Cited by 420Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Reversible memory loss in a mouse transgenic model of Alzheimer’s disease

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Kotilinek, Linda A., Bacskai, Brian, Westerman, Marcus, Kawarabayashi, Takeshi, Younkin, Linda, Hyman, Bradley T., Younkin, Steven, Ashe, Karen H.·2002·The Journal of Neuroscience

DOI 10.1523/jneurosci.22-15-06331.2002PMC PMC6758140

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Abstract

Alzheimer's disease (AD) is a neurodegenerative condition, believed to be irreversible, characterized by inexorable deterioration of memory and intellect, with neuronal loss accompanying amyloid plaques and neurofibrillary tangles. In an amyloid precursor protein transgenic mouse model, Tg2576, little or no neuronal loss accompanies age-related memory impairment or the accumulation of Abeta, a 40-42 aa polypeptide found in plaques. Recently, we have shown inverse correlations between brain Abeta and memory in Tg2576 mice stratified by age (Westerman et al., 2002). Broadening the age range examined obscured this relationship, leading us to propose that small, soluble assemblies of Abeta disrupt cognitive function in these mice. Here we show that memory loss can be fully reversed in Tg2576 mice using intraperitoneally administered BAM-10, a monoclonal antibody recognizing the N terminus of Abeta. The beneficial effect of BAM-10 was not associated with a significant Abeta reduction, but instead eliminated the inverse relationship between brain Abeta and memory. We postulate that BAM-10 acts by neutralizing Abeta assemblies in the brain that impair cognitive function. Our results indicate that a substantial portion of memory loss in Tg2576 mice is not permanent. If these Abeta assemblies contribute significantly to memory loss in AD, then successfully targeting them might improve memory in some AD patients.

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Authors: Kotilinek, L. A., Bacskai, B., Westerman, M., Kawarabayashi, T., Younkin, L., Hyman, B. T., Younkin, S., & Ashe, K. H.
Affiliations: University of Minnesota (US)
Harvard University (US)
Mayo Clinic (US)
Mayo Clinic in Florida (US)
ORCID: Bacskai, Brian
Kawarabayashi, Takeshi
Hyman, Bradley T.
Ashe, Karen H.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2002-08-01
Volume: 22
Issue: 15
Pages: 6331-6335
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.22-15-06331.2002
PMC: PMC6758140
OpenAlex: W1705725530
Cited by: 420
References: 13
Citations by year: 2026: 1 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 3 · 2020: 7 · 2019: 3 · 2018: 6 · 2017: 12 · 2016: 7 · 2015: 10 · 2014: 15 · 2013: 28 · 2012: 14
FWCI: 18.41
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Neuroscience (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Alzheimer's Association
National Institutes of Health
National Institute on Aging (P01AG015453)
National Institute of Mental Health (R01MH065465)
National Institute of Neurological Disorders and Stroke (R01NS033249)
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 › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Alzheimer's disease, memory loss, amyloid-beta, monoclonal antibodies, Tg2576 mice, amyloid precursor protein, cognitive function, age-related memory impairment
MeSH terms: Aging, Alzheimer Disease, Animals, Antibodies, Monoclonal, Behavior, Animal, Brain Chemistry, Cognition, Disease Models, Animal, Female, Immunization, Passive, Injections, Intraperitoneal, Male, Memory, Memory Disorders, Mice, Transgenic, Remission Induction, Spatial Behavior, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice

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Reversible memory loss in a mouse transgenic model of Alzheimer’s disease

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