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İngilizce(English)

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 Although the exact mechanism of action of ALC (Acetyl-L-Carnitine) is currently unknown, studies indicate that it may be related to its activity on cholinergic neural transmission and ability to enhance neuronal metabolism in the mitochondria. Some researchers attribute the cholinergic effects of ALC to the blocking of post-synaptic inhibition potentials, whereas others suggest a direct synaptic stimulation. Based on the enhanced cellular energetics in the mitochondria, human studies show that ALC has the property to stabilize the cell membrane fluidity through the regulation of sphingomyelin levels, and to provide a substrate reservoir for cellular energy production, thereby preventing excessive neuronal degeneration. ALC has also been shown to increase the hippocampal binding of glucocorticoids and nerve growth factor, to reduce the oxidative stress, and to inhibit the excitotoxicity in brain tissue and CSF, thus preventing cell death and ischemia-induced neuronal damage. Regarding the effects on the peripheral nervous system, the benefits of ALC supplementation in patients with peripheral neuropathies may be attributed to its role in nerve regeneration and protection, as well as to its antioxidant, antiapoptotic, and analgesic activity. PUBLISHED ARTICLES : ** Nutrients. 2020 May 12;12(5):1389.doi: 10.3390/nu12051389. Acetyl-L-Carnitine in Dementia and Other Cognitive Disorders: A Critical Update <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284336/pdf/nutrients-12-01389.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284336/pdf/nutrients-12-01389.pdf</a> ** Dement Neurocogn Disord. 2017 Mar;16(1):26-31.doi: 10.12779/dnd.2017.16.1.26. Epub 2017 Mar 31. Cerebral Perfusion Changes after Acetyl-L-Carnitine Treatment in Early Alzheimer's Disease Using Single Photon Emission Computed Tomography <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6427992/pdf/dnd-16-26.pdf" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6427992/pdf/dnd-16-26.pdf</a> ** Free Radic Biol Med. 2007 Feb 1;42(3):371-84.doi: 10.1016/j.freeradbiomed.2006.11.006. Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and alpha-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: implications for Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808543/pdf/nihms-16915.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808543/pdf/nihms-16915.pdf</a> ** Neurochem Res. 2017 Jun;42(6):1661-1675.doi: 10.1007/s11064-017-2288-7. Epub 2017 May 16.&nbsp; L-Carnitine and Acetyl-L-carnitine Roles and Neuroprotection in Developing Brain <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5621476/pdf/nihms877214.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5621476/pdf/nihms877214.pdf</a> ** PLoS One. 2016 May 19;11(5):e0155694.doi:10.1371/journal.pone.0155694.eCollection 2016. Serum Levels of Acyl-Carnitines along the Continuum from Normal to Alzheimer's Dementia <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4873244/pdf/pone.0155694.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4873244/pdf/pone.0155694.pdf</a> 
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ACETYL-L-CARNITINE 

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 Experiments conducted at the University of Hong Kong (China) have demonstrated the neuroprotective effect of Verbena Officinalis extracts. The studies were conducted in vitro on neurons of the cerebral cortex of rats. The in vitro cultured neurons were treated with an aqueous extract of the plant followed by various toxins such as β-amyloid 25–35 (25 μM for 24 h), tunicamycin (1 μg/mL for 16 h), dithiothreitol (0.5 and 1.0 mM for 16 h), hydrogen peroxide (50 μM for 16 h), and UV radiation (32 kJ/cm 2 for 2 h). The cells were then washed with a new medium. Cell lysates were subjected to a caspase activity assay. Cytotoxic activity was determined based on the level of lactate dehydrogenase (LD) in the harvested media. Measurements of the LD level showed that a verbena herb extract at a concentration of 100 μg/mL reduced the mortality of nerve cells exposed to β-amyloid (Aβ) by 9.1 % and dithiothreitol by 9.8 % (0.5 mM DTT) and 29.6 % (1.0 mM DTT). However, the extract did not protect against the effects of tunicamycin, H2O2 , and UV radiation, which may indicate a weaker effect of the extract against the agents directly damaging DNA. Colorimetric caspase-3-like and caspase-2-like activity assays were used to measure the effect of a verbena extract in doses of 25 to 150 μg/mL. The V. officinalis extract already significantly reduced Aβ-triggered activity at a dose of 75 mg/mL by 1.4 times compared to control conditions. This activity was dose dependent. The results obtained prove that extracts from V. officinalis can potentially be used in the prevention of neurodegenerative diseases, with particular emphasis on Alzheimerʼs disease. Verbenalin, hastatoside, aucubin, swertiamarine, acetoside, isoacteoside, jionoside D, cistanoside F, acacetin-7-O-rutinoside, apigenin-7-O-glucoside, glucosyl-6-pedalitin, and acacetin were used to molecular docking. Verbenalin, swertiamarin, and jionoside D have a good binding effect with NLRP3, which may play a role in the treatment of AD by reducing inflammation. Phenylethanoid glycosides including acetoside&nbsp; and isoacteoside have good docking effects with NLRP3 and BACE1, which may reduce the inflammatory response and inhibit Aβ deposition. Apigenin-7-O-glucoside&nbsp; and glucosyl-6-pedalitin were higher than positive drugs in molecular docking with NLRP3, BACE1, and AChE. Acacetin-7-O-rutinoside has a good binding effect on all four protein targets, which is better than that of apigenin-7-O-glucoside, glucosyl-6-pedalitin. Acacetin also has multi-target effects.&nbsp; Aqueous extracts from Verbena Officinalis have been reported to decrease Aβ-induced neurotoxicity such as neurite shorting and DNA condensation in primary cortical neurons. In a recent study, human neuroblastoma SH-SY5Y cells treated with verbenalin showed neuroprotective properties against Aβ-induced cytotoxicity. Verbenalin,was shown to reduce both the intracellular and extracellular expression of APP, which is a precursor to Aβ. Furthermore, verbenalin markedly reduced Aβ 42 in SweAPP/N2a cells. Numerous investigations have demonstrated that the hippocampus and amygdala, as well as other structures of the medial temporal lobe show significant atrophy as AD progresses. Verbenalin reduced the expression of Aβ and tau in the hippocampus of AD animal models, which was consistent with the results of the in vitro assays. Taken together, these findings suggest that verbenalin can be used as an adjuvant therapy for AD owing to its ability to improve AD pathology associated with Aβ and tau. PUBLISHED ARTICLES : ** BMC Pharmacol Toxicol. 2022 Oct 24;23(1):82.doi: 10.1186/s40360-022-00620-3. Cornin protects against cerebral ischemia/reperfusion injury by preventing autophagy via the PI3K/Akt/mTOR pathway <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9594897/pdf/40360_2022_Article_620.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9594897/pdf/40360_2022_Article_620.pdf</a> ** Basic Clin Neurosci. 2020 Jan-Feb;11(1):91-98.doi: 10.32598/bcn.11.1.3. Epub 2020 Jan 1. Evaluating the Antidepressant Effect of Verbena officinalis L. (Vervain) Aqueous Extract in Adult Rats <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253814/pdf/BCN-11-91.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253814/pdf/BCN-11-91.pdf</a> ** Front Plant Sci. 2022 Aug 4;13:955075.doi: 10.3389/fpls.2022.955075. eCollection 2022. Integrating transcriptome and chemical analyses to reveal the anti-Alzheimer's disease components in Verbena officinalis Linn <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9386363/pdf/fpls-13-955075.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9386363/pdf/fpls-13-955075.pdf</a> ** Saudi J Biol Sci. 2018 Sep;25(6):1170-1177.doi: 10.1016/j.sjbs.2017.10.005. Epub 2017 Oct 13. The protective role of verbenalin in rat model of focal cerebral ischemia reperfusion <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6117236/pdf/main.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6117236/pdf/main.pdf</a> ** Molecules. 2022 Dec 8;27(24):8678.doi: 10.3390/molecules27248678. Verbenalin Reduces Amyloid-Beta Peptide Generation in Cellular and Animal Models of Alzheimer's Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9781082/pdf/molecules-27-08678.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9781082/pdf/molecules-27-08678.pdf</a> 
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VERBENA OFFICINALIS

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 Taurine, 2-aminoethanesulfonic acid, is the second most abundant endogenous amino acid after glutamate in the CNS. The chemical plays multiple roles in the body, including thermoregulation, stabilization of protein folding, anti-inflammation, antioxidation, osmoregulation, calcium homeostasis and CNS development. Previous reports in the literature have revealed a lack of taurine in the brains of Alzheimer’s Disease (AD) patients. Arai et al. reported that postmortem brain tissues of AD patients have low concentrations of taurine in the temporal cortex compared with control patients’ brain tissues. Multiple lines of evidence suggest taurine as a therapeutic agent for AD. Recently, taurine was reported to help improve cognitive function and protect against neuropathology in an animal model of AD. Jakaria et al. reported that taurine displayed therapeutic potential against neurological disorders, including AD. Santa-Maria et al. reported that taurine binds to Aβ plaques with weak antifibrillogenic effects. In addition, intravenously administered taurine prevents Aβ neurotoxicity and cognitive impairment. To date, no reports of the possible side effects of taurine have been documented, and due to its nontoxic properties in the body, taurine has been used in foods. Biologically, taurine plays several crucial roles in the modulation of calcium signaling, osmoregulation, and membrane stabilization. The sulfonic acid group in taurine has been reported to bind to Aβ and prevent glycosaminoglycans (GAGs) from binding to Aβ. In AD patients, amyloid peptide binds to GAGs, causing plaques to accumulate in the brain and destroy neurons. Another clinical study reported that 3-amino-1-propane sulfonic acid (3-APS) was designed as an anti-amyloid therapy and significantly reduces Aβ in the brain. Taurine has structural similarity to 3-APS; therefore, we postulated that taurine would eventually bind Aβ directly to inhibit the interaction of GAGs with amyloid peptide. This series of events is thought to eventually led to downregulation of mGluR5. Many studies in rodents also have demonstrated the effects of taurine on AD. Kim et al. reported that taurine significantly ameliorated hippocampus-related cognitive deficits in an AD mouse model. In another recent study, taurine was reported to bind directly to AβO and consequently ameliorated the behavioral deficiencies of AD, such as the loss of learning and memory. Roberto et al. reported that taurine strongly protected neurons against the neurotoxicity of Aβ in vitro. Thy also demonstrated that taurine prevented neurotoxicity caused by Aβ and glutamate receptor agonists in an in vitro study. However, the studies referenced above were all performed based on ex vivo or behavioral observations rather than changes at the molecular level. The progression of AD begins preferentially with a change at the molecular level, and then clinical symptoms appear due to functional and structural changes in the brain. The novelty of the present study is that the therapeutic effects of taurine on AD were evaluated via functional PET. PUBLISHED ARTICLES : ** Sci Rep. 2020 Sep 23;10(1):15551.doi: 10.1038/s41598-020-72755-4. Evaluation of the neuroprotective effect of taurine in Alzheimer's disease using functional molecular imaging <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511343/pdf/41598_2020_Article_72755.pdf"style="color:blue;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511343/pdf/41598_2020_Article_72755.pdf</a> ** J Immunol Res. 2021 Jul 5;2021:7497185.doi: 10.1155/2021/7497185. eCollection 2021. Neuroprotective Effect of Taurine against Cell Death, Glial Changes, and Neuronal Loss in the Cerebellum of Rats Exposed to Chronic-Recurrent Neuroinflammation Induced by LPS <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8277510/pdf/JIR2021-7497185.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8277510/pdf/JIR2021-7497185.pdf</a> ** Mol Med Rep. 2018 Nov;18(5):4516-4522.doi: 10.3892/mmr.2018.9465. Epub 2018 Sep 6. Protective effects of taurine against inflammation, apoptosis, and oxidative stress in brain injury <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6172387/pdf/mmr-18-05-4516.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6172387/pdf/mmr-18-05-4516.pdf</a> ** Redox Biol. 2019 Jun;24:101223.doi: 10.1016/j.redox.2019.101223. Epub 2019 May 21. Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536745/pdf/main.pdf"style="color:blue;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536745/pdf/main.pdf</a> ** Sci Rep. 2014 Dec 12;4:7467.doi: 10.1038/srep07467. Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264000/pdf/srep07467.pdf"style="color:blue;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264000/pdf/srep07467.pdf</a> ** Stem Cell Res. 2015 May;14(3):369-79.doi: 10.1016/j.scr.2015.04.001. Epub 2015 Apr 10. Taurine increases hippocampal neurogenesis in aging mice <a href="https://www.sciencedirect.com/science/article/pii/S1873506115000434?via%3Dihub"style="color:blue;"target="_blank">https://www.sciencedirect.com/science/article/pii/S1873506115000434?via%3Dihub</a> ** Nutr J. 2021 Jun 8;20(1):53.doi: 10.1186/s12937-021-00712-6. The effects of Taurine supplementation on inflammatory markers and clinical outcomes in patients with traumatic brain injury: a double-blind randomized controlled trial <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8186362/pdf/12937_2021_Article_712.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8186362/pdf/12937_2021_Article_712.pdf</a> 
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TAURINE

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 Schisandra Chinensis (SC) is frequently used in China, Korea, and Japan as a tonic for kidney and a treatment for alleviating various symptoms of cognitive deficits and facilitating learning and memory for thousands of years. Recent experience from clinic and laboratory supported the notion that SC was safe and effective in improving cognitive function and reversing cycloheximide-induced amnesia in rats. And also, lignans like Schizarin A, B, C, D, and E were reported to exhibit the antioxidant activity, and some other lignans like gomisin A, C, D, and G along with gallotannins showed excellent inhibitory effects for AChE in several compounds. The SC extract has the potential to reduce AChE activity and relieve the oxidative damage both in vivo and in vitro. Through the assays in PC12 cells and the Alzheimer disease mouse model induced by scopolamine, SC extract exhibited potent neuroprotective effects linked to antioxidative mechanisms. Moreover, based on the determination activity of AChE, the effects of SC may be partly attributed to its potential to inhibit the activity of AChE. Therefore, SC extract could serve as a multifunctional therapeutic remedy for the treatment of Alzheimer disease. The treatment with SC extract was potentially an effective and simple strategy to improve learning and memory abilities in the elderly and may be a feasible method to prevent the development of Alzheimer disease. PUBLISHED ARTICLES : ** Biomed Pharmacother.2018 Jan;97:958-968.doi: 10.1016/j.biopha.2017.10.145. An overview of neuroprotective and cognitive enhancement properties of lignans from Schisandra chinensis <a href="https://www.sciencedirect.com/science/article/pii/S0753332217346243?via%3Dihub"style="color:blue;"target="_blank">https://www.sciencedirect.com/science/article/pii/S0753332217346243?via%3Dihub</a> ** Molecules. 2018 Apr 10;23(4):870.doi: 10.3390/molecules23040870. Effects of Lignans from Schisandra chinensis Rattan Stems against Aβ1-42-Induced Memory Impairment in Rats and Neurotoxicity in Primary Neuronal Cells <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6017482/pdf/molecules-23-00870.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6017482/pdf/molecules-23-00870.pdf</a> ** Oxid Med Cell Longev. 2022 Jul 11;2022:6362617.doi: 10.1155/2022/6362617. eCollection 2022. Explore the Therapeutic Composition and Mechanism of Schisandra chinensis-Acorus tatarinowii Schott on Alzheimer's Disease by Using an Integrated Approach on Chemical Profile, Network Pharmacology, and UPLC-QTOF/MS-Based Metabolomics Analysis <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9293517/pdf/OMCL2022-6362617.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9293517/pdf/OMCL2022-6362617.pdf</a> ** Evid Based Complement Alternat Med. 2020 Feb 20;2020:2804849.doi: 10.1155/2020/ 2804849. In Vitro and In Vivo Anti-AChE and Antioxidative Effects of Schisandra chinensis Extract: A Potential Candidate for Alzheimer's Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053447/pdf/ECAM2020-2804849.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053447/pdf/ECAM2020-2804849.pdf</a> ** Indian J Pharmacol.2020 Mar-Apr;52(2):94-101.doi:10.4103/ijp.IJP_515_19.Epub 2020 Jun 3 Network pharmacology-based study on the mechanism of Schisandra chinensis for treating Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282681/"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282681/</a> ** J Ethnopharmacol.2019 Jun 12;237:354-365.doi:10.1016/j.jep.2019.02.046.Epub 2019 Mar 4. Polysaccharide of Schisandra Chinensis Fructus ameliorates cognitive decline in a mouse model of Alzheimer's disease <a href="https://www.sciencedirect.com/science/article/abs/pii/S037887411833839X?via%3Dihub"style="color:blue;"target="_blank">https://www.sciencedirect.com/science/article/abs/pii/S037887411833839X?via%3Dihub</a> ** Int J Mol Sci. 2018 Jul 6;19(7):1970.doi: 10.3390/ijms19071970. Schisandra chinensis Fructus and Its Active Ingredients as Promising Resources for the Treatment of Neurological Diseases <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073455/pdf/ijms-19-01970.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073455/pdf/ijms-19-01970.pdf</a> ** Molecules. 2019 Mar 27;24(7):1203.doi: 10.3390/molecules24071203. Systematically Characterize the Anti-Alzheimer's Disease Mechanism of Lignans from S. chinensis based on In-Vivo Ingredient Analysis and Target-Network Pharmacology Strategy by UHPLC⁻Q-TOF-MS <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6480032/pdf/molecules-24-01203.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6480032/pdf/molecules-24-01203.pdf</a> ** PLoS One. 2016 Apr 1;11(4):e0152772.doi: 10.1371/journal.pone.0152772. eCollection 2016. Total Lignans of Schisandra chinensis Ameliorates Aβ1-42-Induced Neurodegeneration with Cognitive Impairment in Mice and Primary Mouse Neuronal Cells <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818042/pdf/pone.0152772.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818042/pdf/pone.0152772.pdf</a> 
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SCHISANDRA CHINENSIS

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 Salvia plants are a rich source of polyphenol compounds with over 160 identified polyphenols, comprising an array of phenolic acids and flavonoids. These phenolic compounds include caffeic acid and its derivatives, rosmarinic acid, salvianolic acids, sage-coumarin, lithospermic acids, sagernic acid, and yunnaneic acids. The most prevalent flavonoids include luteolin, apigenin, hispidulin, kaempferol and quercetin. Salvia Miltiorrhiza has been shown to protect mice from Ab-induced neurotoxicity by inhibiting increases in tumour necrosis factor-a (TNF-a), interleukin-6 (IL-6) levels and acetylcholinesterase (AChE) activity. Tanshinones from Salvia Miltiorrhiza can also protect against Ab-induced toxicity by ameliorating mRNA expression of inducible nitric oxide synthase (iNOS), matrix metalloproteinase 2 and nuclear transcription factor-j. In mice exposed to an acute injection of Ab, rosmarinic acid also prevented Ab-induced nitration of proteins (an indirect indicator of peroxynitrite damage) in the hippocampus. Rosmarinic acid also prevented memory impairments induced by Ab toxicity. Protective effects from Ab toxicity have also been observed following the administration of the Salvia constituents, salvianolic acid, carnosic acid and quercetin. In vitro and animal studies have revealed that several Salvia species and their constituents are effective AChE inhibitors. The active constituents, rosmarinic acid, carnosic acid and quercetin, found in several Salvia species can also inhibit AChE activity. In one study, the administration of Salvia Miltiorrhiza to mice mitigated Ab-induced reductions in BDNF. Rosmarinic acid also protected against memory deficits induced by cerebral artery occlusion in mice. PUBLISHED ARTICLES : ** Chin Med. 2019 May 21;14:19. doi: 10.1186/s13020-019-0242-0.eCollection 2019. The effects of bioactive components from the rhizome of Salvia miltiorrhiza (Danshen) on the characteristics of Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528372/pdf/13020_2019_Article_242.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528372/pdf/13020_2019_Article_242.pdf</a> ** Medicine (Baltimore). 2020 Sep 4;99(36):e21924. doi: 10.1097/MD.0000000000021924.&nbsp; Salvia miltiorrhiza improves Alzheimer's disease: A protocol for systematic review and meta-analysis <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7478559/pdf/medi-99-e21924.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7478559/pdf/medi-99-e21924.pdf</a> ** J Neuroinflammation. 2020 Oct 14;17(1):302. doi: 10.1186/s12974-020-01981-4.&nbsp; Tanshinone IIA attenuates neuroinflammation via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7559789/pdf/12974_2020_Article_1981.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7559789/pdf/12974_2020_Article_1981.pdf</a> ** Bioorg Med Chem Lett. 2014 Feb 1;24(3):708-16.doi:10.1016/j.bmcl.2013.12.042. Epub 2013 Dec 18. Danshen diversity defeating dementia <a href="https://www.sciencedirect.com/science/article/pii/S0960894X13014145?via%3Dihub"style="color:blue;"target="_blank">https://www.sciencedirect.com/science/article/pii/S0960894X13014145?via%3Dihub</a> ** Oxid Med Cell Longev. 2019 Jun 24;2019:3281260.doi:10.1155/2019/3281260.eCollection 2019. Current Progress of Research on Neurodegenerative Diseases of Salvianolic Acid B <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612994/pdf/OMCL2019-3281260.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612994/pdf/OMCL2019-3281260.pdf</a> ** Int J Mol Sci. 2018 Feb 3;19(2):458. doi: 10.3390/ijms19020458. Molecular Pharmacology of Rosmarinic and Salvianolic Acids: Potential Seeds for Alzheimer's and Vascular Dementia Drugs <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855680/pdf/ijms-19-00458.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855680/pdf/ijms-19-00458.pdf</a> ** Molecules. 2022 Jul 12;27(14):4463.doi: 10.3390/molecules27144463.&nbsp; A Novel Based-Network Strategy to Identify Phytochemicals from Radix Salviae Miltiorrhizae (Danshen) for Treating Alzheimer's Disease&nbsp; <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9317794/pdf/molecules-27-04463.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9317794/pdf/molecules-27-04463.pdf</a> ** J Biol Res (Thessalon). 2019 Nov 12;26:15.doi:10.1186/s40709-019-0102-1.eCollection 2019 Dec.&nbsp; Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6852914/pdf/40709_2019_Article_102.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6852914/pdf/40709_2019_Article_102.pdf</a> 
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SALVIA OFFICINALIS

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 The salidroside content contributes a lot to the properties of Rhodiola, and is the main active bioactive component in Rhodiola rosea. A number of studies have revealed that salidroside exhibits neuroprotective activities, including anti-Alzheimer’s disease, anti-Parkinson’s disease, anti-Huntington’s disease, anti-stroke, anti-depressive effects, and anti-traumatic brain injury; it is also useful for improving cognitive function, treating addiction, and preventing epilepsy. The mechanisms underlying the potential protective effects of salidroside involvement are the regulation of oxidative stress response, inflammation, apoptosis, hypothalamus-pituitary-adrenal axis, neurotransmission, neural regeneration, and the cholinergic system. Being free of side effects makes salidroside potentially attractive as a candidate drug for the treatment of neurological disorders. It is evident from the available published literature that salidroside has potential use as a beneficial therapeutic medicine with high efficacy and low toxicity to the central nervous system. An in vitro study in Aβ1–42-induced AD PC12 cell lines determined that salidroside reduced cytotoxicity, attenuated reactive oxygen species (ROS) accumulation, and decreased intracellular malondialdehyde by activating antioxidant enzymes in a dose-dependent manner after 3 h pre-incubation with salidroside (1, 5, 10, and 50 mg/mL). Furthermore, pretreatment with salidroside (10, 50, and 100 μM) was shown to significantly inhibit oxidative stress and apoptosis in Aβ25–35-induced SH-SY5Y cells in a concentration-dependent manner in vitro via increasing antioxidant enzyme activities, modulating apoptosis-related protein expression, and restoring anomalies in the mitochondrial membrane potential (MMP) and ROS production. In addition, it was found that salidroside (5, 100, and 200 μM) decreased Aβ levels in Aβ1–42-incubated primary neurons via PI3K/Akt/mTOR signaling. Salidroside (2, 6, and 20 μM) also improved both the longevity and locomotor activity of Tao transgenic Drosophila in a dose-dependent manner. These studies revealed that the protective effects of salidroside were due to the up-regulation of total p-GSK3β and down-regulation of p-tau. PUBLISHED ARTICLES : ** Aging Dis. 2019 Feb 1;10(1):134-146.doi:10.14336/AD.2018.0511.eCollection 2019 Feb. Rosenroot (Rhodiola): Potential Applications in Aging-related Diseases <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345333/pdf/ad-10-1-134.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345333/pdf/ad-10-1-134.pdf</a> ** PLoS One. 2012;7(1):e29641.doi: 10.1371/journal.pone.0029641. Epub 2012 Jan 3. Protective effects of a Rhodiola crenulata extract and salidroside on hippocampal neurogenesis against streptozotocin-induced neural injury in the rat <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3250459/pdf/pone.0029641.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3250459/pdf/pone.0029641.pdf</a> ** Front Pharmacol. 2021 Nov 5;12:736198.doi: 10.3389/fphar.2021.736198. eCollection 2021. Preclinical Evidence and Possible Mechanisms of Rhodiola rosea L. and Its Components for Ischemic Stroke: A Systematic Review and Meta-Analysis <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8602078/pdf/fphar-12-736198.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8602078/pdf/fphar-12-736198.pdf</a> ** Drug Des Devel Ther. 2018 May 24;12:1479-1489.doi: 10.2147/DDDT.S160776. Pharmacological activities, mechanisms of action, and safety of salidroside in the central nervous system <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973445/pdf/dddt-12-1479.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973445/pdf/dddt-12-1479.pdf</a> ** Front Aging Neurosci. 2022 Jan 21;13:809433.doi: 10.3389/fnagi.2021.809433. eCollection 2021. Salidroside Ameliorates Alzheimer's Disease by Targeting NLRP3 Inflammasome-Mediated Pyroptosis <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8814655/pdf/fnagi-13-809433.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8814655/pdf/fnagi-13-809433.pdf</a> ** Chin Med. 2022 Jul 4;17(1):82.doi: 10.1186/s13020-022-00634-3. Salidroside attenuates neuronal ferroptosis by activating the Nrf2/HO1 signaling pathway in Aβ1-42-induced Alzheimer's disease mice and glutamate-injured HT22 cells <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9254541/pdf/13020_2022_Article_634.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9254541/pdf/13020_2022_Article_634.pdf</a> ** Cell Biosci. 2022 Nov 4;12(1):180.doi: 10.1186/s13578-022-00918-z. Salidroside reduces neuropathology in Alzheimer's disease models by targeting NRF2/SIRT3 pathway <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9636768/pdf/13578_2022_Article_918.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9636768/pdf/13578_2022_Article_918.pdf</a> 
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RHODIOLA ROSEA

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 The clearance of neurotoxic amyloid beta (Aβ) remains one of the leading challenges to Alzheimer’s research. Mitochondrial damage mediated oxidative stress has been implicated in the progression of many neurodegenerative diseases including Alzheimer’s Disease. Studies have shown that Resveratrol (RSV) can quench the free radicals-mediated elevated oxidative stress though SIRT1 to maintain via cellular homeostasis in various experimental models. There are persuasive evidences suggesting that RSV can relieve the pathological gripe of amyloid plaques and facilitate attenuation of the expression of BACE1 which is the rate limiting enzyme involved in the production of amyloid plaques. As a result, the neuroprotective potential of RSV in association with SIRT1 pathway is widely being considered in the treatment protocol for Alzheimer’s Disease. Among the natural compounds, RSV has its own place in attracting many researchers to work on its therapeutic applications in AD like condition. Studies have shown that RSV can repress the levels of oxidative stress and free radicals that could mimic the action of caloric restriction (CR) and it increases the expression of genes like AMPK and SIRT1 to maintain homeostasis in animals. Although unmodified RSV appears to have a weak bioavailability, several studies have clearly demonstrated the in vivo neuroprotective properties of the red wine derived polyphenols, strongly supporting the notion that natural metabolites of RSV may have biological activities. Furthermore, recent findings have shed light on the potential role of RSV in transcription and degradation-dependent antiamyloidogenic mechanisms, suggesting that natural metabolites or potent synthetic analogues of RSV may have a therapeutic potential in preventing and/or treating Alzheimer’s Disease. PUBLISHED ARTICLES : ** Front Biosci (Landmark Ed). 2018 Mar 1;23(7):1380-1390.doi: 10.2741/4650. Biophysical interaction of resveratrol with sirtuin pathway: Significance in Alzheimer's disease <a href="https://www.imrpress.com/journal/FBL/23/7/10.2741/4650"style="color:blue;"target="_blank">https://www.imrpress.com/journal/FBL/23/7/10.2741/4650</a> ** Front Aging Neurosci. 2014 Sep 11;6:218.doi: 10.3389/fnagi.2014.00218. Neuroprotective effects of resveratrol in Alzheimer disease pathology <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161050/pdf/fnagi-06-00218.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161050/pdf/fnagi-06-00218.pdf</a> ** Oxid Med Cell Longev. 2018 Oct 30;2018:8152373.doi: 10.1155/2018/8152373. eCollection 2018. Neuroprotective Mechanisms of Resveratrol in Alzheimer's Disease: Role of SIRT1 <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6232815/pdf/OMCL2018-8152373.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6232815/pdf/OMCL2018-8152373.pdf</a> ** Front Pharmacol. 2020 Dec 30;11:619024.doi: 10.3389/fphar.2020.619024. eCollection 2020. Resveratrol and Neuroprotection: Impact and Its Therapeutic Potential in Alzheimer's Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804889/pdf/fphar-11-619024.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804889/pdf/fphar-11-619024.pdf</a> ** Biomed Res Int. 2014;2014:350516.doi: 10.1155/2014/350516. Epub 2014 Nov 26. Resveratrol as a therapeutic agent for Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261550/pdf/BMRI2014-350516.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261550/pdf/BMRI2014-350516.pdf</a> ** Front Aging Neurosci. 2020 Apr 17;12:103.doi: 10.3389/fnagi.2020.00103. eCollection 2020. Resveratrol Derivatives as Potential Treatments for Alzheimer's and Parkinson's Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7180342/pdf/fnagi-12-00103.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7180342/pdf/fnagi-12-00103.pdf</a> ** Ann N Y Acad Sci. 2017 Sep;1403(1):142-149.doi: 10.1111/nyas.13431. Resveratrol for Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664214/pdf/nihms885948.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664214/pdf/nihms885948.pdf</a> ** J Neuroinflammation. 2017 Jan 3;14(1):1.doi: 10.1186/s12974-016-0779-0. Resveratrol regulates neuro-inflammation and induces adaptive immunity in Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5234138/pdf/12974_2016_Article_779.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5234138/pdf/12974_2016_Article_779.pdf</a> ** Int J Mol Sci. 2021 Apr 28;22(9):4628.doi: 10.3390/ijms22094628. Resveratrol, Metabolic Dysregulation, and Alzheimer's Disease: Considerations for Neurogenerative Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8125227/pdf/ijms-22-04628.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8125227/pdf/ijms-22-04628.pdf</a> ** Ageing Res Rev. 2021 May;67:101271.doi: 10.1016/j.arr.2021.101271. Epub 2021 Feb 8. The pleiotropic neuroprotective effects of resveratrol in cognitive decline and Alzheimer's disease pathology: From antioxidant to epigenetic therapy <a href="https://www.sciencedirect.com/science/article/pii/S1568163721000180?via%3Dihub"style="color:blue;"target="_blank">https://www.sciencedirect.com/science/article/pii/S1568163721000180?via%3Dihub</a> 
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RESVERATROL

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 Polygala Tenuifolia Willd. (Polygalaceae), also known as Yuan Zhi, has been reported to be enriched with triterpene saponins, onjisaponins and polygalasaponins (Jin et al. 2014), and it also exhibits protective effects on the central nervous system and is frequently used to treat memory dysfunction, insomnia and neurasthenia (Zhang et al. 2016). As the main pharmacologically active components of P. tenuifolia, polygalasaponins, including polygalasaponin XXXII (PGS 32), tenuifolin, polygalacic acid and senegenin (tenuigenin), have been shown to possess multiplex neuroprotective potential associated with Alzheimer’s Disease, such as anti-b-amyloid (Ab) aggregation (Jia et al. 2004; Park et al. 2019), anti-Tau (Xu et al. 2012), anti-inflammation (Cheong et al. 2011; Wang et al. 2017), antioxidant (Zhang et al. 2011), enhancing central cholinergic system, anti-neuronal apoptosis (Li et al. 2015), promote neuronal proliferation (Park et al. 2008; Zhu et al. 2016). PUBLISHED ARTICLES : ** BMC Complement Med Ther. 2021 Oct 25;21(1):267.doi: 10.1186/s12906-021-03437-5. Active constituent of Polygala tenuifolia attenuates cognitive deficits by rescuing hippocampal neurogenesis in APP/PS1 transgenic mice <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8543956/pdf/12906_2021_Article_3437.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8543956/pdf/12906_2021_Article_3437.pdf</a> ** Biol Pharm Bull. 2006 Sep;29(9):1892-6.doi: 10.1248/bpb.29.1892. Characterization of anti-neurodegenerative effects of Polygala tenuifolia in Abeta(25-35)-treated cortical neurons <a href="https://www.jstage.jst.go.jp/article/bpb/29/9/29_9_1892/_pdf/-char/en"style="color:blue;"target="_blank">https://www.jstage.jst.go.jp/article/bpb/29/9/29_9_1892/_pdf/-char/en</a> ** Biol Pharm Bull. 2004 Jul;27(7):1081-5.doi: 10.1248/bpb.27.1081. Cognitive improving and cerebral protective effects of acylated oligosaccharides in Polygala tenuifolia <a href="https://www.jstage.jst.go.jp/article/bpb/27/7/27_7_1081/_pdf/-char/en"style="color:blue;"target="_blank">https://www.jstage.jst.go.jp/article/bpb/27/7/27_7_1081/_pdf/-char/en</a> ** Evid Based Complement Alternat Med. 2014;2014:392324.doi: 10.1155/2014/392324. Epub 2014 Mar 12. Memory-Enhancing Effects of the Crude Extract of Polygala tenuifolia on Aged Mice <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972950/pdf/ECAM2014-392324.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972950/pdf/ECAM2014-392324.pdf</a> ** Brain Circ. 2018 Jan-Mar;4(1):24-32.doi: 10.4103/bc.bc_2_17. Epub 2018 Apr 18. Neuroprotective effects of tenuigenin on neurobehavior, oxidative stress, and tau hyperphosphorylation induced by intracerebroventricular streptozotocin in rats <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057698/pdf/BC-4-24.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057698/pdf/BC-4-24.pdf</a> ** Pharm Biol. 2020 Dec;58(1):410-416.doi: 10.1080/13880209.2020.1758732. Polygala tenuifolia: a source for anti-Alzheimer's disease drugs <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301717/pdf/IPHB_58_1758732.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301717/pdf/IPHB_58_1758732.pdf</a> ** Acta Pharmacol Sin. 2009 Sep;30(9):1211-9.doi: 10.1038/aps.2009.112. Epub 2009 Aug 17. Polygalasaponin XXXII from Polygala tenuifolia root improves hippocampal-dependent learning and memory <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007183/pdf/aps2009112a.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007183/pdf/aps2009112a.pdf</a> ** Front Psychiatry. 2021 Dec 17;12:688703.doi: 10.3389/fpsyt.2021.688703. Protective Effects and Mechanism of Radix Polygalae Against Neurological Diseases as Well as Effective Substance <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8719339/pdf/fpsyt-12-688703.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8719339/pdf/fpsyt-12-688703.pdf</a> ** PLoS One. 2012;7(9):e45575.doi: 10.1371/journal.pone.0045575. Epub 2012 Sep 21. Senegenin attenuates hepatic ischemia-reperfusion induced cognitive dysfunction by increasing hippocampal NR2B expression in rats <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448627/pdf/pone.0045575.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448627/pdf/pone.0045575.pdf</a> ** BMC Complement Altern Med. 2016 Jan 23;16:26.doi: 10.1186/s12906-016-1006-3. The neuritogenic and neuroprotective potential of senegenin against Aβ-induced neurotoxicity in PC 12 cells <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724108/pdf/12906_2016_Article_1006.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724108/pdf/12906_2016_Article_1006.pdf</a> 
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POLYGALA TENUIFOLIA 

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 Three-dimensional HPLC analysis revealed that a water extract of the herb contained several different chemical compounds including 1,2,3,4,6-penta-O-galloyl-β-d-glucopyranose (PGG). No obvious adverse/toxic were found following treatment with PGG. As was observed with Paeonia suffruticosa, PGG alone inhibited Aβ fibril formation and destabilized pre-formed Aβ fibrils in vitro and in vivo. Our results suggest that both Paeonia suffruticosa and its active constituent PGG have strong inhibitory effects on formation of Aβ fibrils in vitro and in vivo. PGG is likely to be a safe and promising lead compound in the development of disease-modifying drugs to prevent and/or cure Alzheimer’s Disease. PGG inhibited Aβ oligomerization in experiments,. Moreover, treatment of SK-N-SH cells with PGG significantly protected the cells from Aβ1–42 toxicity at concentrations similar to those that inhibited Aβ aggregation. PGG inhibited not only Aβ fibril formation but also neurotoxic Aβ oligomer formation. Furthermore, oral intake of PGG reduced Aβ plaque burden and Aβ peptide content in brain tissue from Tg2576 mice, as did like Paeonia suffruticosa. The decrease in Aβ plaques and Aβ peptide content in brain tissue from Tg2576 mice by PGG may be caused by destabilization of Aβ fibrils. Paeonia suffruticosa seed coat extracts (PSCE) and its 10 stilbenes display good inhibition of AChE and BuChE activities and significantly increase the viability of normal and OGD/R-injured PC12 cells. PSCE improves the cognitive performance of scopolamine-treated mice in behavioural tests. Meanwhile, PSCE increases AChE, ChAT, SOD, and CAT activities and ACh, GSH, IL-4 levels, and decreases IL-1β, IL-6, TNF-α levels in the model animals.&nbsp; Studies demonstrated that paeonol treatment can protect against many of the biochemical, morphological and behavioral changes resulting from amyloid-β administration in a rat model of Alzheimer’s disease. The results suggest that paeonol is a potential therapeutic agent in slowing down the pathogenic processes associated with the disease. A study conducted on ICR mice (albino mice) in a D-galactose assay injected subcutaneously for 60 days at a dose of 50 mg/kg/day showed that paeonol at 50 and 100 mg/kg, together with D-galactose, increased acetylcholine and glutathione levels, restored superoxide dismutase activity and Na+/K+-ATPase levels, and decreased MDA levels and cholinesterase activity. In addition, paeonol alleviated neuronal damage in both the hippocampus and temporal cortex. It was also confirmed that 1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose inhibits the formation and destabilizes the pre-formation of amyloid-β fibrils in in vitro and in vivo models.&nbsp; PUBLISHED ARTICLES : ** Evid Based Complement Alternat Med. 2012;2012:932823.doi: 10.1155/2012/932823.Epub 2012 Mar 13. Paeonol Protects Memory after Ischemic Stroke via Inhibiting β-Secretase and Apoptosis <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312264/pdf/ECAM2012-932823.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312264/pdf/ECAM2012-932823.pdf</a> ** J Oleo Sci. 2021 Aug 5;70(8):1133-1146.doi: 10.5650/jos.ess21040. Epub 2021 Jul 9. Enzyme-assisted Solvent Extraction of High-yield Paeonia suffruticosa Andr. Seed Oil and Fatty Acid Composition and Anti-Alzheimer's Disease Activity <a href="https://www.jstage.jst.go.jp/article/jos/70/8/70_ess21040/_pdf/-char/en"style="color:blue;"target="_blank">https://www.jstage.jst.go.jp/article/jos/70/8/70_ess21040/_pdf/-char/en</a> ** Molecules. 2022 Apr 29;27(9):2829.doi: 10.3390/molecules27092829. Chemical Diversity and Potential Target Network of Woody Peony Flower Essential Oil from Eleven Representative Cultivars ( Paeonia × suffruticosa Andr.) <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9102020/pdf/molecules-27-02829.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9102020/pdf/molecules-27-02829.pdf</a> ** Front Pharmacol. 2022 Aug 12;13:952876.doi:10.3389/fphar.2022.952876.eCollection 2022. Integrating network pharmacology analysis and pharmacodynamic evaluation for exploring the active components and molecular mechanism of moutan seed coat extract to improve cognitive impairment <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9411852/pdf/fphar-13-952876.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9411852/pdf/fphar-13-952876.pdf</a> ** J Neurochem. 2009 Jun;109(6):1648-57.doi:10.1111/j.1471-4159.2009.06069.x.Epub 2009 May 7. A traditional medicinal herb Paeonia suffruticosa and its active constituent 1,2,3,4,6-penta-O-galloyl-beta-D-glucopyranose have potent anti-aggregation effects on Alzheimer's amyloid beta proteins in vitro and in vivo <a href="https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1471-4159.2009.06069.x"style="color:blue;"target="_blank">https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1471-4159.2009.06069.x</a> ** Evid Based Complement Alternat Med. 2016;2016:3704647. doi: 10.1155/2016/3704647. Epub 2016 Dec 22.&nbsp; Neuroprotective Effect of Paeonol Mediates Anti-Inflammation via Suppressing Toll-Like Receptor 2 and Toll-Like Receptor 4 Signaling Pathways in Cerebral Ischemia-Reperfusion Injured Rats <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5215131/pdf/ECAM2016-3704647.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5215131/pdf/ECAM2016-3704647.pdf</a> ** J Integr Neurosci. 2021 Dec 30;20(4):1001-1010. doi: 10.31083/j.jin2004101.&nbsp; Paeonol administration alleviates cognitive deficits and attenuates neural pathological changes in APP/PS1 mice <a href="https://www.imrpress.com/journal/JIN/20/4/10.31083/j.jin2004101"style="color:blue;"target="_blank">https://www.imrpress.com/journal/JIN/20/4/10.31083/j.jin2004101</a> ** Molecules. 2015 Jan 14;20(1):1304-18.doi: 10.3390/molecules20011304.&nbsp; Synthesis and evaluation of paeonol derivatives as potential multifunctional agents for the treatment of Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6272137/pdf/molecules-20-01304.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6272137/pdf/molecules-20-01304.pdf</a> ** PLoS One. 2017 Sep 21;12(9):e0185102.doi:10.1371/journal.pone.0185102.eCollection 2017.&nbsp; Novel derivative of Paeonol, Paeononlsilatie sodium, alleviates behavioral damage and hippocampal dendritic injury in Alzheimer's disease concurrent with cofilin1/phosphorylated-cofilin1 and RAC1/CDC42 alterations in rats <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608314/pdf/pone.0185102.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608314/pdf/pone.0185102.pdf</a> 
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PAEONIA SUFFRUTICOSA

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 Magnesium is one of the most abundant cations in the intracellular environment after potassium. Mg2+ is tightly regulated and kept at basal levels by normal Mg2+ intake, absorption, and metabolism under physiological conditions. Total magnesium levels in the hippocampus of AD patients decreased by 18% compared with that of normal subjects. Although the presence of magnesium deficiency in patients with AD is notable, its severity may be underestimated. The concentration of serum Mg2+ in healthy people ranges from 0.70 mM to 1.05 mM. Mg2+ deficiency is generally determined by measuring the total serum Mg2+ concentration, but it cannot accurately reflect the concentration of magnesium in the human body. Most Mg2+ is stored in bone, muscle, and soft tissue, and the proportion of serum Mg2+ is very low. Even if the human body is in a serious state of Mg2+ depletion, serum magnesium may also be in the normal range. Although the magnesium concentration in AD patients is reduced, the degree of deficiency cannot be accurately evaluated. It is not only difficult to evaluate magnesium deficiency, but also a reasonable supplement of magnesium. Slutsky et al found that following long-term magnesium supplementation, Mg2+ concentration in cerebrospinal fluid only increases by 15%. On one hand, systemic magnesium is closely regulated by renal function. On the other hand, the blood-brain barrier separates the brain from the daily fluctuations of blood magnesium. Hippocampal synapses are very sensitive to small changes in extracellular Mg2+ concentration (increasing the concentration of magnesium by 15% can increase the synaptic density by 50%). Encouragingly, compared with other Mg2+ compounds (such as magnesium chloride, magnesium citrate, and magnesium gluconate), dietary intake of magnesium L-threonate could significantly increase Mg2+ levels in the brain. Therefore, restoring brain magnesium may be a potential way to treat cognitive impairment in patients with AD.&nbsp; PUBLISHED ARTICLES : ** In: Magnesium in the Central Nervous System [Internet]. Adelaide (AU): University of Adelaide Press; 2011. Magnesium in Alzheimer’s disease <a href="https://www.ncbi.nlm.nih.gov/books/NBK507264/pdf/Bookshelf_NBK507264.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/books/NBK507264/pdf/Bookshelf_NBK507264.pdf</a> ** Nutrients. 2018 Jun 6;10(6):730.doi: 10.3390/nu10060730. The Role of Magnesium in Neurological Disorders <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024559/pdf/nutrients-10-00730.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024559/pdf/nutrients-10-00730.pdf</a> ** World J Psychiatry. 2022 Sep 19;12(9):1261-1263.doi: 10.5498/wjp.v12.i9.1261. Magnesium may be an effective therapy for Alzheimer's disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9521536/pdf/WJP-12-1261.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9521536/pdf/WJP-12-1261.pdf</a> ** Int J Mol Sci. 2022 Dec 23;24(1):223.doi: 10.3390/ijms24010223. Magnesium and the Brain: A Focus on Neuroinflammation and Neurodegeneration <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9820677/pdf/ijms-24-00223.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9820677/pdf/ijms-24-00223.pdf</a> ** Front Hum Neurosci. 2013 Oct 29;7:735.doi: 10.3389/fnhum.2013.00735. The role of iron-induced fibrin in the pathogenesis of Alzheimer's disease and the protective role of magnesium <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810650/pdf/fnhum-07-00735.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810650/pdf/fnhum-07-00735.pdf</a> ** CNS Neurosci Ther. 2018 Jan;24(1):70-79.doi: 10.1111/cns.12775. Epub 2017 Nov 10. Magnesium boosts the memory restorative effect of environmental enrichment in Alzheimer's disease mice <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489792/pdf/CNS-24-70.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489792/pdf/CNS-24-70.pdf</a> 
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MAGNESIUM 

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 It is suggested that isoquercetin suppressed reactive oxygen species (ROS) and Lactate dehydrogenase (LDH) release in hippocampal neurons, via the regulation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2‑mediated) nuclear factor erythroid 2‑related factor 2 (Nrf2)&nbsp; expression, which may provide a useful strategy for the moderation of neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease. It acts as a selective SIRT6 activator since it only binds to the SIRT6-selective acyl binding channel through its ability to distinguish between the SIRT6-selective acyl binding channel and an alternative binding site at the entrance of the active binding site of SIRT6. Furthermore, an isoform selectivity study of isoquercetin revealed that the bulky sugar moiety accommodates SIRT6’s acyl channel. Isoquercetin has been reported to exert its cytotoxic/anticancer activity by inhibiting protein kinase B phopsphorylation, and thus surviving protein activates caspases and reduces anti-apoptotic proteins, i.e., Bcl-2 and Mcl-1. PUBLISHED ARTICLES : ** Exp Ther Med. 2017 Apr;13(4):1353-1359.doi: 10.3892/etm.2017.4093. Epub 2017 Jan 31. Isoquercetin activates the ERK1/2-Nrf2 pathway and protects against cerebral ischemia-reperfusion injury in vivo and in vitro <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377244/pdf/etm-13-04-1353.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377244/pdf/etm-13-04-1353.pdf</a> ** Cell J. 2021 Aug;23(3):355-365.doi: 10.22074/cellj.2021.7116. Epub 2021 Jul 17. Neuroprotective Effects of Isoquercetin: An In Vitro and In Vivo Study <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8286454/pdf/Cell-J-23-355.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8286454/pdf/Cell-J-23-355.pdf</a> ** Eur Rev Med Pharmacol Sci. 2022 Dec;26(23):8700-8712.doi: 10.26355/eurrev_202212_30541. Effect of quercetin glycosides on cognitive functions and cerebral blood flow: a randomized, double-blind, and placebo-controlled study <a href="https://www.europeanreview.org/wp/wp-content/uploads/8700-8712.pdf"style="color:blue;"target="_blank">https://www.europeanreview.org/wp/wp-content/uploads/8700-8712.pdf</a> ** Int J Mol Sci. 2021 Apr 17;22(8):4180.doi: 10.3390/ijms22084180. A Comprehensive Analysis into the Therapeutic Application of Natural Products as SIRT6 Modulators in Alzheimer's Disease, Aging, Cancer, Inflammation, and Diabetes <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8073883/pdf/ijms-22-04180.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8073883/pdf/ijms-22-04180.pdf</a> 
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ISOQUERCETIN

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 The anti-anxiety and mild anti-depression property of Ginkgo Biloba Extract is due to reversible inhibition of the two enzymes MAOA and MAOB. The antioxidant, anti-inflammatory and neuroprotective effects mainly contribute to the flavonoid and terpenoid content in Ginkgo Biloba Extract. Alkaloid ketones, amino acids, cyanogenic glycosides and phenols, which are abundant in this plant extract, are the active ingredients responsible for its therapeutic effects. Ginkgo Biloba Extract has positive effects on psychosis, anxiety, schizophrenia and depression. It stimulates cerebral blood circulation and improves problems caused by failure of blood circulation in the brain such as anxiety, stress, poor memory, hearing problems, poor concentration, thinking, social behavior and dementia in Alzheimer's disease. Besides its free radical scavenging properties, it has also been shown to affect the transcription of several genes associated with oxidative stress regulation. Several recent studies have shown that Ginkgo Biloba Extract protects against Aβ-induced neurotoxicity by inhibiting Aβ-induced events such as glucose uptake, reactive oxygen species (ROS) accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis. . Since AβPP processing and amyloidogenesis are hypothesized to be affected by free circulating and intracellular cholesterol levels, Ginkgo Biloba Extract has been reported to inhibit Aβ production in the brain by lowering circulating free cholesterol levels. Ginkgo Biloba Extract may also interfere with Aβ oligomer formation. It is well established that the β-sheet structure of Aβ oligomers is primarily responsible for Aβ neurotoxicity and may also aid in clearance of Aβ via proteolytic cleavage. Therefore, inhibiting the formation of the β-sheet structure of Aβ oligomers may be the main strategy to prevent Aβ toxicity. Ginkgo Biloba Extract has iron chelating properties that can also inhibit Aβ fibril formation. Ginkgo Biloba Extract can also prevent Aβ fibril formation by increasing transthyretin gene expression. The anti-Aβ effect of Ginkgo Biloba Extract on Aβ aggregation was also observed with the flavonoid compounds, ginkgolide J and bilobalide. It has also been shown that Ginkgo Biloba Extract regulates mitochondrial oxidative phosphorylation (OXPHOS) against Aβ-induced oxidative stress, thus helping to maintain the ROS/RNS (reactive oxygen species/reactive nitrogen species) balance in cells. Studies show that Ginkgo Biloba Extract provides beneficial effects on cellular OXPHOS function, thereby helping to improve mitochondrial function against Aβ-induced toxicity. The antioxidant activity in Ginkgo Biloba Extract is related to flavonoid components such as kaempferol and quercetin, which suppress ROS in the body in both in vitro and in vivo models. The flavonoid fraction is directly responsible for the antioxidant effect through ROS scavenging, chelation of pro-oxidative heavy metal ions, and increased expression of antioxidant proteins such as superoxide dismutase (SOD) and glutathione reductase (GSH).&nbsp; PUBLISHED ARTICLES : ** CNS Neurosci Ther. 2019 Feb;25(2):288-298.doi: 10.1111/cns.13095. Treatment of dementia and mild cognitive impairment with or without cerebrovascular disease: Expert consensus on the use of Ginkgo Biloba Extract, EGb 761® <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488894/pdf/CNS-25-288.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488894/pdf/CNS-25-288.pdf</a> ** Front Pharmacol. 2021 Nov 4;12:775034.doi: 10.3389/fphar.2021.775034. eCollection 2021. The Use of Ginkgo Biloba L. as a Neuroprotective Agent in the Alzheimer's Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8599153/pdf/fphar-12-775034.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8599153/pdf/fphar-12-775034.pdf</a> ** Neurotherapeutics. 2019 Jul;16(3):666-674.doi: 10.1007/s13311-019-00767-8. Neuroprotective and Antioxidant Effect of Ginkgo Biloba Extract Against AD and Other Neurological Disorders <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694352/pdf/13311_2019_Article_767.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694352/pdf/13311_2019_Article_767.pdf</a> ** Pharmaceuticals (Basel). 2021 Apr 1;14(4):305.doi: 10.3390/ph14040305. Mild Cognitive Impairment and Mild Dementia: The Role of Ginkgo biloba (EGb 761®) <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8065464/pdf/pharmaceuticals-14-00305.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8065464/pdf/pharmaceuticals-14-00305.pdf</a> ** JAMA. 2008 Nov 19;300(19):2253-62.doi: 10.1001/jama.2008.683. Ginkgo biloba for prevention of dementia: a randomized controlled trial <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823569/pdf/nihms103555.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823569/pdf/nihms103555.pdf</a> ** Front Pharmacol. 2021 Aug 3;12:721216.doi: 10.3389/fphar.2021.721216. eCollection 2021. Ginkgo Biloba Extract Is Comparable With Donepezil in Improving Functional Recovery in Alzheimer's Disease: Results From a Multilevel Characterized Study Based on Clinical Features and Resting-State Functional Magnetic Resonance Imaging <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369572/pdf/fphar-12-721216.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369572/pdf/fphar-12-721216.pdf</a> ** Front Pharmacol. 2020 Feb 21;10:1688.doi: 10.3389/fphar.2019.01688. An Updated Review of Randomized Clinical Trials Testing the Improvement of Cognitive Function of Ginkgo Biloba Extract in Healthy People and Alzheimer's Patients <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047126/pdf/fphar-10-01688.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047126/pdf/fphar-10-01688.pdf</a> 
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GINKGO BILOBA

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 An important nutrient that is known to affect brain development and aging is choline. Choline is essential for several biological functions of cells. For example, choline metabolites acetylcholine and phosphatidylcholine, respectively, contribute to proper signaling functions for normal cholinergic neurotransmission and the structural integrity of cell membranes. Brain choline uptake is decreased in older adults and the lower supply of extracellular choline may contribute to aging-related cognitive decline. Not surprisingly, higher dietary choline is associated with better cognitive performance in elderly individuals. One method to increase dietary choline is through supplementation with citicoline (CDP-choline or cytidine-5-diphosphate choline). Compared with choline moiety obtained through other dietary sources such as phosphatidylcholine, choline in citicoline has been suggested to be less prone to conversion to trimethylamine (TMA) and trimethylamine N-oxide (TMAO),which have been implicated in the pathogenesis of cardiovascular disease. Citicoline is a naturally occurring mononucleotide comprised of cytosine, ribose, pyrophosphate, and choline. It is produced by the body as an intermediate product of phosphatidylcholine and sphingomyelin biosynthesis. The neuroprotective actions of citicoline include activating the biosynthesis of structural phospholipids in the neuronal membranes, increasing cerebral metabolism, noradrenaline, and dopamine levels in the central nervous system, preventing the loss of cardiolipin (an exclusive inner mitochondrial phospholipid enriched with unsaturated fatty acids), and protecting cell membranes by accelerating re-synthesis of phospholipids. Unsurprisingly, citicoline supplementation has shown beneficial effects on memory function and behavior in populations with awide range of impairments such as those with mild to moderate vascular cognitive impairment, vascular dementia, or senile dementia. PUBLISHED ARTICLES : ** Nutr. 2021 Aug 7;151(8):2153-2160.doi: 10.1093/jn/nxab119. Citicoline and Memory Function in Healthy Older Adults: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8349115/pdf/nxab119.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8349115/pdf/nxab119.pdf</a> ** J Neurochem. 2002 Jan;80(1):12-23.doi: 10.1046/j.0022-3042.2001.00697.x. Citicoline: neuroprotective mechanisms in cerebral ischemia <a href="https://onlinelibrary.wiley.com/doi/epdf/10.1046/j.0022-3042.2001.00697.x"style="color:blue;"target="_blank">https://onlinelibrary.wiley.com/doi/epdf/10.1046/j.0022-3042.2001.00697.x</a> ** Clin Interv Aging. 2013;8:131-7.doi: 10.2147/CIA.S38420. Epub 2013 Feb 5. Effectiveness and safety of citicoline in mild vascular cognitive impairment: the IDEALE study <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569046/pdf/cia-8-131.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569046/pdf/cia-8-131.pdf</a> ** J Pharmacol Sci. 2011;116(2):232-7.doi: 10.1254/jphs.11013fp. Epub 2011 May 25. Neuroprotective effects of citidine-5-diphosphocholine on impaired spatial memory in a rat model of cerebrovascular dementia <a href="https://pubmed.ncbi.nlm.nih.gov/21613753/"style="color:blue;"target="_blank">https://pubmed.ncbi.nlm.nih.gov/21613753/</a> ** Clin Interv Aging. 2012;7:113-8.doi: 10.2147/CIA.S29366. Retrospective and observational study to assess the efficacy of citicoline in elderly patients suffering from stupor related to complex geriatric syndrome <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3363302/pdf/cia-7-113.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3363302/pdf/cia-7-113.pdf</a> ** Clin Interv Aging. 2015; 10: 1421–1429. Published online 2015 Sep 3. doi: 10.2147/CIA.S87886 The role of citicoline in cognitive impairment: pharmacological characteristics, possible advantages, and doubts for an old drug with new perspectives <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562749/pdf/cia-10-1421.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562749/pdf/cia-10-1421.pdf</a> 
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CITICHOLINE

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 Its positive effects on brain aging have been generally attributed to its two major triterpene saponosides; asiatic and madecassic acids as well as their heterosides; asiaticoside and madecassoside, respectively. The hydroalcoholic extract of the plant was tested in vitro against acetylcholinesterase (AChE), the key enzyme taking a critical role in the pathogenesis of Alzheimers disease (Since deficit in the level of acetylcholine (ACh), which is hydrolyzed by AChE, has been identified in the brains of AD patients, inhibition of AChE as well as its sister enzyme butyrylcholinesterase (BChE) has become a rational target in drug development against AD. The extract was found to inhibit AChE with 50% of inhibition rate at 150 μg/mL concentration by the spectrophotometric method of Ellman. Awad et al. investigated inhibitory property of C. asiatica extract towards glutamic acid decarboxylase (GAD) and γ-aminobutyric acid transaminase (GABA-T), which are the enzymes responsible for GABA metabolism and found out that the extract stimulated the activity of GAD over 40%. The aqueous extract of C. asiatica caused a serious decrease in malondialdehyde (MDA) and an increase in glutathione and CAT levels were recorded, which led to a final suggestion by the authors that C. asiatica extract has a positive effect on memory that is also related to its remarkable antioxidant effect. PUBLISHED ARTICLES :&nbsp; ** Evid Based Complement Alternat Med. 2012;2012:946259.doi: 10.1155/2012/946259. Epub 2012 May 14. Centella asiatica (L.) Urban: From Traditional Medicine to Modern Medicine with Neuroprotective Potential <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359802/pdf/ECAM2012-946259.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359802/pdf/ECAM2012-946259.pdf</a> ** 2021 Dec 16;12:788312.doi: 10.3389/fphar.2021.788312. eCollection 2021. Centella asiatica Alters Metabolic Pathways Associated With Alzheimer's Disease in the 5xFAD Mouse Model of ß-Amyloid Accumulation <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8717922/pdf/fphar-12-788312.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8717922/pdf/fphar-12-788312.pdf</a> ** J Alzheimers Dis. 2015;45(3):933-46.doi: 10.3233/JAD-142217. Centella asiatica Attenuates Amyloid-β-Induced Oxidative Stress and Mitochondrial Dysfunction <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412033/pdf/nihms677848.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412033/pdf/nihms677848.pdf</a> ** Neurosci Lett. 2017 Apr 12;646:24-29.doi: 10.1016/j.neulet.2017.02.072. Epub 2017 Mar 6. Centella asiatica attenuates Aβ-induced neurodegenerative spine loss and dendritic simplification <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5533098/pdf/nihms860326.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5533098/pdf/nihms860326.pdf</a> ** Int J Alzheimers Dis. 2012;2012:381974.doi: 10.1155/2012/381974. Epub 2012 Feb 15. Centella asiatica Extract Improves Behavioral Deficits in a Mouse Model of Alzheimer's Disease: Investigation of a Possible Mechanism of Action <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296229/pdf/IJAD2012-381974.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296229/pdf/IJAD2012-381974.pdf</a> ** Antioxidants (Basel). 2019 Dec 8;8(12):630.doi: 10.3390/antiox8120630. Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296229/pdf/IJAD2012-381974.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296229/pdf/IJAD2012-381974.pdf</a> ** Int J Mol Sci. 2019 Apr 16;20(8):1871.doi: 10.3390/ijms20081871. Centella asiatica Protects d-Galactose/AlCl3 Mediated Alzheimer's Disease-Like Rats via PP2A/GSK-3β Signaling Pathway in Their Hippocampus <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6514756/pdf/ijms-20-01871.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6514756/pdf/ijms-20-01871.pdf</a> ** Front Physiol. 2021 Oct 14;12:712317.doi: 10.3389/fphys.2021.712317. eCollection 2021. Hypoxia-Induced Neuroinflammation in Alzheimer's Disease: Potential Neuroprotective Effects of Centella asiatica <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8551388/pdf/fphys-12-712317.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8551388/pdf/fphys-12-712317.pdf</a> ** Front Pharmacol. 2021 Jun 29;12:687935.doi: 10.3389/fphar.2021.687935. Mitoprotective Effects of Centella asiatica (L.) Urb.: Anti-Inflammatory and Neuroprotective Opportunities in Neurodegenerative Disease <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8275827/pdf/fphar-12-687935.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8275827/pdf/fphar-12-687935.pdf</a> ** Malays J Med Sci. 2016 Jan;23(1):4-14. Recent Updates in Neuroprotective and Neuroregenerative Potential of Centella asiatica <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4975583/pdf/2ramjms231.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4975583/pdf/2ramjms231.pdf</a> 
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CENTELLA ASIATICA

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 Choline alphoscerate (alpha glycerylphosphorylcholine, Alpha-GPC) is a choline-containing phospholipid with cognition enhancing capabilities, proposed for countering the cognitive impairment in Alzheimer’s Disease, stroke, and other types of adult-onset dementias. From a pharmacological point of view, Alpha-GPC is considered as a parasympathetic agent, which is used both as a registered drug or as a nutraceutical in several countries. Preclinical studies have shown that Alpha-GPC increases acetylcholine release and levels, as well as facilitates learning and memory. It has been shown that Alpha-GPC increases acetylcholine levels in the aging brain. Acetylcholine is a neuro-transmitter contributing to communication between nerve cells, and between neurons and their skeletal muscles and autonomic targets. It also plays a key role in the brain’s ability to store and recall information. In clinical studies, Alpha-GPC was found to improve cognition, behavioral, and functional outcomes in patients with Alzheimer’s Disease, stroke, and cerebral ischemic attacks. PUBLISHED ARTICLES : ** Nutrients. 2021 Jun 18;13(6):2091.doi: 10.3390/nu13062091. Alpha-Glycerylphosphorylcholine Increases Motivation in Healthy Volunteers: A Single-Blind, Randomized, Placebo-Controlled Human Study <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8235064/pdf/nutrients-13-02091.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8235064/pdf/nutrients-13-02091.pdf</a> ** J Alzheimers Dis. 2023;92(1):59-70.doi: 10.3233/JAD-221189. Activity of Choline Alphoscerate on Adult-Onset Cognitive Dysfunctions: A Systematic Review and Meta-Analysis <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10041421/pdf/jad-92-jad221189.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10041421/pdf/jad-92-jad221189.pdf</a> ** J Clin Med. 2022 Oct 13;11(20):6052.doi: 10.3390/jcm11206052. Effect of Choline Alphoscerate on the Survival of Glioblastoma Patients: A Retrospective, Single-Center Study <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9605462/pdf/jcm-11-06052.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9605462/pdf/jcm-11-06052.pdf</a> ** Front Cell Neurosci. 2022 Sep 23;16:988759.doi: 10.3389/fncel.2022.988759. Effects of choline containing phospholipids on the neurovascular unit: A review <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9541750/pdf/fncel-16-988759.pdf"style="color:blue;"target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9541750/pdf/fncel-16-988759.pdf</a> ** J Neurochem. 2019 May;149(4):499-517.doi: 10.1111/jnc.14560. Epub 2018 Nov 8. Distinct disruptions in Land's cycle remodeling of glycerophosphocholines in murine cortex mark symptomatic onset and progression in two Alzheimer's disease mouse models <a href="https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.14560"style="color:blue;"target="_blank">https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.14560</a> 
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ALPHA GPC

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