Although type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) are two
independent diseases, evidences from epidemiological, pathophysiological and animal studies
have indicated a close pathophysiological relationship between these diseases. Due to the
pathophysiological similarity of T2DM and AD, which includes insulin resistance and deficiency,
protein aggregation, oxidative stress, inflammation, autophagocytosis and advanced
glycation end products; AD is often referred to as “type 3 diabetes”. In addition to the targeted
regimens usually used for treating T2DM and AD individually, currently, anti-diabetic
drugs are successfully used to reduce the cognitive decline in AD patients. Therefore, if a
common pathophysiology of T2DM and AD could be clearly determined, both diseases
could be managed more efficiently, possibly by shared pharmacotherapy in addition to understanding
the broader spectrum of preventive strategies. The aim of this review is to discuss
the pathophysiological bridge between T2DM and AD to lay the foundation for the
future treatment strategies in the management of both diseases.
Keywords: Type 2 diabetes mellitus, Alzheimer’s disease, pathophysiology, linkage, inflammation,
oxidative stress, treatment.
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