Neuron Loss and Behavioral Deficits in the TBA42 Mouse Model Expressing N-Truncated Pyroglutamate Amyloid-β3–42
| Autor: | Julius N. Meißner, Yvonne Bouter, Thomas A. Bayer |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Genetically modified mouse
Amyloid Spatial Learning Hippocampus Mice Transgenic Hippocampal formation Pathogenesis Mice 03 medical and health sciences 0302 clinical medicine Alzheimer Disease Animals Humans Muscle Strength Maze Learning CA1 Region Hippocampal 030304 developmental biology Neurons 0303 health sciences Amyloid beta-Peptides Movement Disorders Cell Death Working memory Mental Disorders General Neuroscience Age Factors General Medicine Peptide Fragments Disease Models Animal Psychiatry and Mental health Clinical Psychology Toxicity Geriatrics and Gerontology Neuron death Psychology Neuroscience Psychomotor Performance 030217 neurology & neurosurgery |
| Zdroj: | Journal of Alzheimer's Disease. 45:471-482 |
| ISSN: | 1875-8908 1387-2877 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|