Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States
Open accessAbstract
During aging, the cellular milieu of the brain exhibits tell-tale signs of compromised bioenergetics, impaired adaptive neuroplasticity and resilience, aberrant neuronal network activity, dysregulation of neuronal Ca2+ homeostasis, the accrual of oxidatively modified molecules and organelles, and inflammation. These alterations render the aging brain vulnerable to Alzheimer’s and Parkinson’s diseases and stroke. Emerging findings are revealing mechanisms by which sedentary overindulgent lifestyles accelerate brain aging, whereas lifestyles that include intermittent bioenergetic challenges (exercise, fasting, and intellectual challenges) foster healthy brain aging. Here we provide an overview of the cellular and molecular biology of brain aging, how those processes interface with disease-specific neurodegenerative pathways, and how metabolic states influence brain health.
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Diffusion MRI indicates age-related changes in white matter connectivity between prefrontal and posterior cortical regions and within posterior sensory cortices.
“Diffusion MRI methods have shown age-related changes in white matter connectivity between prefrontal and posterior cortical regions, and within posterior sensory cortices.25–27”
From Maintenance, reserve and compensation: the cognitive neuroscience of healthy ageing (2018) · cites this paper as [27]
The 'Aberrant Neuronal Network Activity' section says white matter integrity is compromised during normal aging and describes age-related changes in functional connectivity. It does not say that diffusion MRI showed changes specifically between prefrontal and posterior cortical regions or within posterior sensory cortices. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn neurons, mitochondria generate ATP through oxidative phosphorylation in order to sustain synaptic transmission and cell maintenance/repair.
“In neurons, mitochondria generate ATP through oxidative phosphorylation in order to sustain synaptic transmission and cell maintenance/repair.73,75”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [73]
Mitochondrial dysfunction is a known hallmark of the aging brain and neurodegenerative disorders.
“Mitochondrial dysfunction is a known hallmark of the aging brain73,74 and neurodegenerative disorders.75,76,77”
From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [73]
Chronic neuroinflammation is a common feature of the aged brain.
“Chronic neuroinflammation is a common feature of the aged brain”
From Dietary Restriction and Neuroinflammation: A Potential Mechanistic Link (2019) · cites this paper as [21]
Brain ageing and Alzheimer's disease share common alterations, such as a loss of proteostasis, oxidative stress, and inflammation, which are exacerbated in Alzheimer's disease.
“Brain ageing and AD share common alterations, such as a loss of proteostasis, oxidative stress, and inflammation, which are exacerbated in AD.99”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [99]
The study details ligand-receptor interactions among nearly all cell types in the brain that are modified by aging.
“Given that cell non-autonomous changes are also known to regulate aging-dependent changes 2,3 , we also detail ligand-receptor interactions among nearly all the cell types in the brain that are modified by aging.”
From Single-cell transcriptomic profiling of the aging mouse brain (2019) · cites this paper as [3]
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Plumbagin, a novel Nrf2/ARE activator, protects against cerebral ischemia
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Hypothalamic PGC-1α Protects Against High-Fat Diet Exposure by Regulating ERα
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Exercise and BDNF reduce Aβ production by enhancing α‐secretase processing of APP
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Self-citationParkinson's Disease Is Not Simply a Prion Disorder
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shRNA targeting α-synuclein prevents neurodegeneration in a Parkinson’s disease model
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The etiology of Parkinson's disease with emphasis on the MPTP story
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Mitochondrial DNA Oxidative Damage and Repair in Aging and Alzheimer's Disease
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Genomic integrity and the ageing brain
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The Global Burden of Ischemic Stroke: Findings of the GBD 2010 Study
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Recruiting adaptive cellular stress responses for successful brain ageing
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Why size matters – balancing mitochondrial dynamics in Alzheimer's disease
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Novel ketone diet enhances physical and cognitive performance
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Self-citation
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Effects of intermittent fasting on health, aging, and disease
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Self-citationMaintenance, reserve and compensation: the cognitive neuroscience of healthy ageing
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Synergy between amyloid-β and tau in Alzheimer’s disease
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NAD+ in Brain Aging and Neurodegenerative Disorders
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Self-citationMolecular mechanisms of dietary restriction promoting health and longevity
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“Actually, the hallmarks of aging that are common to neurons and other cells have been described recently (Mattson and Arumugam, 2018).”
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Aging Hallmarks and Progression and Age-Related Diseases: A Landscape View of Research Advancement
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Metabolic Network Analysis Reveals Altered Bile Acid Synthesis and Metabolism in Alzheimer’s Disease
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“As illustrated by aging and degenerative brain diseases, human brains maintain many mental abilities despite significant loss of neural mass and function ( 78 ).”
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Blood-to-brain communication in aging and rejuvenation
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Diet in Parkinson’s Disease: Critical Role for the Microbiome
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Evaluating Large Language Models in Theory of Mind Tasks
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A Primary Care Agenda for Brain Health: A Scientific Statement From the American Heart Association
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Glucose metabolism, neural cell senescence and Alzheimer's disease
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Neural ageing and synaptic plasticity: prioritizing brain health in healthy longevity
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The killifish visual system as an in vivo model to study brain aging and rejuvenation
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- Authors
- Mattson, M. P., & Arumugam, T. V.
- Affiliations
- Johns Hopkins University (US)
- National University of Singapore (SG)
- Corresponding author
- Mattson, Mark P.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 27
- Issue
- 6
- Pages
- 1176-1199
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC6039826
- OpenAlex
- W2806146174
- Semantic Scholar
- 5213382f66849c05c4e2b4d50f639a4251ce1cb7
- Cited by
- 1,242
- References
- 352
- Citations by year
- 2026: 190 · 2025: 206 · 2024: 167 · 2023: 185 · 2022: 173 · 2021: 166 · 2020: 95 · 2019: 52 · 2018: 7
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG000312-15)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- brain aging, metabolic status, neurodegeneration, Alzheimer's disease, Parkinson's disease, stroke, oxidative stress, inflammation, homeostasis, physical activity, fasting, intellectual challenge, sedentary lifestyle, bioenergetics
- MeSH terms
- Aging, Alzheimer Disease, Animals, Brain, Energy Metabolism, Homeostasis, Humans, Inflammation, Neuronal Plasticity, Neurons, Oxidation-Reduction, Parkinson Disease, Calcium Signaling, Mice, Rats
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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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