Short-term exercise in aged Tg2576 mice alters neuroinflammation and improves cognition
Open accessAbstract
Exercise is a treatment paradigm that can ameliorate cognitive dysfunction in Alzheimer disease (AD) and AD mouse models. Since exercise is also known to alter the peripheral immune response, one potential mechanism for the cognitive improvement following exercise may be by modulating the inflammatory repertoire in the central nervous system. We investigated the effects of voluntary exercise in the Tg2576 mouse model of AD at a time-point at which pathology has already developed. Inflammatory mRNA markers are increased in sedentary Tg2576 mice versus non-transgenic controls. We demonstrate that short-term voluntary wheel running improved spatial learning in aged transgenic mice as compared to sedentary Tg2576 controls. Inflammatory profiles of the Tg2576 and non-transgenic mice were different following exercise with the non-transgenic mice showing a broader response as compared to the Tg2576. Notably, exercising Tg2576 exhibited increases in a few markers including CXCL1 and CXCL12, two chemokines that may affect cognition.
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Mice show greater improvements in acquisition and retention based learning in hippocampus-dependent tasks following long-term exercise rather than shorter regimes of exercise.
“Further work illustrates that mice show greater improvements in acquisition and retention based learning in hippocampus-dependent tasks following long-term exercise rather than shorter regimes of exercise (Handschin and Spiegelman, 2008; Parachikova et al., 2008; Ploeger et al., 2009).”
From Exercise-Mediated Neurogenesis in the Hippocampus via BDNF (2018) · cites this paper as Parachikova et al., 2008
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- Authors
- Parachikova, A., Nichol, K. E., & Cotman, C. W.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Parachikova, A.
- ORCID
- Cotman, C.W.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2008-04
- Volume
- 30
- Issue
- 1
- Pages
- 121-129
- ISSN
- 0969-9961 (ISSN-L)
- PMC
- PMC2386749
- OpenAlex
- W2053298975
- Cited by
- 193
- References
- 4
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 7 · 2021: 9 · 2020: 13 · 2019: 9 · 2018: 15 · 2017: 3 · 2016: 14 · 2015: 13 · 2014: 10 · 2013: 16 · 2012: 26
- FWCI
- 9.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (P01AG000538, AG 16573, AG-000538, P50AG016573)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- voluntary exercise, wheel running, Alzheimer's disease, Tg2576 mice, neuroinflammation, cognitive impairment, spatial learning, aged mice, chemokines, CXCL1, CXCL12, inflammatory gene expression, sedentary behavior
- MeSH terms
- Aging, Alzheimer Disease, Animals, Behavior, Animal, Cognition, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Inflammation, Mice, Inbred C57BL, Mice, Transgenic, RNA, Messenger, Time Factors, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Maze Learning, Microarray Analysis, Mice, Chemokine CXCL1, Chemokine CXCL2
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