Jency Thomas
La Trobe University, Australia
Title: Effect of Diabetes on hippocampal gene expression
Biography
Biography: Jency Thomas
Abstract
Diabetes is a metabolic disorder that leads to other health complications over a period of time and is the cause for considerable morbidity and mortality world-wide. The complications of diabetes in the peripheral tissues are well characterized including coronary heart disease, retinal degeneration, renal disorders, and also micro and macro vascular complications. Over the last few decades much emphasis has been placed on the complications of diabetes that occur in the central nervous system (CNS). One such neuropathology due to diabetes in CNS is cognitive impairment. The hippocampus, the limbic structure, is involved in higher brain functions and appears to be particularly vulnerable to diabetes. presents a study on the comparison of gene expression profile in the hippocampus of a streptozotocin (STZ) induced diabetic mice and a vehicle treated control animals. Here it is demonstrated that diabetes causes significant alterations in the genes that plays a crucial role in synaptic function and plasticity and also for neurogenesis, both of which are required for normal cognitive functions. Six weeks after diabetes was established in these mice, a number of genes had altered expression including genes involved in epigenetic regulation, and this included histone deacetylase (Hdac) 4, 9 and 11. Interestingly Hdac 4 and 9 are abundantly present in the hippocampus and are required for hippocampal dependent learning, memory and synaptic plasticity. Glycogen synthase kinase beta (Gsk3β) which has been shown to have a crucial role in metabolic and neurodevelopmental functions and considered to be an important regulator of synaptic functions, also exhibited significant decrease in the STZ induced diabetic mice as opposed to the buffer treated control group. The marked decrease of these genes that are crucial for higher functions in the hippocampus underscores the impact of uncontrolled diabetes on the hippocampus. Furthermore genes that have been linked to neurological disorder and cognitive dysfunction such as apolipoprotien E (ApoE) showed increased expression in diabetic mice as opposed to the non- diabetic control group. These findings implicate the abnormal transcription of genes which could disrupt normal cognitive functions in the hippocampus and also underscores epigenetic mechanisms involved in disease conditions like diabetes.