Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
By Tiantian Guo, Denghong Zhang, Yuzhe Zeng, Timothy Y. Huang, Huaxi Xu, Yingjun Zhao. Molecular Neurodegeneration, 2020
755 citations recorded by the source corpus.
Alzheimer’s disease (AD) is the most common neurodegenerative disorder seen in age-dependent dementia. There is currently no effective treatment for AD, which may be attributed in part to lack of a clear underlying mechanism. Studies within the last few decades provide growing evidence for a central role of amyloid β (Aβ) and tau, as well as glial contributions to various molecular and cellular pathways in AD pathogenesis. Herein, we review recent progress with respect to Aβ- and tau-associated mechanisms, and discuss glial dysfunction in AD with emphasis on neuronal and glial receptors that mediate Aβ-induced toxicity. We also discuss other critical factors that may affect AD pathogenesis, including genetics, aging, variables related to environment, lifestyle habits, and describe the potential role of apolipoprotein E (APOE), viral and bacterial infection, sleep, and microbiota. Although we have gained much towards understanding various aspects underlying this devastating neurodegenerative disorder, greater commitment towards research in molecular mechanism, diagnostics and treatment will be needed in future AD research.
Subfields: Neurology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/9d0c9bccae6d6e0750c119c605d172661f0365b1
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Citations in the corpus
- Recent advances in Alzheimer’s disease: mechanisms, clinical trials and new drug development strategies (2024, background): “182,479,480 In the extensively researched A β hypothesis, A β stands as the most direct drug target.”
- Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “233,234 A β protein triggered mitochondrial fi ssion, synaptic loss, and neuronal damage, at least partially via S-nitrosylation of Drp1 to activate GTPase activity.”