Journal
NEUROBIOLOGY OF DISEASE
Volume 84, Issue -, Pages 22-38Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2015.04.008
Keywords
Diabetes; Alzheimer's disease; Beta amyloid; Amylin; Tau; Neurodegeneration
Categories
Funding
- National Health and Medical Research Council (NHMRC) [APP1009295, APP1045507]
- Hollywood Private Hospital
- McCusker Alzheimer's Disease Research Foundation
- Curtin Senior Research Fellowship [CRF140196]
- Department of Health WA Merit Award
Ask authors/readers for more resources
A growing body of evidence links type-2 diabetes (T2D) with dementia and neurodegenerative diseases such as Alzheimer's disease (AD). AD is the most common form of dementia and is characterised neuropathologically by the accumulation of extracellular beta amyloid (A beta) peptide aggregates and intracellular hyper-phosphorylated tau protein, which are thought to drive and/or accelerate inflammatory and oxidative stress processes leading to neurodegeneration. Although the precise mechanism remains unclear, T2D can exacerbate these neurodegenerative processes. Brain atrophy, reduced cerebral glucose metabolism and CNS insulin resistance are features of both AD and T2D. Cell culture and animal studies have indicated that the early accumulation of A beta may play a role in CNS insulin resistance and impaired insulin signalling. From the viewpoint of insulin resistance and impaired insulin signalling in the brain, these are also believed to initiate other aspects of brain injury, including inflammatory and oxidative stress processes. Here we review the clinical and experimental pieces of evidence that link these two chronic diseases of ageing, and discuss underlying mechanisms. The evaluation of treatments for the management of diabetes in preclinical, and clinical studies and trials for AD will also be discussed. (C) 2015 Elsevier Inc All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available