Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 39, Issue 1, Pages 145-162Publisher
IOS PRESS
DOI: 10.3233/JAD-131238
Keywords
Alzheimer's disease; amyloid-beta; diabetes; glycogen synthase kinase-3 beta; learning and memory; pathological aging of the brain; senescence-accelerated mice; synaptophysin; tau
Categories
Funding
- Westside Institute for Science and Education
- Department of Pediatrics, University of Illinois at Chicago, Children's Hospital of the University of Illinois, Chicago, IL
- National Institute of Health [AG039625, NS079614]
- Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Rehabilitation RD [B6285R, I0880R]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS079614] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R21AG039625] Funding Source: NIH RePORTER
- Veterans Affairs [I01RX000880] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Alzheimer's disease (AD) is an age-dependent neurodegenerative disease constituting similar to 95% of late-onset non-familial/sporadic AD, and only similar to 5% accounting for early-onset familial AD. Availability of a pertinent model representing sporadic AD is essential for testing candidate therapies. Emerging evidence indicates a causal link between diabetes and AD. People with diabetes are >1.5-fold more likely to develop AD. Senescence-accelerated mouse model (SAMP8) of accelerated aging displays many features occurring early in AD. Given the role played by diabetes in the pre-disposition of AD, and the utility of SAMP8 non-transgenic mouse model of accelerated aging, we examined if high fat diet-induced experimental type 2 diabetes in SAMP8 mice will trigger pathological aging of the brain. Results showed that compared to non-diabetic SAMP8 mice, diabetic SAMP8 mice exhibited increased cerebral amyloid-beta, dysregulated tau-phosphorylating glycogen synthase kinase 3 beta, reduced synaptophysin immunoreactivity, and displayed memory deficits, indicating Alzheimer-like changes. High fat diet-induced type 2 diabetic SAMP8 mice may represent the metabolic model of AD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available