ABSTRACT
Type 3 Diabetes (T3D) is a neuroendocrine disorder that represents the progression of Type 2 Diabetes Mellitus (T2DM) to Alzheimer's disease (AD). T3D contributes in the increase of the total load of Alzheimer's patients worldwide. The protein network based strategies were used for the analysis of protein interactions and hypothesis was derived describing the possible routes of communications among proteins. The hypothesis provides the insight on the probable mechanism of the disease progression for T3D. The current study also suggests that insulin degrading enzyme (IDE) could be the major player which holds the capacity to shift T2DM to T3D by altering metabolic pathways like regulation of beta-cell development, negative regulation of PI3K/AKT pathways and amyloid beta degradation.
Subject(s)
Alzheimer Disease/metabolism , Diabetes Mellitus, Type 2/metabolism , Proteins/metabolism , Databases, Protein , Humans , Protein Binding , Protein Interaction Maps , Signal TransductionABSTRACT
Epidemiological studies have proved that, there are pathophysiological connections between Type 2 Diabetes Mellitus (T2DM) and Alzheimer's disease (AD). Diabetic patients have higher incidences of cognitive impairment and hence they are more at the risk of developing AD. Some of the recent evidences have majorly stated the effects of insulin resistance in the disturbance of various biological processes and signaling pathways. Both hyperglycemia and hypoglycemic conditions contributes in dysfunctioning of cognitive abilities and functions. The present review summarizes the evidences which establish the possible links between the two pathologies on the account of molecular, biochemical and at histopathological level. The information regarding their interactions was collected from different databases and journals. The gathered information will clearly establish the link among the two pathologies and will be helpful in future for the development of drugs for Type 3 Diabetes.
