Mitochondrial Dysfunction, Oxidative Stress, Neuroinflammation, and Metabolic Alterations in the Progression of Alzheimer's Disease: A Meta-Analysis of In Vivo Magnetic Resonance Spectroscopy Studies
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Accumulating evidence demonstrates that metabolic changes in the brain associated with neuroinflammation, oxidative stress, and mitochondrial dysfunction play an important role in the pathophysiology of mild cognitive impairment (MCI) and Alzheimer's disease (AD). However, the neural signatures associated with these metabolic alterations and underlying molecular mechanisms are still elusive. Accordingly, we reviewed the literature on in vivo human brain 1 H and 31 P-MRS studies and use meta-analyses to identify patterns of brain metabolic alterations in MCI and AD. 40 and 39 studies on MCI and AD, respectively, were classified according to brain regions. Our results indicate decreased N-acetyl aspartate and creatine but increased myo-inositol levels in both MCI and AD, decreased glutathione level in MCI as well as disrupted energy metabolism in AD. In addition, the hippocampus shows the strongest alterations in most of these metabolites. This meta-analysis also illustrates progressive metabolite alterations from MCI to AD. Taken together, it suggests that 1) neuroinflammation and oxidative stress may occur in the early stages of AD, and likely precede neuron loss in its progression; 2) the hippocampus is a sensitive region of interest for early diagnosis and monitoring the response of interventions; 3) targeting bioenergetics associated with neuroinflammation/oxidative stress is a promising approach for treating AD.
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Aβ deposition, tau hyperphosphorylation, and neuroinflammation exacerbate metabolic impairment by further disrupting glucose transport and mitochondrial function.
“On the other hand, Aβ deposition, tau hyperphosphorylation, and neuroinflammation exacerbate metabolic impairment by further disrupting glucose transport and mitochondrial function [75].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [75]
The Discussion (page unavailable) links Aβ to microglial activation and describes neuroinflammation, mitochondrial dysfunction, and metabolic alterations as intertwined in Alzheimer’s disease. It does not say that Aβ deposition, tau hyperphosphorylation, and neuroinflammation worsen metabolism by disrupting glucose transport and mitochondrial function; it also notes that mitochondrial dysfunction may precede amyloid deposition. Searches for glucose transport and tau hyperphosphorylation did not establish those specific mechanisms. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThese mitochondrial changes reduce ATP production and amplify ROS generation, establishing a vicious cycle of bioenergetic failure and oxidative damage.
“These changes not only reduce ATP production but also amplify ROS generation, establishing a vicious cycle of bioenergetic failure and oxidative damage [75].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [75]
The Introduction links mitochondrial abnormalities in Alzheimer’s disease to cellular energy deficits and excess ROS, and the Discussion says mitochondrial dysfunction could cause ROS overproduction and oxidative stress. But the paper does not establish reduced ATP production or a self-reinforcing cycle of bioenergetic failure and oxidative damage; its Results report no significant difference in ATP levels between AD patients and healthy controls. The Discussion describes these processes as intertwined while cautioning that their causal order is unclear. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAβ exacerbates mitochondrial dysfunction by impairing respiratory enzyme activity, disrupting mitochondrial dynamics, and interacting directly with mitochondrial proteins such as Aβ-binding alcohol dehydrogenase.
“In AD, Aβ exacerbates mitochondrial dysfunction by impairing respiratory enzyme activity, disrupting mitochondrial dynamics, and interacting directly with mitochondrial proteins, such as Aβ-binding alcohol dehydrogenase.”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [75]
The Introduction (page unavailable) reports reduced mitochondrial enzyme activity and altered mitochondrial structure in AD, supporting the background link to mitochondrial dysfunction. It does not say that Aβ causes those changes, disrupts mitochondrial dynamics, or binds Aβ-binding alcohol dehydrogenase. The Discussion (page unavailable) instead notes that mitochondrial dysfunction may precede amyloid plaques. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIncreased oxidative stress, mitochondrial dysfunction, neuroinflammation, and metabolic alterations may be critical in initiation of neurodegeneration in AD.
“increased levels of oxidative stress, mitochondrial dysfunction, neuroinflammation, and metabolic alterations, which are prominent features of aging, may all be critical in the initiation of the neurodegeneration occurring in AD (Song et al., 2021)”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Song et al., 2021
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Hein, Z. M., Karikalan, B., Gopalakrishna, P. K., Dhevi, K., Alkatiri, A., Hussan, F., Mohd Moklas, M. A., Jagadeesan, S., Che Ramli, M. D., Che Mohd Nassir, C. M. N., et al. (2026) · Molecular Neurobiology · doi:10.1007/s12035-025-05602-0 · Cited by 43 · see citing works
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The Power Struggle: Kynurenine Pathway Enzyme Knockouts and Brain Mitochondrial Respiration
Juhász, L., Spisák, K., Szolnoki, B. Z., Nászai, A., Szabó, Á., Rutai, A., Tallósy, S. P., Szabó, A., Toldi, J., Tanaka, M., et al. (2025) · Journal of Neurochemistry · doi:10.1111/jnc.70075 · Cited by 15 · see citing works
- Authors
- Song, T., Song, X., Zhu, C., Patrick, R., Skurla, M., Santangelo, I., Green, M., Harper, D., Ren, B., Forester, B. P., Öngür, D., & Du, F.
- Affiliations
- Harvard University (US)
- McLean Hospital (US)
- Corresponding author
- Du, Fei
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2021-12
- Volume
- 72
- Pages
- 101503
- ISSN
- 1568-1637 (ISSN-L)
- PMC
- PMC8662951
- OpenAlex
- W3209041513
- Cited by
- 346
- References
- 176
- Citations by year
- 2026: 85 · 2025: 96 · 2024: 86 · 2023: 54 · 2022: 25
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 339 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Ageing Research Reviews (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (K24MH104449, P50MH115846, R01AG066670, R01MH095809, R01MH114982)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
- Keywords
- Alzheimer's disease, mild cognitive impairment, mitochondrial dysfunction, oxidative stress, neuroinflammation, brain energy metabolism, N-acetylaspartate, creatine, myo-inositol, glutathione, hippocampus, 31P NMR, 1H magnetic resonance spectroscopy, early diagnosis, bioenergetics
- MeSH terms
- Neuroinflammatory Diseases, Alzheimer Disease, Humans, Mitochondria, Magnetic Resonance Spectroscopy, Oxidative Stress, Disease Progression, Cognitive Dysfunction
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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.
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