Calcium signaling and neurodegenerative diseases

被引：379

作者：

Bezprozvanny, Ilya ^{[1
]}

机构：

[1] Univ Texas SW Med Ctr Dallas, Dept Physiol, Dallas, TX 75390 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2009年 / 15卷 / 03期

关键词：

AMYOTROPHIC-LATERAL-SCLEROSIS; SPINOCEREBELLAR ATAXIA TYPE-6; TRANSGENIC MOUSE MODEL; HUNTINGTONS-DISEASE; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; MITOCHONDRIAL DYSFUNCTION; MUTANT HUNTINGTIN; ALPHA-SYNUCLEIN; CORTICAL-NEURONS;

D O I：

10.1016/j.molmed.2009.01.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD) and spinocerebellar ataxias (SCAs), present an enormous medical, social, financial and scientific problem. Recent evidence indicates that neuronal calcium (Ca(2+)) signaling is abnormal in many of these disorders. Similar, but less severe, changes in neuronal Ca(2+) signaling occur as a result of the normal aging process. The role of aberrant neuronal Ca(2+) signaling in the pathogenesis of neurodegenerative disorders is discussed here. The potential utility of Ca(2+) blockers for treatment of these disorders is also highlighted. It is reasoned that Ca(2+) blockers will be most beneficial clinically when used in combination with other disease-specific therapeutic approaches.

引用

页码：89 / 100

页数：12

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