Reviews
| Rev Diabet Stud,
2006,
3(4):161-168 |
DOI 10.1900/RDS.2006.3.161 |
Diabetes and Alzheimer's Disease - Is There a Connection?
Anders A.F. Sima1,2, Zhen-guo Li1
1Departments of Pathology, Wayne State University, School of Medicine, Detroit, MI 48201, USA.
2Departments of Neurology, Wayne State University, School of Medicine, Detroit, MI 48201, USA.
Address correspondence to: Anders A.F. Sima, email: asima@med.wayne.edu
Abstract
It has been known for some time that diabetes may be associated with impaired cognitive function. During the last decade, epidemiological data have emerged suggesting a linkage between diabetes, particularly type 2 diabetes, and Alzheimer's disease (AD). There is evidence to suggest that impaired activities of neurotrophic factors such as insulin, IGF-1 and NGF, which occur in both diabetes and AD, may provide a mechanistic link between the two disorders. An additional probable factor that has been less evaluated to date is hypercholesterolemia, a common accompaniment to type 2 diabetes. Increased cholesterol availability is believed to play a crucial role in the abnormal metabolism of amyloid precursor protein leading to accumulation of amyloid-β. Impaired insulin signaling in particular appears to be involved in hyperphosphorylation of the tau protein, which constitutes neurofibrillary tangles in AD. The linkage between abnormal amyloid metabolism and phosphor-tau is likely to be provided by the activation of caspases both by increased amyloid-β and by impaired insulin signaling. Although the details of many of these components still await evaluation, it appears clear that commonalities exist in the underlying pathogenesis of diabetes and Alzheimer’s disease. In this review we provide a brief update on linkages between these two diverse but common disorders.
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| Rev Diabet Stud,
2006,
3(4):169-177 |
DOI 10.1900/RDS.2006.3.169 |
Pathogenesis of Fulminant Type 1 Diabetes
Akihisa Imagawa, Toshiaki Hanafusa
First Department of Internal Medicine, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki 569-8686, Japan.
Address correspondence to: Akihisa Imagawa, email: aimag@poh.osaka-med.ac.jp
Abstract
Fulminant type 1 diabetes is a new subtype of type 1 diabetes. The term was established in 2000. It is a syndrome characterized by a markedly rapid and almost complete destruction of pancreatic β-cells. Several lines of evidence suggest that both genetic factors, such as human leukocyte antigen (HLA), and environmental factors, such as viral infection, contribute to the development of this disease. It is also suggested that autoimmune processes contribute less critically to fulminant type 1 diabetes than to classic type 1A diabetes. Based on the findings made to date, both viral infection and the subsequent immune reaction in genetically susceptible individuals cause β-cell destruction and lead to fulminant type 1 diabetes.
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