Is sporadic Alzheimer disease the brain type of non-insulin dependent diabetes mellitus? A challenging hypothesis

被引:239
作者
Hoyer, S [1 ]
机构
[1] Univ Heidelberg, Dept Pathochem & Gen Neurochem, D-69120 Heidelberg, Germany
关键词
sporadic Alzheimer disease; brain; insulin; insulin receptor; advanced glycation end products; non-insulin dependent diabetes mellitus;
D O I
10.1007/s007020050067
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The hypothesis is forwarded that sporadic late-onset Alzheimer disease is caused by non-insulin dependent diabetes mellitus which is confined to the brain. This hypothesis is based on the findings of Frolich and coworkers (this volume) who clearly demonstrate a perturbation of the neuronal insulin/ insulin receptor signal transduction pathway which is considered to be the pathobiochemical basis for the drastic reduction in glucose/energy metabolism in Alzheimer brain. As a consequence of this abnormality, advanced glycation end products are formed. Munch et al. (this volume) evaluate the impacts of the latter related to oxidative stress and the formation of P-amyloid and neurofibrillary tangles.
引用
收藏
页码:415 / 422
页数:8
相关论文
共 44 条
[41]  
VLASSARA H, 1994, LAB INVEST, V70, P138
[42]  
WILDEBODE C, 1997, J BIOL CHEM, V42, P16085
[43]   Changes in membrane properties during energy depletion-induced cell injury studied with fluorescence microscopy [J].
Wu, YK ;
Sun, FF ;
Tong, DM ;
Taylor, BM .
BIOPHYSICAL JOURNAL, 1996, 71 (01) :91-100
[44]   RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease [J].
Yan, SD ;
Chen, X ;
Fu, J ;
Chen, M ;
Zhu, HJ ;
Roher, A ;
Slattery, T ;
Zhao, L ;
Nagashima, M ;
Morser, J ;
Migheli, A ;
Nawroth, P ;
Stern, D ;
Schmidt, AM .
NATURE, 1996, 382 (6593) :685-691