Correlation of the clinical severity of Alzheimer's disease with an aberration in mitochondrial DNA (mtDNA)

Brown, Abraham M.; Sheu, Rex K.-F.; Mohs, Richard; Haroutunian, Vahram; Blass, John P.

doi:10.1385/jmn:16:1:41

Cited by 40Alzheimer's disease research and treatmentsMitochondrial Function and PathologyDementia and Cognitive Impairment Research

Correlation of the clinical severity of Alzheimer's disease with an aberration in mitochondrial DNA (mtDNA)

Brown, Abraham M., Sheu, Rex K.-F., Mohs, Richard, Haroutunian, Vahram, Blass, John P.·2001·Journal of Molecular Neuroscience

DOI 10.1385/jmn:16:1:41

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Abstract

Controversy exists about which of the well-established neurobiological abnormalities in Alzheimer's disease (AD) relate directly to the clinical disabilities. Because of an interest in the mitochondrial lesion in AD, we tested the correlation between clinical disability (measured by the Clinical Dementia Rating [CDR] scale) and an anomaly in mitochondrial DNA (mtDNA) in AD brain. Simultaneous polymerase chain reaction (PCR) amplification of the CO1 gene in mtDNA and CO1 pseudogenes in nuclear DNA (nDNA) were performed in samples from AD and non-AD brain, and the ratios of mtDNA/nDNA amplicons calculated. This approach utilizes PCR amplification of endogenous nDNA as a normalization standard for the amplification of mtDNA. We examined total DNA from the brains of Caucasian residents of a Jewish nursing home (86 AD and 26 non-AD "controls"). These patients had been closely followed clinically until death and then autopsied. In this sample, the degree of cognitive impairment in the AD patients correlated with the reduction in the amplification of the mtDNA gene (p = 0.23; p = 0.034), but not with the density of neuritic plaques (p = 0.109). These results agree with the suggestion that the well-documented impairment in brain-energy metabolism in AD may be a direct cause of the clinical disability.

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AD subject brains and blood cells contain less PCR-amplifiable mtDNA.
“In aggregate, AD subject brains and blood cells contain less PCR-amplifiable mtDNA [47, 105, 109-111].”
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Authors: Brown, A. M., Sheu, R. K.-F., Mohs, R., Haroutunian, V., & Blass, J. P.
Affiliations: Cornell University (US)
Veterans Health Administration (US)
Corresponding author: Blass, John P.
ORCID: Brown, Abraham M.
Mohs, Richard
Haroutunian, Vahram
Venue: Journal of Molecular Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2001
Volume: 16
Issue: 1
Pages: 41-48
ISSN: 0895-8696 (ISSN-L)
DOI: 10.1385/jmn:16:1:41
OpenAlex: W2069862107
Cited by: 40
References: 41
Citations by year: 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 1 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 4 · 2015: 1 · 2014: 1 · 2013: 3 · 2012: 1
FWCI: 1.20
Type: journal article
Language: en
Open access: closed
Locations: Journal of Molecular Neuroscience (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, mitochondrial DNA, mtDNA/nDNA ratio, CO1 gene, Clinical Dementia Rating, cognitive impairment, brain energy metabolism, neuritic plaques
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Brain, Disability Evaluation, DNA Mutational Analysis, DNA, Mitochondrial, Female, Humans, Male, Middle Aged, Mutation, Nerve Degeneration, Neurons, Polymerase Chain Reaction, Disease Progression

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Correlation of the clinical severity of Alzheimer's disease with an aberration in mitochondrial DNA (mtDNA)

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