EVALUATING THE ASSOCIATION BETWEEN TYPE 2 DIABETES AND ALZHEIMER’S DISEASE BY BIOMARKERS, PATHOLOGICAL TRAITS & MANAGEMENT
European Journal of Molecular & Clinical Medicine,
2022, Volume 9, Issue 9, Pages 474-499
AbstractIn recent years, extensive research has indicated that, in addition to the traditional process of neurodegenerative disease, neurodegeneration can also be caused by a variety of unconventional pathways. One of these is type 2 diabetes mellitus, a dysmetabolic condition that has been widely investigated. The majority of our knowledge of glucose metabolic dysfunction in neurodegeneration comes from investigations in Alzheimer's disease (AD) models. Type 3 diabetes is a term given to Alzheimer's disease since it is significantly associated with hyperglycemia. The pathophysiology of Alzheimer's disease is first discussed., from the aspects of typical protein aggregation and the newer T2DM-dependent pathways, which are validated by evidence from T2DM patients such as epidemiological, neuroimaging, and pathological evaluations. Second, we analyzed the several routes through which neurodegeneration is exacerbated in diabetic conditions, taking Alzheimer's disease as an instance. Finally, recent scientific advancements in metabolic disorders-driven neurodegeneration are highlighted, as well as some of the major developments in AD management.
Methods: We reviewed the literatures that are found in PubMed and google scholar searches.
Results: Aside from the established causes of Alzheimer's disease, T2DM sheds new light on the disease's pathophysiology in a variety of ways. It's a two-way interplay whose molecular and signaling mechanisms only have recently been explored. This is our attempt to reconcile them all together to derive a comprehensive molecular explanation for T2DM neurodegeneration.
Conclusion: The relation within T2DM and Alzheimer's disease has been observed and investigated thoroughly. It's encouraging to learn that these investigations have resulted in some advancements in the treatment of AD.
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