Facilitation of memory impairment and cholinergic disturbance in a mouse model of Alzheimer's disease by mild ischemic burden
| Autor: | Norito Yamagata, Kotaro Takasaki, Takuya Watanabe, Michihiro Fujiwara, Katsunori Iwasaki |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Genetically modified mouse
medicine.medical_specialty Ischemia Hippocampus Brain Ischemia Brain ischemia Amyloid beta-Protein Precursor Mice Alzheimer Disease Internal medicine medicine Animals Humans Memory impairment Carotid Stenosis Maze Learning Memory Disorders Amyloid beta-Peptides General Neuroscience Brain medicine.disease Acetylcholine Mice Mutant Strains Endocrinology Cholinergic Alzheimer's disease Psychology Neuroscience medicine.drug |
| Zdroj: | Neuroscience Letters. 536:74-79 |
| ISSN: | 0304-3940 |
| Popis: | Epidemiological studies suggest that cerebral ischemia may contribute to the onset and progression of Alzheimer's disease (AD). However, the mechanism by which ischemic events trigger the onset and progression of AD is poorly understood. Acetylcholine (ACh) is one of the key factors in memory, and cholinergic disturbance is a primary feature of AD. To clarify whether cholinergic disturbance is implicated in the exacerbation of AD symptoms by cerebral ischemia, memory impairment and hippocampal ACh release were examined in young (4-6 month-old) Tg2576 (Tg) mice, an AD transgenic mouse model, and in age-matched control mice with or without transient cerebral ischemia (bilateral common carotid artery occlusion: 2VO). 2VO induced memory impairment and decreased high-K(+)-evoked ACh release in Tg mice, but not in control mice. There were no differences in memory and ACh release between sham-operated control and Tg mice. Increases in β-amyloid (Aβ) 40 and Aβ42 were also observed in 2VO-operated Tg mice compared with sham-operated Tg mice, but no evident amyloid plaques or neuronal loss were found in the hippocampus of these mice. These results suggest that the memory of Tg mice is affected by 2VO, and the memory impairment may be due to cholinergic dysfunction induced by Aβ. Our findings support the idea that cerebral hypoperfusion could be a risk factor for AD. |
| Databáze: | OpenAIRE |
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