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Updated: Jan 6, 2026

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
Published on: October 30, 2018
Targeting the awry Aβ pathway in Alzheimer's disease: hype and hurdles
Hayder M Al-Kuraishy1, Ghassan M Sulaiman2, Ali I Al-Gareeb3
1Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Abstract:
Alzheimer's disease (AD) is the most common neurodegenerative brain disease due to the progressive accumulation of amyloid protein (Aβ) and neurofibrillary tangles (NFTs). These neuropathological changes trigger excitotoxicity, inflammation, oxidative stress, and neuronal apoptosis. Therefore, targeting Aβ may be operative in the management of AD. However, suppression of normal Aβ, which regulates brain cognitive function, may induce cognitive impairment in healthy individuals. Therefore, this review aims to discuss the potential physiological role of normally present Aβ and neurotoxic Aβ in healthy brains and AD patients, respectively. In addition, in this review, we discussed and explained how targeting neurotoxic Aβ could be effective in the management of AD.
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