Related Experiment Videos
Senescence-accelerated mouse. Neurochemical studies on aging
Y Nomura1, Y Yamanaka, Y Kitamura
1Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Annals of the New York Academy of Sciences
|June 15, 1996
Summary
The senescence-accelerated mouse model (SAMP8) shows increased gliosis and amyloid precursor protein (APP) fragments, indicating accelerated brain aging and potential memory dysfunction in these mice.
Area of Science:
- Neuroscience
- Aging Research
- Animal Models
Background:
- Senescence-accelerated mouse (SAMP8) models exhibit accelerated aging and memory deficits.
- Gliosis, indicated by PK-11195 binding and GFAP immunoreactivity, is a hallmark of aging in the brain.
Purpose of the Study:
- To investigate the relationship between aging, gliosis, and amyloid precursor protein (APP) processing in the SAMP8 mouse brain.
- To characterize neurochemical and molecular changes associated with accelerated aging in SAMP8 mice.
Main Methods:
- Quantification of [3H] PK-11195 binding as a marker of gliosis in SAMP8 cerebral cortex and hippocampus.
- Assessment of glial fibrillary acidic protein (GFAP) immunoreactivity.
- Analysis of amyloid precursor protein (APP)-like immunoreactivity and its fragments in SAMP8 brain tissue.
Main Results:
- Markedly increased [3H] PK-11195 binding and GFAP immunoreactivity in aging SAMP8 brains, indicating significant astrocytosis.
- Elevated APP-like immunoreactivity and 27-kDa carboxyl-terminal fragments of APP were observed in SAMP8 brains.
- Reactive astrocytes were found surrounding areas of spongy degeneration, with anti-APP antibody staining.
Conclusions:
- SAMP8 mice exhibit pronounced astrocytosis and increased production of APP-derived fragments, consistent with accelerated brain aging.
- These findings highlight the utility of the SAMP8 model for studying age-related neurodegenerative processes, including those involving gliosis and amyloid pathology.