A Possible Link of Gut Microbiota Alteration in Type 2 Diabetes and Alzheimer’s Disease Pathogenicity: An Update
CNS & Neurological Disorders - Drug Targets,
Mohammad Z. Alam, Qamre Alam, Mohammad A. Kamal, Adel M. Abuzenadah and Absarul HaqueAffiliation:
Fundamental and Applied Biology Group, Recombinant DNA Technology Unit, King Fahd Medical Research Centre, King Abdulaziz University, P. O. Box 80216, Jeddah 21589, Saudi Arabia.
AbstractImbalances in gut microbiota are associated with metabolic disorder, which are a group of obesity-related metabolic abnormalities that increase an individual’s risk of developing type 2 diabetes (T2D) and Alzheimer’s disease (AD). Although a number of risk factors have been postulated that may trigger the development of AD, the root cause of this disease is still a matter of debate. This review further investigates the etiology of AD by accumulating the current role played by gut microbiota in human, and trying to establish an inter-link between T2D and AD pathogenesis. There is a growing body of evidence which suggests that obesity is associated with alteration in the normal gut flora, reduced bacterial diversity, metabolic pathways and altered representation of bacterial genes. Obesity and T2D are considered to be induced as a result of changes within the composition of gut microbiota. The evidence gathered so far clearly advocates the involvement of gut microbes in causing obesity, a state of chronic and low-grade inflammation. Hence, understanding the microbiota of the gut is significant in relation to inflammation, as it is a key contributor for diabetes which has a direct relation to the AD pathogenesis. Comparative analysis of gut microbiota may enable further novel insight into the complex biology of AD, which is very important in order to take preventive measure such as early diagnosis, identification of new therapeutic targets and development of novel drugs.
Alzheimer's disease, Inflammation, Insulin resistance, Macrobiotic, obesity, Tall–like receptor, type-2 diabetes.
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