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Front Neurosci. 2019 Jan 25;12:898. doi: 10.3389/fnins.2018.00898. eCollection 2018.

Potential Role of Mic60/Mitofilin in Parkinson's Disease.

Author information

1
Department of Neurology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
2
Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA, United States.
3
Division of Neuropathology, Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
4
Cellular and Molecular Pathology (CMP) Program, Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
5
Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, United States.
6
Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, PA, United States.

Abstract

There are currently no treatments that hinder or halt the inexorable progression of Parkinson's disease (PD). While the etiology of PD remains elusive, evidence suggests that early dysfunction of mitochondrial respiration and homeostasis play a major role in PD pathogenesis. The mitochondrial structural protein Mic60, also known as mitofilin, is critical for maintaining mitochondrial architecture and function. Loss of Mic60 is associated with detrimental effects on mitochondrial homeostasis. Growing evidence now implicates Mic60 in the pathogenesis of PD. In this review, we discuss the data supporting a role of Mic60 and mitochondrial dysfunction in PD. We will also consider the potential of Mic60 as a therapeutic target for treating neurological disorders.

KEYWORDS:

Mic60/mitofilin; Parkinson’s disease; mitochondria; mitochondrial dynamics; neurodegeneration

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