The Clinical and Biological Relationship between Type II Diabetes Mellitus and Alzheimer's Disease

被引:107
作者
Nicolls, Mark R. [1 ]
机构
[1] Univ Colorado, Div Pulm Sci & Crit Care Med, Hlth Sci Ctr, Denver, CO 80262 USA
关键词
Type II Diabetes Mellitus; Alzheimer's disease; islet; pancreas; islet transplantation;
D O I
10.2174/1567205043480555
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The clinical relationship between Type II diabetes mellitus and Alzheimer's disease has been debated for over a decade. While several studies have not shown a clear clinical correlation, others have demonstrated that Type II diabetes is an independent risk factor for Alzheimer's disease. Why diabetes would increase the likelihood of Alzheimer's disease is not immediately clear, although recent studies have demonstrated an impact of insulin abnormalities, insulin resistance and advanced glycation end products on both the development of neural amyloid plaques and neurofibrillary tangles. Although endodermal in embryologic development, the pancreas is a highly innervated organ that shares a number of molecular similarities with brain at the level of the transcriptome and proteome. Type II diabetes and Alzheimer's disease are characterized by localized amyloid deposits that progress during the course of the disease. Comparing amyloid deposition in the brain and pancreas reveals some striking pathophysiologic similarities. Neurodegeneration in pancreatic islets, as manifested by neurofibrillary tangles, is less well studied than in Alzheimer's disease but may also occur. This review summarizes what is currently known about the clinical and biological relationships and similarities between Type II diabetes and Alzheimer's disease.
引用
收藏
页码:47 / 54
页数:8
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共 125 条
[1]   Huntington's disease of the endocrine pancreas: Insulin deficiency and diabetes mellitus due to impaired insulin gene expression [J].
Andreassen, OA ;
Dedeoglu, A ;
Stanojevic, V ;
Hughes, DB ;
Browne, SE ;
Leech, CA ;
Ferrante, RJ ;
Habener, JF ;
Beal, MF ;
Thomas, MK .
NEUROBIOLOGY OF DISEASE, 2002, 11 (03) :410-424
[2]   Notch signalling controls pancreatic cell differentiation [J].
Apelqvist, Å ;
Li, H ;
Sommer, L ;
Beatus, P ;
Anderson, DJ ;
Honjo, T ;
de Angelis, MH ;
Lendahl, U ;
Edlund, H .
NATURE, 1999, 400 (6747) :877-881
[3]  
Arrigo AP, 1998, BIOL CHEM, V379, P19
[4]   Processing of pro-islet amyloid polypeptide (proIAPP) by the prohormone convertase PC2 [J].
Badman, MK ;
Shennan, KIJ ;
Jermany, JL ;
Docherty, K ;
Clark, A .
FEBS LETTERS, 1996, 378 (03) :227-231
[5]  
BEAUMONT K, 1993, MOL PHARMACOL, V44, P493
[6]   An insulin-degrading enzyme inhibitor decreases amylin degradation, increases amylin-induced cytotoxicity, and increases amyloid formation in insulinoma cell cultures [J].
Bennett, RG ;
Hamel, FG ;
Duckworth, WC .
DIABETES, 2003, 52 (09) :2315-2320
[7]   Cell-permeable peptide inhibitors of JNK novel blockers of β-cell death [J].
Bonny, C ;
Oberson, A ;
Negri, S ;
Sauser, C ;
Schorderet, DF .
DIABETES, 2001, 50 (01) :77-82
[8]   IB1, a JIP-1-related nuclear protein present in insulin-secreting cells [J].
Bonny, C ;
Nicod, P ;
Waeber, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (04) :1843-1846
[9]   Vascular risks and incident dementia: Results from a cohort study of the very old [J].
Brayne, C ;
Gill, C ;
Huppert, FA ;
Barkley, C ;
Gehlhaar, E ;
Girling, DM ;
O'Connor, DW ;
Paykel, ES .
DEMENTIA AND GERIATRIC COGNITIVE DISORDERS, 1998, 9 (03) :175-180
[10]   NONENZYMATIC GLYCOSYLATION AND THE PATHOGENESIS OF DIABETIC COMPLICATIONS [J].
BROWNLEE, M ;
VLASSARA, H ;
CERAMI, A .
ANNALS OF INTERNAL MEDICINE, 1984, 101 (04) :527-537