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Cited by 72Mitochondrial Function and PathologyAlzheimer's disease research and treatmentsAutophagy in Disease and Therapy

Role of mitochondrial-mediated signaling pathways in Alzheimer disease and hypoxia

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Carvalho, Cristina, Correia, Sónia C., Santos, Renato X., Cardoso, Susana, Moreira, Paula I., Clark, Timothy A., Zhu, Xiongwei, Smith, Mark A. +1 more·2009·Journal of Bioenergetics and Biomembranes
DOI 10.1007/s10863-009-9247-1PMC PMC4054815
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Abstract

Development of effective treatments for Alzheimer's disease is complicated by the poor understanding of its pathophysiology. Recent work suggests mitochondria may play a primary role in neurodegeneration, due to alterations in mitochondria turnover and that the brain is specifically susceptible, due to high energy demand. Mitochondria are the major source of cellular energy through oxidative phosphorylation and regulate intracellular calcium levels and survival pathways. Hypoxia has been implicated in several neurodegenerative diseases including Alzheimer's disease. During hypoxic events, mitochondrial complex III produces high levels of reactive oxygen species (ROS). These ROS seem to have a primary role in the regulation of the transcription factor hypoxia inducible factor 1alpha that triggers death effectors. Here we discuss the role of mitochondria in AD putting focus on the activation of hypoxia-mediated mitochondrial pathways, which could eventually lead to cell degeneration and death.

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  • Disruption of the communication networks between mitochondria and the rest of the cell is thought to contribute to aging and neurodegeneration.

    “Disruption of the communication networks between mitochondria and the rest of the cell is thought to contribute to aging and neurodegeneration [50, 51].”

    From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [51]

    The “Mitochondria and the brain” section (page unavailable) says that excess reactive oxygen species activate anomalous signaling and discusses mitochondrial damage during aging. The “Is mitochondrial dysfunction a necessary step in neurodegeneration?” section (page unavailable) links mitochondrial dysfunction to Alzheimer’s disease. The copy does not specifically say that disrupted communication between mitochondria and the rest of the cell contributes to aging. (LLM, conf=0.82)

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Authors
Carvalho, C., Correia, S. C., Santos, R. X., Cardoso, S., Moreira, P. I., Clark, T. A., Zhu, X., Smith, M. A., & Perry, G.
Affiliations
  • Centro de Neurociências e Biologia Celular (PT)
  • The University of Texas at San Antonio (US)
  • Case Western Reserve University (US)
Corresponding author
Perry, George
ORCID
Venue
Journal of Bioenergetics and Biomembranes
Publisher
Springer Science and Business Media LLC
Published
2009-10
Volume
41
Issue
5
Pages
433-440
ISSN
  • 0145-479X (ISSN-L)
  • 1573-6881
DOI
10.1007/s10863-009-9247-1
PMC
PMC4054815
OpenAlex
W2083174388
Cited by
72
References
10
Citations by year
2026: 2 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 8 · 2021: 2 · 2020: 6 · 2019: 8 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 8 · 2014: 5 · 2013: 4 · 2012: 3
FWCI
0.29
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Journal of Bioenergetics and Biomembranes (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of General Medical Sciences (R25GM060655)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
Alzheimer's disease, hypoxia, mitochondria, mitochondrial pathway, reactive oxygen species, hypoxia-inducible factor-1α, neurodegeneration, oxidative phosphorylation, mitochondrial complex III, cell death, intracellular calcium
MeSH terms
Alzheimer Disease, Hypoxia, Brain, Humans, Mitochondria, Models, Neurological, Nerve Degeneration, Signal Transduction, Cell Death, Reactive Oxygen Species

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