Inducible proteoplathies

被引:83
作者
Walker, Lary C. [1 ]
LeVine, Harry, III
Mattson, Mark P.
Jucker, Mathias
机构
[1] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA
[2] Emory Univ, Dept Neurol, Atlanta, GA 30322 USA
[3] Univ Kentucky, Sanders Brown Ctr Aging, Dept Mol & Cellular Biochem, Lexington, KY 40536 USA
[4] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA
[5] Univ Tubingen, Dept Cellular Neurol, Hertie Inst Clin Brain Res, D-72076 Tubingen, Germany
关键词
D O I
10.1016/j.tins.2006.06.010
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Numerous degenerative diseases are characterized by the aberrant polymerization and accumulation of specific proteins. These proteopathies include neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease and the prion diseases, in addition to diverse systemic disorders, particularly the amyloidoses. The prion diseases have been shown to be transmissible by an alternative conformation of the normal cellular prion protein. Other proteopathies have been thought to be non-transmissible, but there is growing evidence that some systemic and cerebral amyloidoses can be induced by exposure of susceptible hosts to cognate molecular templates. As we review here, the mechanistic similarities among these diseases provide unprecedented opportunities for elucidating the induction of protein misfolding and assembly in vivo, and for developing an integrated therapeutic approach to degenerative proteopathies.
引用
收藏
页码:438 / 443
页数:6
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