[This abstract first appeared in: Dementia: the Latest Evidence Newsletter RWHT Volume 1 Issue 3 October 2010].
Alzheimer’s disease and Type 2 Diabetes are both complex diseases. Known risks for both include high cholesterol, obesity and vasculopathy. These risk factors are interrelated. Previous research has linked diabetes with the risk of dementia. New opportunities may soon become available for the more effective treatment of both diseases.
New research has revealed a molecular mechanism in the gene SorCS1 which is shared by Alzheimer’s and Type 2 diabetes. This could lead to new drugs to treat both diseases. The research found that the brains of mice genetically deficient in SorCS1 showed increased levels of amyloid-beta (Abeta i.e. Aβ), which is known to play a role in the onset of Alzheimer’s disease.
Conversely, brain cells engineered for high levels of SorCS1 generated low levels of Abeta.
The SorCS1-deficient mice also were found to have abnormally low levels of another protein called Vps35 (linked to Alzheimer’s disease in a previous study).
The authors propose that dysfunction of SorCS1 may contribute to disturbances of the amyloid-β peptide (Aβ) and the Aβ precursor protein (APP) which seem to be underlying factors in Alzheimer’s disease and the insulin/glucose disturbance in diabetes mellitus.
Put simply, it seems likely that low SorCS1 may cause low Vps35 and lead to the increased formation of Abeta. New drug targets to treat both Type 2 Diabetes and Alzheimer’s disease by increasing levels of SorCS1 or Vps35 are now on the research agenda.
Lane, RF. Raines, SM. Steele, JW. [et al], (2010). Diabetes-associated SorCS1 regulates Alzheimer’s amyloid-beta metabolism: evidence for involvement of SorL1 and the retromer complex. The Journal of Neuroscience, September 29th 2010, Vol.30(39), pp.13110-5.