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Mol Neurodegener. 2019 Apr 5;14(1):16. doi: 10.1186/s13024-019-0314-8.

Glial phagocytic clearance in Parkinson's disease.

Author information

1
Axe Neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Quebec, QC, Canada.
2
Département de Médecine Moléculaire, Faculté de Médecine, Université Laval, Quebec, QC, Canada.
3
Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
4
Department of Biology, University of Padova, Via Ugo Bassi 58/B, 35131, Padova, Italy. laura.civiero@unipd.it.

Abstract

An emerging picture suggests that glial cells' loss of beneficial roles or gain of toxic functions can contribute to neurodegenerative conditions. Among glial cells, microglia and astrocytes have been shown to play phagocytic roles by engulfing synapses, apoptotic cells, cell debris, and released toxic proteins. As pathogenic protein accumulation is a key feature in Parkinson's disease (PD), compromised phagocytic clearance might participate in PD pathogenesis. In contrast, enhanced, uncontrolled and potentially toxic glial clearance capacity could contribute to synaptic degeneration. Here, we summarize the current knowledge of the molecular mechanisms underlying microglial and astrocytic phagocytosis, focusing on the possible implication of phagocytic dysfunction in neuronal degeneration. Several endo-lysosomal proteins displaying genetic variants in PD are highly expressed by microglia and astrocytes. We also present the evidence that lysosomal defects can affect phagocytic clearance and discuss the therapeutic relevance of restoring or enhancing lysosomal function in PD.

KEYWORDS:

Parkinson’s disease; Phagocytosis; Reactive astrocytes; Reactive microglia

PMID:
30953527
PMCID:
PMC6451240
DOI:
10.1186/s13024-019-0314-8
[Indexed for MEDLINE]
Free PMC Article

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