Regular exercise prevents non-cognitive disturbances in a rat model of Alzheimer's disease
Open accessAbstract
Previously, we reported that in a rat model of sporadic Alzheimer's disease (AD) generated by exogenous administration of Aβ₁₋₄₂ (250 pmol/d for 2 wk) via mini-osmotic pump, the animals exhibited learning and memory impairment, which could be attributed to the deleterious alterations in the levels of cognition-related signalling molecules. We showed that 4 wk of treadmill exercise totally prevented these impairments. Here, we evaluated the effect of exercise on non-cognitive function and basal synaptic transmission in the Cornu Ammonis 1 (CA1) area using the same AD model. Our results indicated that the anxiety behaviour of Aβ-treated rats was prevented by 4 wk of treadmill exercise. Exercised/Aβ-infused rats spent a longer time in the centre area of the open field (OF), elevated plus maze (EPM) paradigms and the light area of the light-dark (LD) box, which were similar to those of control and exercise rats. Furthermore, under basal conditions the aberrant up-regulation of calcineurin (PP2B) and reduction of phosphorylated Ca²⁺/calmodulin dependent protein kinase II (p-CaMKII) levels induced by AD-like pathology were normalised by the exercise regimen. We conclude that regular exercise may exert beneficial effects on both cognitive and non-cognitive functions in this AD model.
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HIIT regulates hippocampal oxidative stress, BDNF, and inflammatory mediators in laboratory animals.
“Additionally, this training method regulates hippocampal oxidative stress, BDNF, and in ammatory mediators in laboratory animals.”
HIIT through increases in H2O2 and TNF-α can lead to a significant improvement in BDNF and GDNF concentrations.
“High-Intensity Interval Training (HIIT) through increases in H 2 O 2 and TNF-α can lead to a signi cant improvement in BDNF (Brain-Derived Neurotrophic Factor) and GDNF (Glial Derived Neurotrophic Factor) concentrations”
Training with interval bouts that need maximum effort will result in better neurotrophic gain.
“Thus, training with interval bouts that need maximum effort will result in better neurotrophic gain (27).”
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- Authors
- Dao, A. T., Zagaar, M. A., Salim, S., Eriksen, J. L., & Alkadhi, K. A.
- Affiliations
- University of Houston (US)
- Corresponding author
- Alkadhi, Karim A.
- Venue
- The International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-11-14
- Volume
- 17
- Issue
- 04
- Pages
- 593-602
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- PMC
- PMC4097602
- OpenAlex
- W1994504660
- Cited by
- 39
- References
- 55
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 3 · 2018: 5 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 3
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Houston
- National Institutes of Health
- National Institute on Aging (R15 AG103327, R15AG039008)
- National Institute of Mental Health (R15MH093918)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, treadmill exercise, physical activity, amyloid-beta, anxiety-like behavior, synaptic transmission, hippocampal CA1, calcineurin, CaMKII, learning and memory impairment, rat model
- MeSH terms
- Alzheimer Disease, Animals, Anxiety, Behavior, Animal, Disease Models, Animal, Male, Motor Activity, Synaptic Transmission, Physical Conditioning, Animal, Random Allocation, Rats, Wistar, Calcineurin, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, CA1 Region, Hippocampal
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