Models of repair mechanisms for future treatment modalities of Parkinson's disease

被引：22

作者：

Isacson, O ^{[1
]}

机构：

[1] Harvard Univ, Neuroregenerat Labs, McLean Hosp, Sch Med, Belmont, MA 02478 USA

来源：

BRAIN RESEARCH BULLETIN | 2002年 / 57卷 / 06期

关键词：

oxidative stress; protein damage; cellular damage; age; trophic factors; prevention; stem cells; neurological diseases;

D O I：

10.1016/S0361-9230(01)00773-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Parkinson's disease is one of the most likely neurological disorders to be fully treatable by drugs and new therapeutic modalities. The age-dependent and multifactorial nature of its pathogenesis allows for many strategies of intervention and repair. Most data indicate that the selectively vulnerable dopaminergic neurons in the substantia nigra of patients that have developed Parkinson's disease can be modified by protective and reparative therapies. First, the oxidative stress, protein abnormalities, and cellular inclusions typically seen could be dealt with by anti-oxidants, trophic factors, and proteolytic enhancements. Secondly, if the delay of degeneration is not sufficient, then immature dopamine neurons can be placed in the parkinsonian brain by transplantation. Such neurons can be derived from stem cell sources or even stimulated to repair from endogenous stem cells. Novel molecular and cellular treatments provide new tools to prevent and alleviate Parkinson's disease. (C) 2002 Elsevier Science Inc.

引用

页码：839 / 846

页数：8

共 147 条

[91] Intrastriatal implantation of fibroblasts genetically engineered to produce brain-derived neurotrophic factor prevents degeneration of dopaminergic neurons in a rat model of Parkinson's disease [J].