Abstract
Alzheimer’s disease (AD) is the most common type of dementia which characterized by a progressive loss of memory and cognitive function due to degeneration of synapses and axons. Currently, there is no cure for AD. Deposition of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles (NFTs) are two hallmark pathologic changes in the brains of Alzheimer’s patients. Autophagy is the major mechanism in cells responsible for removing protein aggregates. Accumulation of immature autophagic vacuoles (AVs) in dystrophic neurites of Alzheimer patients’ brains suggests that autophagy process is disrupted. Till now, it is far from clear what role autophagy plays in AD, a causative role, a protective role, or just a consequence of the disease process itself. To design more effective therapeutic strategies towards this devastating disorder, it is essential to understand the exact role of autophagy played during different stages of AD.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia in the elderly, which is characterized by a progressive deficiency in memory and cognitive functions (Scheltens et al, 2016)
The abundance of autophagic vacuoles (AVs) in the brains of AD animal models and AD patients is in sharp contrast to the rarely-observed AVs in normal brains, which suggests that the accumulation of pathogenic proteins such as Aβ and tau in AD may be caused by defective autophagy-lysosome proteolysis pathway (Cataldo et al, 2004; Yang et al, 2011a)
Inhibiting the delivery of autophagosomes to lysosomes induces a rapid AVs accumulation in neurites, with very similar morphology to what has seen in the AD brain, which further suggests that defective axonal transportation of AVs may play a role in AD pathogenesis (Boland et al, 2008)
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia in the elderly, which is characterized by a progressive deficiency in memory and cognitive functions (Scheltens et al, 2016). The abundance of AVs in the brains of AD animal models and AD patients is in sharp contrast to the rarely-observed AVs in normal brains, which suggests that the accumulation of pathogenic proteins such as Aβ and tau in AD may be caused by defective autophagy-lysosome proteolysis pathway (Cataldo et al, 2004; Yang et al, 2011a).
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