- Author:
Nirmal VERMA
1
;
Florin DESPA
Author Information
- Publication Type:Review
- Keywords: Dementia; Diabetes mellitus; Obesity
- MeSH: Amyloid; Brain Injuries; Brain; Dementia; Diabetes Mellitus; Humans; Insulin; Models, Animal; Obesity; Plaque, Amyloid; Presenilin-1; Rodentia
- From:Diabetes & Metabolism Journal 2019;43(5):560-567
- CountryRepublic of Korea
- Language:English
- Abstract: The link of diabetes with co-occurring disorders in the brain involves complex and multifactorial pathways. Genetically engineered rodents that express familial Alzheimer's disease-associated mutant forms of amyloid precursor protein and presenilin 1 (PSEN1) genes provided invaluable insights into the mechanisms and consequences of amyloid deposition in the brain. Adding diabetes factors (obesity, insulin impairment) to these animal models to predict success in translation to clinic have proven useful at some extent only. Here, we focus on contributing factors to diabetic brain injury with the aim of identifying appropriate animal models that can be used to mechanistically dissect the pathophysiology of diabetes-associated cognitive dysfunction and how diabetes medications may influence the development and progression of cognitive decline in humans with diabetes.