Neuron Loss and Behavioral Deficits in the TBA42 Mouse Model Expressing N-Truncated Pyroglutamate Amyloid-β3–42
Abstract
Pyroglutamate-modified amyloid-β (Aβ) at amino acid position three (Aβ(pE3-42)) is gaining considerable attention as a potential key player in the pathogenesis of Alzheimer's disease (AD). Aβ(pE3-42) is abundant in AD brain and has a high aggregation propensity, stability, and cellular toxicity. The aim of the present work was to study the effect of Aβ(pE3-42) expression on neuron loss and associated behavioral deficits using the TBA42 transgenic mouse model. Expression of pyroglutamate Aβ(3-42) triggers hippocampal CA1 neuron loss and behavioral deficits in the TBA42 mouse model. Mice elicited significant neuron death (-35% at the age of 12 months), deficits in the spatial reference memory, working memory, loss of anxiety, and severe motor deficits in an age-dependent manner. These results support a major pathological function of pyroglutamate Aβ in AD.
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In TBA42 mice, intraneuronal Aβ accumulation was evident by 3 months of age in the CA1 pyramidal layer, and an ~35% loss of CA1 pyramidal neurons was found in aged TBA42 mice.
“A more thorough behavioral analysis confirmed the severe motor phenotype and revealed additional deficits in spatial reference memory in the Morris water maze, as well as an ~35% loss of CA1 pyramidal neurons in aged TBA42 mice [100].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [100]
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References 58 · Cited by 16
- Authors
- Meißner, J. N., Bouter, Y., & Bayer, T. A.
- Affiliations
- Universitätsmedizin Göttingen (DE)
- Corresponding author
- Bayer, Thomas A.
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2015-03-18
- Volume
- 45
- Issue
- 2
- Pages
- 471-482
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W1712313334
- Cited by
- 16
- References
- 58
- Citations by year
- 2024: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 3 · 2015: 3
- FWCI
- 2.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- GRO (submittedVersion)
- Funders
- Universitätsmedizin Göttingen
- Georg-August-Universität Göttingen
- Studienstiftung des Deutschen Volkes
- 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 › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- pyroglutamate amyloid-beta
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Mental Disorders, Disease Models, Animal, Humans, Mice, Transgenic, Movement Disorders, Neurons, Peptide Fragments, Psychomotor Performance, Amyloid beta-Peptides, Cell Death, Maze Learning, Mice, Muscle Strength, CA1 Region, Hippocampal, Spatial Learning
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