神经病动物模型。

Bailliere's clinical neurology Pub Date : 1996-03-01
H Schmalbruch, C Krarup
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引用次数: 0

摘要

动物的神经病变要么是由基因决定的,要么是由化合物或物理损伤引起的。小鼠和大鼠的糖尿病可能是自发的或诱发的,但人类糖尿病神经病变的真正副本尚未获得。疼痛性神经病发生在神经收缩或神经瘤形成后。小鼠突变体迟发性沃勒氏变性证明了这一过程在损伤轴突再生中的关键作用。令人惊讶的是,在癌症患者中严重的顺铂的神经毒性作用尚未明确地在动物中重现。突变体或转基因动物的遗传决定疾病可能影响外周轴突的髓鞘形成。“震颤鼠”缺乏髓磷脂,可能与人类的CMT IA相对应。小鼠、大鼠和狗的感觉神经病变与人类疾病的关系尚不清楚。实验动物的运动神经病变引起了人们的极大兴趣,因为最近发现的运动神经营养因子引起了人们的高度期望。大多数描述的突变没有得到适当的研究,小鼠突变“运动神经元病”(mind)最终被发现患有巴顿氏病。少数几个研究更彻底的模型中,没有一个可能是人类疾病的复制品,尽管它们可能同样有助于测试新的疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Animal models of neuropathies.

Neuropathy in animals is either genetically determined or is provoked by chemical compounds or physical injury. Diabetes in mice and rats may be spontaneous or induced, but a true copy of diabetic neuropathy in man is not yet available. Painful neuropathy occurs after nerve constriction or neuroma formation. A mouse mutant with delayed Wallerian degeneration demonstrates the pivotal role of this process for the regeneration of injured axons. Surprisingly, the neurotoxic effect of cisplatin which is severe in cancer patients has not yet unambiguously been reproduced in animals. Genetically determined diseases in mutants or transgenic animals may affect the myelination of peripheral axons. 'Trembler mice' are deficient in myelin and possibly correspond to CMT IA in man. The relation of sensory neuronopathies in mice, rats and dogs to human diseases is not yet clear. Motor neuronopathies in experimental animals have attracted much interest, because the recent discovery of motoneuronotrophic factors has raised high hopes. Most of the mutants described have not been appropriately studied, and the mouse mutant 'motoneurone disease' (mnd) eventually was found to have Batten's disease. None of the few more thoroughly studied models is probably a copy of human disease, although they may none the less help to test new therapies.

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