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REVIEW: Effect of Tau Protein on Mitochondrial Functions

Khoren K. Epremyan1,a*, Tatyana N. Goleva1, and Renata A. Zvyagilskaya1

1Bach Institute of Biochemistry, Federal Research Center of Biotechnology, Russian Academy of Sciences, 119071 Moscow, Russia

* To whom correspondence should be addressed.

Received April 27, 2022; Revised July 4, 2022; Accepted July 6, 2022
Alzheimer’s disease is the most common age-related progressive neurodegenerative disorder of brain cortex and hippocampus leading to cognitive impairment. Accumulation of extracellular amyloid plaques and intraneuronal neurofibrillary tangles are believed to be the main hallmarks of the disease. Origin of Alzheimer’s disease is not totally clear, multiple initiator factors are likely to exist. Intracellular impacts of Alzheimer’s disease include mitochondrial dysfunction, oxidative stress, ER-stress, disruption of autophagy, severe metabolic challenges leading to massive neuronal apoptosis. Mitochondria are the key players in all these processes. This formed the basis for the so-called mitochondrial cascade hypothesis. This review provides current data on the molecular mechanisms of the development of Alzheimer’s disease associated with mitochondria. Special attention was paid to the interaction between Tau protein and mitochondria, as well as to the promising therapeutic approaches aimed at preventing development of neurodegeneration.
KEY WORDS: Alzheimer’s disease, Tau protein, bioenergetics, mitochondria

DOI: 10.1134/S0006297922080028