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 443

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

Published Papers

There is no accepted submissions to this special issue at this moment.
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