Year: 2019
Type: dissertation
Abstract: Regulation of blood glucose is responsible for maintaining a continuous supply of energy moving throughout the human body; excess glucose is toxic, while insufficient glucose can lead to impairment in insulin secretion, ketoacidosis, coma, and death1. Fluctuating continuously between fasting and post-eating modes, blood glucose homeostasis is regulated by a negative feedback system regulating as needed to preserve adequate insulin synthesis, secretion, and the body’s need for glucose-derived energy2,3. Dysregulation of the glucose-insulin feedback loop can contribute to the pathogenesis of various detrimental health disorders, including two of the most common chronic and debilitating diseases of Western Society, Alzheimer’s Disease (AD) and Type 2 Diabetes (T2D)4. While T2D is a chronic metabolic disorder, and AD is a chronic neurodegenerative disorder, there are potential pathophysiological connections between the two. Metabolic changes associated with T2D such as hyperglycemia and obesity, have been shown to induce known pathologies associated with AD such as Amyloid Beta (Aβ) plaques, neurofibrillary tangles (NFTs), and neuronal death5. Metabolic connections between AD/T2D suggest a common disease mechanism. Understanding the relationship between these two diseases could lead to new potential therapeutic treatments for AD. I hypothesize that correlation between T2D and AD shared pathologies indicates causation for the development of AD and AD-like dementia; thus, identifying additional biomarkers for early stages of AD could potentially lead to new diagnostic tests to help delay the onset of AD.
Author: Dilia Ayala
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W3087434990