Mitophagy Impairments as Culprit of Alzheimer’s Disease

Shalini Mani, Geeta Swargiary, Manisha Singh, Mahima Rawal

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Dementia is considered as a common term which includes different disease known to affect memory and other cognitive abilities too. Amongst different brain diseases, which can cause dementia, Alzheimer’s disease (AD) is reported to be the most common form and nearly 60–70% of dementia cases are AD patients. The major events of AD primarily include protein aggregation, neuronal injury, synaptic failure, and consequently neuronal death in the hippocampal region of the brain. In the recent past, defects in mitochondrial function are also reported as a central aspect of different neurodegenerative diseases, including AD. To maintain the mitochondrial dynamics and neuronal health, the aged and dysfunctional mitochondria are efficiently removed by a specific process called mitophagy. Several studies have revealed that mitochondrial turnover is regulated by the integration of different cellular pathways. In this chapter, the mechanism of different mitophagy pathways and the possible molecular defect leading to mitophagy impairment in AD are discussed. This chapter also provides a glimpse of different therapeutic approaches to enhance mitophagy in neurons of AD brain and combat such diseases. Though there are lots of developments in mitophagybased therapeutic interventions of AD; however, the associated limitations need to be addressed.

Original languageEnglish
Title of host publicationCurrent Thoughts on Dementia
Subtitle of host publicationFrom Risk Factors to Therapeutic Interventions
PublisherSpringer Nature
Pages115-143
Number of pages29
ISBN (Electronic)9789811676062
ISBN (Print)9789811676055
DOIs
StatePublished - 1 Jan 2022
Externally publishedYes

Keywords

  • Alzheimer’s disease
  • Amyloid β
  • Dementia
  • Mitochondria
  • Mitophagy
  • Parkin
  • Tau

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