Aberrant Mitochondrial Metabolism in Alzheimer's Disease Links Energy Stress with Ferroptosis Article Swipe
Francesca Alves
,
Darius J.R. Lane
,
Adam Wahida
,
Md. Jakaria
,
Paweł Kalinowski
,
Adam Southon
,
Abdel Ali Belaidi
,
Teresa Samperi‐Esteve
,
Triet Phu Minh Nguyen
,
Lei Peng
,
Marcus Krueger
,
Stefan Mueller
,
Marcus Conrad
,
Puja Agarwal
,
Sue E. Leurgans
,
Julie Schneider
,
Ashley I. Bush
,
Scott Ayton
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1002/advs.202504175
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1002/advs.202504175
Alzheimer's disease (AD) is defined by β‐amyloid plaques and tau‐containing neurofibrillary tangles, but the ensuing cellular derangements that culminate in neurodegeneration remain elusive. Here, a mechanistic link between two AD pathophysiological hallmarks: energy insufficiency and oxidative stress is revealed. It is demonstrated that mitochondrial function and glutathione (GSH) flux are coupled, impacting neuronal ferroptosis susceptibility. Analysis of proteomic data from the inferior temporal cortex of 625 subjects along a continuum of clinical and pathological changes in AD, reveals a prominent depletion of mitochondrial proteins. Biogenetic insufficiency in AD is reflected by a concurrent loss of GSH, which requires 2 ATP for its synthesis, and genetic and pharmacologic ATP depletion models confirm that ATP is rate‐limiting for GSH. Accordingly, an unbiased association analysis uncovers mitochondrial proteins in positive correlation with total GSH (t‐GSH) in AD subjects. But mitochondria also consume GSH via the SLC25A39 transporter. It is found that mitochondrial inhibition either increases or decreases ferroptosis susceptibility in cellular models, depending on contextual factors that dictate whether mitochondria act as a net GSH producer or consumer, respectively. Mitochondria therefore control GSH flux, and loss of energy output is consequently demonstrated as a liability for ferroptosis in AD.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/advs.202504175
- OA Status
- gold
- Cited By
- 4
- References
- 71
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4412111007
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4412111007Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1002/advs.202504175Digital Object Identifier
- Title
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Aberrant Mitochondrial Metabolism in Alzheimer's Disease Links Energy Stress with FerroptosisWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2025Year of publication
- Publication date
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2025-07-08Full publication date if available
- Authors
-
Francesca Alves, Darius J.R. Lane, Adam Wahida, Md. Jakaria, Paweł Kalinowski, Adam Southon, Abdel Ali Belaidi, Teresa Samperi‐Esteve, Triet Phu Minh Nguyen, Lei Peng, Marcus Krueger, Stefan Mueller, Marcus Conrad, Puja Agarwal, Sue E. Leurgans, Julie Schneider, Ashley I. Bush, Scott AytonList of authors in order
- Landing page
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https://doi.org/10.1002/advs.202504175Publisher landing page
- Open access
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://doi.org/10.1002/advs.202504175Direct OA link when available
- Concepts
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Energy metabolism, Disease, Mitochondrion, Oxidative stress, Metabolism, Stress (linguistics), Neuroscience, Biology, Cell biology, Medicine, Biochemistry, Internal medicine, Endocrinology, Philosophy, LinguisticsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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4Total citation count in OpenAlex
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2025: 4Per-year citation counts (last 5 years)
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71Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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