Cited by 517Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMemory and Neural Mechanisms

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Environmental Enrichment Mitigates Cognitive Deficits in a Mouse Model of Alzheimer's Disease

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Jankowsky, Joanna L., Melnikova, Tatiana, Fadale, Daniel J., Xu, Guilian M., Slunt, Hilda H., Gonzales, Victoria, Younkin, Linda H., Younkin, Steven G., Borchelt, David R., Savonenko, Alena V.·2005·The Journal of Neuroscience

DOI 10.1523/jneurosci.5080-04.2005PMC PMC4440804

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Abstract

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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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)
ORCID: Jankowsky, Joanna L.
Xu, Guilian M.
Younkin, Steven G.
Borchelt, David R.
Savonenko, Alena V.
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
DOI: 10.1523/jneurosci.5080-04.2005
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: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)
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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Environmental Enrichment Mitigates Cognitive Deficits in a Mouse Model of Alzheimer's Disease

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