Cited by 323Autophagy in Disease and TherapyNeuroinflammation and Neurodegeneration MechanismsGenetics, Aging, and Longevity in Model Organisms

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Autophagy and Microglia: Novel Partners in Neurodegeneration and Aging

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Plaza-Zabala, Ainhoa, Sierra-Torre, Virginia, Sierra, Amanda·2017·International Journal of Molecular Sciences

DOI 10.3390/ijms18030598PMC PMC5372614

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Abstract

Autophagy is emerging as a core regulator of Central Nervous System (CNS) aging and neurodegeneration. In the brain, it has mostly been studied in neurons, where the delivery of toxic molecules and organelles to the lysosome by autophagy is crucial for neuronal health and survival. However, we propose that the (dys)regulation of autophagy in microglia also affects innate immune functions such as phagocytosis and inflammation, which in turn contribute to the pathophysiology of aging and neurodegenerative diseases. Herein, we first describe the basic concepts of autophagy and its regulation, discuss key aspects for its accurate monitoring at the experimental level, and summarize the evidence linking autophagy impairment to CNS senescence and disease. We focus on acute, chronic, and autoimmunity-mediated neurodegeneration, including ischemia/stroke, Alzheimer’s, Parkinson’s, and Huntington’s diseases, and multiple sclerosis. Next, we describe the actual and potential impact of autophagy on microglial phagocytic and inflammatory function. Thus, we provide evidence of how autophagy may affect microglial phagocytosis of apoptotic cells, amyloid-β, synaptic material, and myelin debris, and regulate the progression of age-associated neurodegenerative diseases. We also discuss data linking autophagy to the regulation of the microglial inflammatory phenotype, which is known to contribute to age-related brain dysfunction. Overall, we update the current knowledge of autophagy and microglia, and highlight as yet unexplored mechanisms whereby autophagy in microglia may contribute to CNS disease and senescence.

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2 retracted

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Correction: Neuronal Hyperactivity Disturbs ATP Microgradients, Impairs Microglial Motility, and Reduces Phagocytic Receptor Expression Triggering Apoptosis/Microglial Phagocytosis Uncoupling
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Authors: Plaza-Zabala, A., Sierra-Torre, V., & Sierra, A.
Affiliations: Achucarro Basque Center for Neuroscience, 48170 Zamudio, Spain
Ikerbasque (ES)
Corresponding author: Sierra, Amanda
ORCID: Sierra, Amanda
Venue: International Journal of Molecular Sciences
Publisher: MDPI AG
Published: 2017-03-09
Volume: 18
Issue: 3
Pages: 598
ISSN: 1422-0067 (ISSN-L)
DOI: 10.3390/ijms18030598
PMC: PMC5372614
OpenAlex: W2594094135
Cited by: 323
References: 169
Citations by year: 2026: 23 · 2025: 24 · 2024: 25 · 2023: 42 · 2022: 37 · 2021: 55 · 2020: 38 · 2019: 39 · 2018: 32 · 2017: 8
FWCI: 4.24
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
Locations: International Journal of Molecular Sciences (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Spanish Ministry of Economy and Competitiveness (BFU2015-66689, RYC-2013-12817)
BBVA Foundation Grant for Researchers and Cultural Creators
Basque Government (PI_2016_1_0011)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords: autophagy, microglia, neurodegeneration, brain aging, microglial phagocytosis, neuroinflammation, Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, amyloid-beta clearance, myelin debris, autophagy regulation, autophagy monitoring
MeSH terms: Aging, Animals, Autophagy, Central Nervous System, Humans, Microglia, Neurodegenerative Diseases

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Autophagy and Microglia: Novel Partners in Neurodegeneration and Aging

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