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ISSN (Online): 1996-3181

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Review Article

Amyloid Beta Peptide-Mediated Alterations in Mitochondrial Dynamics and its Implications for Alzheimer’s Disease

Author(s): Luis Ángel Monsalvo-Maraver, Marisol Maya-López, Edgar Rangel-López, Isaac Túnez, Alexey A. Tinkov, Anatoly Skalny, Beatriz Ferrer, Michael Aschner* and Abel Santamaría*

Volume 22, Issue 7, 2023

Published on: 11 August, 2022

Page: [1039 - 1056] Pages: 18

DOI: 10.2174/1871527321666220616094036

open access plus

Abstract

Alzheimer’s disease (AD) is considered the most frequent neurodegenerative disorder worldwide, compromising cognitive function in patients, with an average incidence of 1-3% in the open population. Protein aggregation into amyloidogenic plaques and neurofibrillary tangles, as well as neurodegeneration in the hippocampal and cortical areas, represent the neuropathological hallmarks of this disorder. Mechanisms involved in neurodegeneration include protein misfolding, augmented apoptosis, disrupted molecular signaling pathways and axonal transport, oxidative stress, inflammation, and mitochondrial dysfunction, among others. It is precisely through a disrupted energy metabolism that neural cells trigger toxic mechanisms leading to cell death. In this regard, the study of mitochondrial dynamics constitutes a relevant topic to decipher the role of mitochondrial dysfunction in neurological disorders, especially when considering that amyloid-beta peptides can target mitochondria. Specifically, the amyloid beta (Aβ) peptide, known to accumulate in the brain of AD patients, has been shown to disrupt overall mitochondrial metabolism by impairing energy production, mitochondrial redox activity, and calcium homeostasis, thus highlighting its key role in the AD pathogenesis. In this work, we review and discuss recent evidence supporting the concept that mitochondrial dysfunction mediated by amyloid peptides contributes to the development of AD.

Keywords: Amyloid beta-peptide, protein aggregation, mitochondrial function, energy metabolism alterations, mitophagy, neurodegeneration, Alzheimer’s disease.

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