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Brain-derived neurotrophic factor protects neurons by stimulating mitochondrial function through protein kinase A.脑源性神经营养因子通过蛋白激酶 A 刺激线粒体功能来保护神经元。
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AMPA receptor modulation through sequential treatment with perampanel and aniracetam mitigates post-stroke damage in experimental model of ischemic stroke.通过依次使用吡仑帕奈和阿尼西坦治疗来调节AMPA受体,可减轻缺血性中风实验模型中的中风后损伤。
Naunyn Schmiedebergs Arch Pharmacol. 2023 Dec;396(12):3529-3545. doi: 10.1007/s00210-023-02544-z. Epub 2023 May 25.
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Regulation of the Soluble Amyloid Precursor Protein α (sAPPα) Levels by Acetylcholinesterase and Brain-Derived Neurotrophic Factor in Lung Cancer Cell Media.乙酰胆碱酯酶和脑源性神经营养因子对肺癌细胞培养基中可溶性淀粉样前体蛋白α(sAPPα)水平的调节。
Int J Mol Sci. 2022 Sep 15;23(18):10746. doi: 10.3390/ijms231810746.
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Alzheimer's Disease: Key Insights from Two Decades of Clinical Trial Failures.阿尔茨海默病:二十年临床试验失败的关键洞察。
J Alzheimers Dis. 2022;87(1):83-100. doi: 10.3233/JAD-215699.
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Brain-derived neurotrophic factor in Alzheimer's disease and its pharmaceutical potential.阿尔茨海默病中的脑源性神经营养因子及其药物潜力。
Transl Neurodegener. 2022 Jan 28;11(1):4. doi: 10.1186/s40035-022-00279-0.
6
Mitochondrial Dysfunction in Alzheimer's Disease: A Biomarker of the Future?阿尔茨海默病中的线粒体功能障碍:未来的生物标志物?
Biomedicines. 2021 Jan 11;9(1):63. doi: 10.3390/biomedicines9010063.
7
Metabotropic Glutamate Receptors in Alzheimer's Disease Synaptic Dysfunction: Therapeutic Opportunities and Hope for the Future.代谢型谷氨酸受体在阿尔茨海默病突触功能障碍中的作用:治疗机遇与未来希望。
J Alzheimers Dis. 2020;78(4):1345-1361. doi: 10.3233/JAD-201146.
8
Alzheimer's Disease "Non-amyloidogenic" p3 Peptide Revisited: A Case for Amyloid-α.阿尔茨海默病“非淀粉样变性”p3 肽再探:淀粉样蛋白-α的作用。
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9
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Deciphering the neuroprotective and neurogenic potential of soluble amyloid precursor protein alpha (sAPPα).解析可溶性淀粉样前体蛋白 α(sAPPα)的神经保护和神经发生潜能。
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阿尼西坦:预防阿尔茨海默病中淀粉样β斑块积累的循证模型。

Aniracetam: An Evidence-Based Model for Preventing the Accumulation of Amyloid-β Plaques in Alzheimer's Disease.

机构信息

Research Department, Brain Fit For Life, LLC, Lewes, DE, USA.

出版信息

J Alzheimers Dis. 2024;98(4):1235-1241. doi: 10.3233/JAD-231247.

DOI:10.3233/JAD-231247
PMID:38552113
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11091568/
Abstract

Alzheimer's disease is the leading cause of dementia in the world. It affects 6 million people in the United States and 50 million people worldwide. Alzheimer's disease is characterized by the accumulation of amyloid-β plaques (Aβ), an increase in tau protein neurofibrillary tangles, and a loss of synapses. Since the 1990s, removing and reducing Aβ has been the focus of Alzheimer's treatment and prevention research. The accumulation of Aβ can lead to oxidative stress, inflammation, neurotoxicity, and eventually apoptosis. These insults impair signaling systems in the brain, potentially leading to memory loss and cognitive decline. Aniracetam is a safe, effective, cognitive-enhancing drug that improves memory in both human and animal studies. Aniracetam may prevent the production and accumulation of Aβ by increasing α-secretase activity through two distinct pathways: 1) increasing brain derived neurotrophic factor expression and 2) positively modulating metabotropic glutamate receptors. This is the first paper to propose an evidence-based model for aniracetam reducing the accumulation and production of Aβ.

摘要

阿尔茨海默病是世界上导致痴呆症的主要原因。它影响了美国的 600 万人和全球的 5000 万人。阿尔茨海默病的特征是淀粉样β斑块(Aβ)的积累,tau 蛋白神经原纤维缠结的增加,以及突触的丧失。自 20 世纪 90 年代以来,去除和减少 Aβ一直是阿尔茨海默病治疗和预防研究的重点。Aβ的积累会导致氧化应激、炎症、神经毒性,最终导致细胞凋亡。这些损伤会破坏大脑中的信号系统,可能导致记忆丧失和认知能力下降。阿尼西坦是一种安全、有效、增强认知的药物,在人类和动物研究中都能改善记忆力。阿尼西坦可能通过两种不同的途径增加 α-分泌酶的活性来预防 Aβ的产生和积累:1)增加脑源性神经营养因子的表达,2)积极调节代谢型谷氨酸受体。这是第一篇提出阿尼西坦减少 Aβ积累和产生的循证模型的论文。