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Front. Mol. Neurosci. | doi: 10.3389/fnmol.2018.00144

Microglial phagocytosis and its regulation: a therapeutic target in Parkinson's disease?

  • 1Health Sciences, Università degli studi Magna Græcia di Catanzaro, Italy
  • 2Biomedical Sciences, Università degli studi di Cagliari, Italy

The role of phagocytosis in the neuroprotective function of microglia has been appreciated for a long time, but only more recently a dysregulation of this process has been recognized in Parkinson’s disease. Indeed, microglia play several critical roles in central nervous system, such as clearance of dying neurons and pathogens as well as immunomodulation, and to fulfill these complex tasks they engage distinct phenotypes. Regulation of phenotypic plasticity and phagocytosis in microglia can be impaired by defects in molecular machinery regulating critical homeostatic mechanisms, including autophagy. Here, we briefly summarize current knowledge on molecular mechanisms of microglia phagocytosis, and the neuro-pathological role of microglia in PD. Then we focus more in detail on the possible functional role of microglial phagocytosis in the pathogenesis and progression of PD. Evidence in support of either a beneficial or deleterious role of phagocytosis in dopaminergic degeneration is reported. Altered expression of target-recognizing receptors and lysosomal receptor CD68, as well as the emerging determinant role of α-synuclein in phagocytic function is discussed. We finally discuss the rationale to consider phagocytic processes as a therapeutic target to prevent or slow down dopaminergic degeneration.

Keywords: Microglia, Phagocytosis, Cytokines, alpha-Synuclein, parkinson.

Received: 15 Jan 2018; Accepted: 09 Apr 2018.

Edited by:

Caterina Scuderi, Sapienza Università di Roma, Italy

Reviewed by:

Björn Spittau, Universitätsmedizin Rostock, Germany
Cataldo Arcuri, University of Perugia, Italy  

Copyright: © 2018 Janda, Boi and Carta. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Anna R. Carta, Università degli studi di Cagliari, Biomedical Sciences, Cagliari, Italy,