Researchers have identified a protein that may contribute to the progression of Alzheimer's disease pathology in type-2 diabetes, reports a new study of male mice and human brain tissue. The research could have implications for future drug development.
The cause of sporadic, late onset Alzheimer's disease is unknown. However, type-2-diabetes is associated with an increased Alzheimer's risk, which may provide a clue to its origin.
Bonds et al. examined the relationship between diabetes and Alzheimer's disease and found that a protein called caveolin-1 (Cav-1) is depleted in the temporal lobe of humans with diabetes and in a diabetic mouse model. Depletion of Cav-1 causes the upregulation of amyloid precursor protein and b-amyloid levels. Importantly, restoring Cav-1 levels in mice reduced Alzheimer's pathology and improved learning and memory deficits, revealing a potential mechanism responsible for the increased risk of Alzheimer's disease in this population.
Manuscript title: Depletion of Caveolin-1 in Type-2 Diabetes Model Induces Alzheimer's disease Pathology Precursors
Please contact firstname.lastname@example.org for full-text PDF and to join SfN's journals media list.
JNeurosci, the Society for Neuroscience's first journal, was launched in 1981 as a means to communicate the findings of the highest quality neuroscience research to the growing field. Today, the journal remains committed to publishing cutting-edge neuroscience that will have an immediate and lasting scientific impact, while responding to authors' changing publishing needs, representing breadth of the field and diversity in authorship.
About The Society for Neuroscience
The Society for Neuroscience is the world's largest organization of scientists and physicians devoted to understanding the brain and nervous system. The nonprofit organization, founded in 1969, now has nearly 37,000 members in more than 90 countries and over 130 chapters worldwide.