Mitochondrial Damage and Dysfunction in Neurodegenerative Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Mitochondria".

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 471

Special Issue Editors


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Guest Editor
Department of Ophthalmology, University of California, Irvine, CA 92697, USA
Interests: age-related macular degeneration; AMD; mitochondrial genetics; aging diseases
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Assistant Guest Editor
Department of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA 92697, USA

Special Issue Information

Dear Colleagues,

Mitochondria are the primary source of cellular energy production and healthy mitochondria are critical for protecting neurons.  Although mitochondrial defects affect several tissues and organs, the brain, which is the most energy-demanding organ, is particularly vulnerable to mitochondrial impairment and bioenergetic deficit.  Mitochondria play a vital role in brain function and cognition by regulating synaptic transmission.

Aging, a major risk factor for most neurodegenerative diseases, triggers many detrimental changes in cells, including mitochondrial DNA damage and subsequent loss of mitochondrial functions. These events are major features of many neurodegenerative diseases, including, but not limited to, Alzheimer’s and Parkinson’s diseases. Defective mitochondria may act as biomarkers for neurodegeneration.

Mitochondria targeting drugs and mitochondrial-derived peptides protect mitochondria and may be therapeutic against many neurodegenerative diseases.  The cytoprotective mechanisms involve a wide range of pathways including apoptosis, inflammation, oxidative stress, ER stress, complement, autophagy, etc.

This Special Issue aims at summarizing the current knowledge on the role of mitochondria in neurodegenerative diseases and potential therapeutic perspectives.  We strongly encourage manuscript submissions that highlight novel mitochondria-targeting therapeutic approaches for neurogenerative diseases and/or provide novel mechanistic insights into the non-canonical mitochondria-driven pathways involved in neuronal activity.

We look forward to receiving your expert contributions.

Prof. Dr. Maria Cristina Kenney
Guest Editor

Dr. Sonali Nashine
Assistant Guest Editor

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Keywords

  • mitochondria
  • Alzheimer’s disease
  • Parkinson’s disease
  • neuroinflammation
  • lewy body formation
  • neurodegeneration

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Published Papers

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