Trauma-like exposure alters neuronal apoptosis, Bin1, Fkbp5 and NR2B expression in an amyloid-beta (1–42) rat model of Alzheimer's disease

Faborode, Oluwaseun Samuel; Review, Ernest Dalle Writing -; Editing,; Mabandla, Musa V.

doi:10.1016/j.nlm.2022.107611

Cited by 1 publication

(1 citation statement)

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“…However, when various pathogenic factors are present, the Aβ metabolism is disrupted, causing its accumulation that affects neurological function [ 66 ] . In the early stage of AD, extensive aggregation and accumulation of Aβ may occur in the brain, leading to pathological changes, including impaired autophagy [ 67 ] , apoptosis [ 68 ] , and oxidative stress [ 69 ] as well as abnormal growth of axons [ 70 ] .…”

Section: Amyloid-beta Metabolismmentioning

confidence: 99%

Impaired autophagy in amyloid-beta pathology: A traditional review of recent Alzheimer's research

Yuan¹,

Wang²,

Huang³

et al. 2023

J Biomed Res

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Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. The major pathological changes in AD progression are the generation and accumulation of amyloid-beta (Aβ) peptides as well as the presence of abnormally hyperphosphorylated tau proteins in the brain. Autophagy is a conserved degradation pathway that eliminates abnormal protein aggregates and damaged organelles. Previous studies have suggested that autophagy plays a key role in the production and clearance of Aβ peptides to maintain a steady-state of Aβ peptides levels. However, a growing body of evidence suggests that autophagy is significantly impaired in the pathogenesis of AD, especially in Aβ metabolism. Therefore, this article reviews the latest studies concerning the mechanisms of autophagy, the metabolism of Aβ peptides, and the defective autophagy in the production and clearance of Aβ peptides. Here, we also summarize the established and new strategies for targeting autophagy in vivo and through clinical AD trials to identify gaps in our knowledge and to generate further questions.

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