» Articles » PMID: 31936292

Mitophagy in Alzheimer's Disease and Other Age-Related Neurodegenerative Diseases

Overview
Journal Cells
Publisher MDPI
Date 2020 Jan 16
PMID 31936292
Citations 100
Authors
Affiliations
Soon will be listed here.
Abstract

Mitochondrial dysfunction is a central aspect of aging and neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. Mitochondria are the main cellular energy powerhouses, supplying most of ATP by oxidative phosphorylation, which is required to fuel essential neuronal functions. Efficient removal of aged and dysfunctional mitochondria through mitophagy, a cargo-selective autophagy, is crucial for mitochondrial maintenance and neuronal health. Mechanistic studies into mitophagy have highlighted an integrated and elaborate cellular network that can regulate mitochondrial turnover. In this review, we provide an updated overview of the recent discoveries and advancements on the mitophagy pathways and discuss the molecular mechanisms underlying mitophagy defects in Alzheimer's disease and other age-related neurodegenerative diseases, as well as the therapeutic potential of mitophagy-enhancing strategies to combat these disorders.

Citing Articles

Hippocampal mitophagy alterations in MAPT-associated frontotemporal dementia with parkinsonism.

Richardson T, Hou X, Fiesel F, Wszolek Z, Dickson D, Springer W Acta Neuropathol Commun. 2025; 13(1):41.

PMID: 39994734 PMC: 11849217. DOI: 10.1186/s40478-025-01955-8.


Targeted drug delivery in neurodegenerative diseases: the role of nanotechnology.

Dhariwal R, Jain M, Mir Y, Singh A, Jain B, Kumar P Front Med (Lausanne). 2025; 12:1522223.

PMID: 39963432 PMC: 11831571. DOI: 10.3389/fmed.2025.1522223.


DNA repair pathways in the mitochondria.

King D, Copeland W DNA Repair (Amst). 2025; 146:103814.

PMID: 39914164 PMC: 11848857. DOI: 10.1016/j.dnarep.2025.103814.


High glucose induces renal tubular epithelial cell senescence by inhibiting autophagic flux.

Zhang Y, Zhao Y, Liu Y, Fang Y, Sun L, Wei S Hum Cell. 2025; 38(2):43.

PMID: 39789393 DOI: 10.1007/s13577-024-01156-w.


Underneath the Gut-Brain Axis in IBD-Evidence of the Non-Obvious.

Boldyreva L, Evtushenko A, Lvova M, Morozova K, Kiseleva E Int J Mol Sci. 2024; 25(22).

PMID: 39596193 PMC: 11594934. DOI: 10.3390/ijms252212125.


References
1.
Devi L, Raghavendran V, Prabhu B, Avadhani N, Anandatheerthavarada H . Mitochondrial import and accumulation of alpha-synuclein impair complex I in human dopaminergic neuronal cultures and Parkinson disease brain. J Biol Chem. 2008; 283(14):9089-100. PMC: 2431021. DOI: 10.1074/jbc.M710012200. View

2.
Ryu D, Mouchiroud L, Andreux P, Katsyuba E, Moullan N, Nicolet-Dit-Felix A . Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nat Med. 2016; 22(8):879-88. DOI: 10.1038/nm.4132. View

3.
Lee S, Sato Y, Nixon R . Lysosomal proteolysis inhibition selectively disrupts axonal transport of degradative organelles and causes an Alzheimer's-like axonal dystrophy. J Neurosci. 2011; 31(21):7817-30. PMC: 3351137. DOI: 10.1523/JNEUROSCI.6412-10.2011. View

4.
Hou Y, Lautrup S, Cordonnier S, Wang Y, Croteau D, Zavala E . NAD supplementation normalizes key Alzheimer's features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency. Proc Natl Acad Sci U S A. 2018; 115(8):E1876-E1885. PMC: 5828618. DOI: 10.1073/pnas.1718819115. View

5.
Dragicevic N, Mamcarz M, Zhu Y, Buzzeo R, Tan J, Arendash G . Mitochondrial amyloid-beta levels are associated with the extent of mitochondrial dysfunction in different brain regions and the degree of cognitive impairment in Alzheimer's transgenic mice. J Alzheimers Dis. 2010; 20 Suppl 2:S535-50. DOI: 10.3233/JAD-2010-100342. View