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Environmental Enrichment Mitigates Cognitive Deficits in a Mouse Model of Alzheimer's Disease
Open accessAbstract
Epidemiological studies suggest that individuals with greater education or more cognitively demanding occupations have diminished risk of developing dementia. We wanted to test whether this effect could be recapitulated in rodents using environmental enrichment, a paradigm well documented to attenuate behavioral deficits induced by various pathological insults. Here, we demonstrate that learning and memory deficits observed in a transgenic mouse model of Alzheimer's disease can be ameliorated by enrichment. Female transgenic mice overexpressing amyloid precursor protein and/or presenilin-1 and nontransgenic controls were placed into enriched or standard cages at 2 months of age and tested for cognitive behavior after 6 months of differential housing. Enrichment significantly improved performance of all genotypes in the radial water maze and in the classic and repeated-reversal versions of the Morris water maze. However, enrichment did not benefit all genotypes equally. Mice overproducing amyloid-β (Aβ), particularly those with amyloid deposits, showed weaker memory for the platform location in the classic Morris water maze and learned new platform positions in the repeated-reversals task less quickly than their nontransgenic cagemates. Nonetheless, enrichment normalized the performance of Aβ-overproducing mice to the level of standard-housed nontransgenic mice. Moreover, this functional preservation occurred despite increased neuritic plaque burden in the hippocampus of double-transgenic animals and elevated steady-state Aβ levels, because both endogenous and transgene-derived Aβ are increased in enriched animals. These results demonstrate that the generation of Aβ in vivo and its impact on the function of the nervous system can be strongly modulated by environmental factors.
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“there are many examples of environmental and/or microglial gene manipulation in mouse models of amyloidosis in which cognition improved in the absence of a decrease, or even in the presence of an increase, in plaques.61,62”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [61]
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Metadata
- Authors
- Jankowsky, J. L., Melnikova, T., Fadale, D. J., Xu, G. M., Slunt, H. H., Gonzales, V., Younkin, L. H., Younkin, S. G., Borchelt, D. R., & Savonenko, A. V.
- Affiliations
- California Institute of Technology (US)
- Johns Hopkins University (US)
- Mayo Clinic in Florida (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-05-25
- Volume
- 25
- Issue
- 21
- Pages
- 5217-5224
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC4440804
- OpenAlex
- W2059212904
- Cited by
- 517
- References
- 86
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 14 · 2023: 23 · 2022: 25 · 2021: 27 · 2020: 18 · 2019: 20 · 2018: 27 · 2017: 24 · 2016: 32 · 2015: 34 · 2014: 19 · 2013: 29 · 2012: 26
- FWCI
- 17.45
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by)
- Funders
- American Health Assistance Foundation
- John Douglas French Alzheimer's Foundation
- National Institutes of Health
- National Institute on Aging (AG 15453, AG06656, K01AG026144, P01AG015453, K01AG26144, R01AG006656)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- environmental enrichment, Alzheimer's disease, amyloid-beta, amyloid precursor protein, presenilin 1, cognitive impairment, learning and memory, Morris water maze, neuritic plaques, hippocampus, transgenic mice
- MeSH terms
- Age Factors, Alzheimer Disease, Analysis of Variance, Animals, Behavior, Animal, Cognition Disorders, Disease Models, Animal, Environment, Enzyme-Linked Immunosorbent Assay, Female, Hippocampus, Humans, Immunohistochemistry, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Time Factors, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Maze Learning, Mice, Presenilin-1
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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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