Abstract

CAUSE OF NEURODEGENERATION THROUGH GABA RECEPTOR AND GAD ENZYME IN HYPERGLYCEMIC PATIENT

Piyush Tripathi, Bhartendu Sharma^*and Kritika

Abstract

Worldwide (6% of the population) suffers from diabetes mellitus (DM), the most prevalent endocrine condition. It is brought on by insufficient or insufficient insulin production by the pancreas, which increases blood glucose levels or falls. It has been demonstrated to harm numerous bodily systems, including the heart, kidneys, blood vessels, eyes, and nerves—insulin-dependent diabetes mellitus (IDDM, Type I). T1DM is caused by the autoimmune destruction of pancreatic beta cells where the hormone insulin is produced, which is essential for glucose metabolism. In diabetes, hyperglycemia is caused by inadequate insulin action. Numerous insulin receptors exist in the brain, particularly in the hippocampus and cerebral cortex, whose regions hold significance for memory and cognitive function, respectively. In the brain, insulin is broken down by the insulin-degrading enzyme (IDE). This enzyme also disassembles the amyloid beta protein. By encouraging the release of extracellular amyloid β peptide and upregulating IDE expression, insulin regulates the synthesis and elimination of amyloid β from the brain. Moreover, glucose and insulin can also affect the brain. Along with its impacts on acute metabolic effects, nutrition intake regulation, and energy storage monitoring, insulin also affects cognition further, leading to various neurodegenerative diseases.

Keywords: Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Glutamic Acid Decarboxylase, Gamma-aminobutyric acid, Dementia, Neurocognitive Diseases.