Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease

Md Ataur Rahman, MD Hasanur Rahman, A. N.M. Mamun-Or-rashid, Hongik Hwang, Sooyoung Chung, Bonglee Kim, Hyewhon Rhim

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Alzheimer’s disease (AD) is one of the most prevailing neurodegenerative diseases in the world, which is characterized by memory dysfunction and the formation of tau and amyloid ꞵ (Aꞵ) aggregates in multiple brain regions, including the hippocampus and cortex. The formation of senile plaques involving tau hyperphosphorylation, fibrillar A , and neurofibrillary tangles (NFTs) is used as a pathological marker of AD and eventually produces aggregation or misfolded protein. Importantly, it has been found that the failure to degrade these aggregate-prone proteins leads to pathological consequences, such as synaptic impairment, cytotoxicity, neuronal atrophy, and memory deficits associated with AD. Recently, increasing evidence has suggested that the autophagy pathway plays a role as a central cellular protection system to prevent the toxicity induced by aggregation or misfolded proteins. Moreover, it has also been revealed that AD-related protein aggresomes could be selectively degraded by autophagosome and lysosomal fusion through the autophagy pathway, which is known as aggrephagy. Therefore, the regulation of autophagy serve as a useful approach to modulate the formation of aggresomes associated with AD. This review focuses on the recent improvements in the application of natural compounds and small molecules as a potential therapeutic approach for AD prevention and treatment via aggrephagy.

Original languageEnglish
Article number1027
Issue number5
StatePublished - May 2022


  • Alzheimer’s disease (AD)
  • aggregation
  • aggrephagy
  • aggresome
  • autophagosomes
  • autophagy


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