Mitochondria in Aging and Alzheimer’s Disease: Focus on Mitophagy

Author:

Pradeepkiran Jangampalli Adi1,Baig Javaria1,Selman Ashley1,Reddy P. Hemachandra12345ORCID

Affiliation:

1. Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA

2. Department of Nutritional Sciences, College of Human Sciences, Texas Tech University, Lubbock, TX, USA

3. Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX, USA

4. Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX, USA

5. Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA

Abstract

Alzheimer’s disease (AD) is characterized by the accumulation of amyloid β and phosphorylated τ protein aggregates in the brain, which leads to the loss of neurons. Under the microscope, the function of mitochondria is uniquely primed to play a pivotal role in neuronal cell survival, energy metabolism, and cell death. Research studies indicate that mitochondrial dysfunction, excessive oxidative damage, and defective mitophagy in neurons are early indicators of AD. This review article summarizes the latest development of mitochondria in AD: 1) disease mechanism pathways, 2) the importance of mitochondria in neuronal functions, 3) metabolic pathways and functions, 4) the link between mitochondrial dysfunction and mitophagy mechanisms in AD, and 5) the development of potential mitochondrial-targeted therapeutics and interventions to treat patients with AD.

Funder

NIH grants

Publisher

SAGE Publications

Subject

Neurology (clinical),General Neuroscience

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