Alzheimer’s disease (AD) has become one of the most threatening diseases in the elderly, and type 2 diabetes mellitus (T2DM) is a major health problem in the world, representing 7.4% of the population. Several studies have produced epidemiological, clinical, and pathological evidence of the relationship between AD and T2DM. Laboratory research using animal models has identified mechanisms shared by both T2DM and AD. Particularly, there is an increase of tau phosphorylation and cleavage, which is known to be particularly toxic to neurons and to form a nucleation for neurofibrillary tangles. Also, alterations in synaptic plasticity are associated to tau pathology through the direct abnormal interaction of pathological tau with synaptic proteins and indirectly through Tau-activated neuroinflammatory processes. Many T2DM complications are potentiated or initiated by the accumulation of specific forms of advanced glycation end products (AGEs) and their interaction with its receptors (RAGE). AGEs promote β-amyloid aggregation and cytotoxicity, while glycation of tau may enhance their aggregation. Therefore, this review addresses the analysis of the common mechanisms where the major molecular players of these two diseases participate and contribute to a better understanding of these diseases in their pathogenic relationship.
Part of the book: Neurodegenerative Diseases