skip to main content
DOE PAGES title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington’s disease

Abstract

Mitochondrial dysfunction and ensuing oxidative damage is typically thought to be a primary cause of Huntington's disease, Alzheimer's disease, and Parkinson disease. There is little doubt that mitochondria (MT) become defective as neurons die, yet whether MT defects are the primary cause or a detrimental consequence of toxicity remains unanswered. Oxygen consumption rate (OCR) and glycolysis provide sensitive and informative measures of the functional status MT and the cells metabolic regulation, yet these measures differ depending on the sample source; species, tissue type, age at measurement, and whether MT are measured in purified form or in a cell. The effects of these various parameters are difficult to quantify and not fully understood, but clearly have an impact on interpreting the bioenergetics of MT or their failure in disease states. A major goal of the review is to discuss issues and coalesce detailed information into a reference table to help in assessing mitochondrial dysfunction as a cause or consequence of Huntington's disease.

Authors:
ORCiD logo [1];  [1]
  1. Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States). Molecular Biophysics and Integrated Bioimaging Division
Publication Date:
Research Org.:
Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
Sponsoring Org.:
National Institutes of Health (NIH)
OSTI Identifier:
1393099
Grant/Contract Number:  
AC02-05CH11231; NS060115; CA092584
Resource Type:
Accepted Manuscript
Journal Name:
Mechanisms of Ageing and Development
Additional Journal Information:
Journal Volume: 161; Journal Issue: Part A; Journal ID: ISSN 0047-6374
Publisher:
Elsevier
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; 59 BASIC BIOLOGICAL SCIENCES

Citation Formats

Polyzos, Aris A., and McMurray, Cynthia T. The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington’s disease. United States: N. p., 2016. Web. doi:10.1016/j.mad.2016.09.003.
Polyzos, Aris A., & McMurray, Cynthia T. The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington’s disease. United States. doi:10.1016/j.mad.2016.09.003.
Polyzos, Aris A., and McMurray, Cynthia T. Mon . "The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington’s disease". United States. doi:10.1016/j.mad.2016.09.003. https://www.osti.gov/servlets/purl/1393099.
@article{osti_1393099,
title = {The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington’s disease},
author = {Polyzos, Aris A. and McMurray, Cynthia T.},
abstractNote = {Mitochondrial dysfunction and ensuing oxidative damage is typically thought to be a primary cause of Huntington's disease, Alzheimer's disease, and Parkinson disease. There is little doubt that mitochondria (MT) become defective as neurons die, yet whether MT defects are the primary cause or a detrimental consequence of toxicity remains unanswered. Oxygen consumption rate (OCR) and glycolysis provide sensitive and informative measures of the functional status MT and the cells metabolic regulation, yet these measures differ depending on the sample source; species, tissue type, age at measurement, and whether MT are measured in purified form or in a cell. The effects of these various parameters are difficult to quantify and not fully understood, but clearly have an impact on interpreting the bioenergetics of MT or their failure in disease states. A major goal of the review is to discuss issues and coalesce detailed information into a reference table to help in assessing mitochondrial dysfunction as a cause or consequence of Huntington's disease.},
doi = {10.1016/j.mad.2016.09.003},
journal = {Mechanisms of Ageing and Development},
number = Part A,
volume = 161,
place = {United States},
year = {2016},
month = {9}
}

Journal Article:
Free Publicly Available Full Text
Publisher's Version of Record

Citation Metrics:
Cited by: 6 works
Citation information provided by
Web of Science

Save / Share: