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Common pathological processes in Alzheimer disease and type 2 diabetes: a review.

Biomedical Sciences Research Institute Computer Science Research Institute Environmental Sciences Research Institute Nanotechnology & Advanced Materials Research Institute

Li, Lin and Holscher, Christian (2007) Common pathological processes in Alzheimer disease and type 2 diabetes: a review. Brain research reviews, 56 (2). pp. 384-402. [Journal article]

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Abstract

Alzheimer disease (AD) and type 2 diabetes mellitus (T2DM) are conditions that affect a large number of people in the industrialized countries. Both conditions are on the increase, and finding novel treatments to cure or prevent them are a major aim in research. Somewhat surprisingly, AD and T2DM share several molecular processes that underlie the respective degenerative developments. This review describes and discusses several of these shared biochemical and physiological pathways. Disturbances in insulin signalling appears to be the main common impairment that affects cell growth and differentiation, cellular repair mechanisms, energy metabolism, and glucose utilization. Insulin not only regulates blood sugar levels but also acts as a growth factor on all cells including neurons in the CNS. Impairment of insulin signalling therefore not only affects blood glucose levels but also causes numerous degenerative processes. Other growth factor signalling systems such as insulin growth factors (IGFs) and transforming growth factors (TGFs) also are affected in both conditions. Also, the misfolding of proteins plays an important role in both diseases, as does the aggregation of amyloid peptides and of hyperphosphorylated proteins. Furthermore, more general physiological processes such as angiopathic and cytotoxic developments, the induction of apoptosis, or of non-apoptotic cell death via production of free radicals greatly influence the progression of AD and T2DM. The increase of detailed knowledge of these common physiological processes open up the opportunities for treatments that can prevent or reduce the onset of AD as well as T2DM.

Item Type:Journal article
Faculties and Schools:Faculty of Life and Health Sciences
Faculty of Life and Health Sciences > School of Biomedical Sciences
Research Institutes and Groups:Biomedical Sciences Research Institute
Biomedical Sciences Research Institute > Molecular Medicine
Biomedical Sciences Research Institute > Molecular Medicine > Neuroscience & Neurodegenerative Diseases
ID Code:11234
Deposited By:Dr Christian Holscher
Deposited On:04 Feb 2010 09:36
Last Modified:10 Jun 2010 10:48

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