Brain‐derived neurotrophic factor as a regulator of systemic and brain energy metabolism and cardiovascular health
Open accessAbstract
Overweight sedentary individuals are at increased risk for cardiovascular disease, diabetes, and some neurological disorders. Beneficial effects of dietary energy restriction (DER) and exercise on brain structural plasticity and behaviors have been demonstrated in animal models of aging and acute (stroke and trauma) and chronic (Alzheimer's and Parkinson's diseases) neurological disorders. The findings described later, and evolutionary considerations, suggest brain‐derived neurotrophic factor (BDNF) plays a critical role in the integration and optimization of behavioral and metabolic responses to environments with limited energy resources and intense competition. In particular, BDNF signaling mediates adaptive responses of the central, autonomic, and peripheral nervous systems from exercise and DER. In the hypothalamus, BDNF inhibits food intake and increases energy expenditure. By promoting synaptic plasticity and neurogenesis in the hippocampus, BDNF mediates exercise‐ and DER‐induced improvements in cognitive function and neuroprotection. DER improves cardiovascular stress adaptation by a mechanism involving enhancement of brainstem cholinergic activity. Collectively, findings reviewed in this paper provide a rationale for targeting BDNF signaling for novel therapeutic interventions in a range of metabolic and neurological disorders.
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In the hippocampus, BDNF promotes the production and survival of new neurons from stem cells and the integration of new neurons into existing neuronal circuits.
“In the hippocampus, BDNF promotes the production and survival of new neurons from stem cells and the integration of new neurons into existing neuronal circuits [141], reviewed in [160].”
From The neuropathology of sport (2014) · cites this paper as [160]
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- Authors
- Rothman, S. M., Griffioen, K. J., Wan, R., & Mattson, M. P.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Rothman, Sarah M.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2012-04-30
- Volume
- 1264
- Issue
- 1
- Pages
- 49-63
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC3411899
- OpenAlex
- W2135826654
- Cited by
- 185
- References
- 134
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 12 · 2023: 7 · 2022: 10 · 2021: 13 · 2020: 11 · 2019: 13 · 2018: 17 · 2017: 19 · 2016: 14 · 2015: 20 · 2014: 14 · 2013: 11 · 2012: 4
- FWCI
- 1.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (Z99 AG999999)
- National Institute on Aging
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- brain-derived neurotrophic factor, energy metabolism, cardiovascular health, hypocaloric diet, physical activity, hypothalamus, dietary intake, energy expenditure, synaptic plasticity, hippocampal neurogenesis, cognitive function, neuroprotection, cholinergic activity, brainstem, obesity, diabetes mellitus, neurological disorders, BDNF signaling
- MeSH terms
- Animals, Autonomic Nervous System, Cardiovascular Diseases, Central Nervous System, Cognition, Eating, Energy Metabolism, Hippocampus, Humans, Hypothalamus, Neuronal Plasticity, Obesity, Exercise, Brain-Derived Neurotrophic Factor, Caloric Restriction, Mice
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.
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