Assessing the Clinical Correlation between Alzheimer's disease and Type-2 Diabetes Mellitus: Current Strategies and Emerging Perspectives

This article aims to provide a brief overview of novel therapeutic approaches for combating type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). The most prevalent disorders in elderly patients are type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD), raising worldwide concern. Recent research indicates that insulin resistance develops in patients with AD, owing to insufficient glucose absorption by the human body. Amyloid precursor protein (APP), present on the cellular membrane of neurons, helps develop and repair damaged brain neurons. Insulin resistance, hyperinsulinemia and elevated blood sugar levels (hyperglycemia) are the three primary clinical features of T2DM. The first is insulin resistance, which appears because of diminished or poor insulin sensitivity in the liver, muscles and fat cells. The linkable pathophysiology of AD and DM starts from the abnormal formation of ⍺ cells and β cells in the pancreas, which leads to an increase in the action of glycogen synthase kinase (GSK), glucose, insulin and TNF⍺ in the cell tissue in the skeletal muscle, which leads to insulin resistance in the liver and ultimately mitochondrial dysfunction, which promotes the formation amyloid β plaques which hinder the neuronal signalling. Along with these factors, glucagon-like peptide-1(GLP-1) receptor signalling also plays an essential role in reducing the pathogenicity of the disease. APP significantly affects insulin gene expressions and glucose-dependent insulin release through the pancreas and is also helpful in suppressing neurodegenerative cascades that help improve both diabetes and neurodegenerative illness. This article also explores recent research studies demonstrating various therapy approaches that help in the amelioration of AD and T2DM.