Cited by 263Mitochondrial Function and PathologyAutophagy in Disease and TherapyParkinson's Disease Mechanisms and Treatments

Mitochondrial involvement in brain function and dysfunction: relevance to aging, neurodegenerative disorders and longevity

Open access
Calabrese, V., Scapagnini, G., Giuffrida Stella, A. M., Bates, T. E., Clark, J. B.·2001·Neurochemical Research

Abstract

It is becoming increasingly evident that the mitochondrial genome may play a key role in neurodegenerative diseases. Mitochondrial dysfunction is characteristic of several neurodegenerative disorders, and evidence for mitochondria being a site of damage in neurodegenerative disorders is partially based on decreases in respiratory chain complex activities in Parkinson's disease, Alzheimer's disease, and Huntington's disease. Such defects in respiratory complex activities, possibly associated with oxidant/antioxidant balance perturbation, are thought to underlie defects in energy metabolism and induce cellular degeneration. Efficient functioning of maintenance and repair process seems to be crucial for both survival and physical quality of life. This is accomplished by a complex network of the so-called longevity assurance processes, which are composed of genes termed vitagenes. A promising approach for the identification of critical gerontogenic processes is represented by the hormesis-like positive effect of stress. In the present review, we discuss the role of energy thresholds in brain mitochondria and their implications in neurodegeneration. We then review the evidence for the role of oxidative stress in modulating the effects of mitochondrial DNA mutations on brain age-related disorders and also discuss new approaches for investigating the mechanisms of lifetime survival and longevity.

Integrity signals

Registry

Crossref · 10.1023/a:1010955807739

Cites

196 of 196 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • AD has been related to genetic mutations, including in the gene encoding the Aβ precursor protein peptide, mutations in presenilins genes, and presence of the APOE ε4 allele.

    “AD has been related to genetic mutations, among them in the gene encoding the Aβ precursor protein peptide, mutations in the presenilins genes (Calabrese et al., 2001) and the presence of the APOE ε4 allele (Martínez-Lazcano et al., 2010).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Calabrese, V., Scapagnini, G., Giuffrida Stella, A. M., Bates, T. E., & Clark, J. B.
Affiliations
  • University of Catania (IT)
  • UCL Queen Square Institute of Neurology (GB)
Venue
Neurochemical Research
Published
2001-06
Volume
26
Issue
6
Pages
739-764
ISSN
  • 0364-3190 (ISSN-L)
  • 1573-6903
OpenAlex
W1595816980
Cited by
263
References
196
Citations by year
2026: 4 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 9 · 2020: 8 · 2019: 1 · 2018: 5 · 2017: 13 · 2016: 9 · 2015: 8 · 2014: 9 · 2013: 14 · 2012: 16
FWCI
5.31
Type
journal article
Language
en
Open access
Locations
  • Neurochemical Research (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Figshare (submittedVersion, cc-by)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
mitochondrial dysfunction, neurodegenerative diseases, brain aging, longevity, Parkinson's disease, Alzheimer's disease, Huntington's disease, respiratory chain complexes, oxidative stress, mitochondrial DNA mutations, energy metabolism, vitagenes, hormesis, stress response, brain mitochondria
MeSH terms
Aging, Animals, Brain, Humans, Longevity, Mitochondria, Neurodegenerative Diseases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review