Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms

By J. Kerr, Bryan A. Adriaanse, N. Greig, Mark P. Mattson, M. Z. Cader, V. A. Bohr, Evandro Fei Fang. Trends in Neurosciences, 2017

753 citations recorded by the source corpus.

Neurons affected in Alzheimer’s disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid β-peptide (Aβ) and Tau pathologies. Emerging findings suggest that the autophagy – lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria. Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy. Interventions that bolster mitochondrial health and/or stimulate mitophagy may therefore forestall the neurodegenerative process in AD.

Subfields: Epidemiology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/7511f45723cfe196c4f48c99b7dd818514ef95d6

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In Physiology

Huaxi Xu

Citations in the corpus

Recent advances in Alzheimer’s disease: mechanisms, clinical trials and new drug development strategies (2024, background): “231 In summary, abnormalities of autophagy are intimately related to the onset and progression of AD.”
Aging and aging-related diseases: from molecular mechanisms to interventions and treatments (2022, methodology): “The development of strategies to treat this impairment of mitophagy would benefit from the screening and identification of new mitophagy regulators.(521,522) Recently, a research team used a combination of unsupervised machine learning (including vector representation of molecular structure, pharmac”
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “In addition, defects in autophagy/lysosome pathways that remove damaged mitochondria are also impaired in AD, thereby enhancing the accumulation of dysfunctional mitochondria [518].”
Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, neutral): “246,352,353 In the nervous system of AD patients, mitochondrial ﬁ ssion is more universal.”