美國西北大學費因伯格醫(yī)學院開發(fā)的一類新的藥物,，初步顯示出對老年癡呆癥,，帕金森氏癥,，多發(fā)性硬化癥和創(chuàng)傷性腦損傷的治療效果,，這主要是通過減少大腦的炎癥實現(xiàn)的。西北大學最近獲批了這一類新藥的專利,，并已授權生物技術公司完成了首次1期臨床試驗,。
該類藥物針對一類特定類型的大腦炎癥。這種炎癥是這些神經(jīng)系統(tǒng)疾病和腦外傷和中風的一個共同特點,。這種大腦的炎癥,，也被稱為神經(jīng)炎癥，被越來越多地認為在這些以漸進性破壞為特征的慢性疾病和腦損傷中發(fā)揮重大作用,。
相比目前正在進行測試的防止大腦發(fā)生斑塊的治療方法,，新藥物--mw151和mw189--通過緩解大腦炎癥，提供了一種完全不同的對老年癡呆癥的治療方法,。淀粉樣斑塊是一個疾病的指標,，但不是一個已被證實的病因。
一項發(fā)表在神經(jīng)學雜志（Journal of Neuroscience）的新臨床研究報告說,，給予老年癡呆癥易患小鼠,，某種西北大學研發(fā)的新藥MW01-2-151SRM ，可以防止小鼠老年癡呆的全面發(fā)生。本研究,，還確定了該藥物最佳的治療時間窗,。研究者說，該藥物可以口服并容易穿過血腦屏障,。西北大學費因伯格醫(yī)學院分子藥理學和生物化學沃特森教授說,，"這種藥物可能成為預防老年癡呆癥發(fā)生發(fā)展的藥物庫的一員。"
其他研究同時證實了,，該藥物對帕金森氏癥,，多發(fā)性硬化癥和創(chuàng)傷性腦損傷的治療效果。（生物谷bioon.com）
本文編譯自New drug could treat Alzheimer's, multiple sclerosis and brain injury
doi:10.1016/j.cell.2011.10.017
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Early Stage Drug Treatment That Normalizes Proinflammatory Cytokine Production Attenuates Synaptic Dysfunction in a Mouse Model That Exhibits Age-Dependent Progression of Alzheimer's Disease-Related Pathology
Adam D. Bachstetter1,Christopher M. Norris1,2,Pradoldej Sompol1,Donna M. Wilcock1,3,Danielle Goulding1,Janna H. Neltner1,4,Daret St. Clair1,5,7,D. Martin Watterson8, andLinda J. Van Eldik1,6
Overproduction of proinflammatory cytokines in the CNS has been implicated as a key contributor to pathophysiology progression in Alzheimer's disease (AD), and extensive studies with animal models have shown that selective suppression of excessive glial proinflammatory cytokines can improve neurologic outcomes. The prior art, therefore, raises the logical postulation that intervention with drugs targeting dysregulated glial proinflammatory cytokine production might be effective disease-modifying therapeutics if used in the appropriate biological time window. To test the hypothesis that early stage intervention with such drugs might be therapeutically beneficial, we examined the impact of intervention with MW01-2-151SRM (MW-151), an experimental therapeutic that selectively attenuates proinflammatory cytokine production at low doses. MW-151 was tested in an APP/PS1 knock-in mouse model that exhibits increases in AD-relevant pathology progression with age, including increases in proinflammatory cytokine levels. Drug was administered during two distinct but overlapping therapeutic time windows of early stage pathology development. MW-151 treatment attenuated the increase in microglial and astrocyte activation and proinflammatory cytokine production in the cortex and yielded improvement in neurologic outcomes, such as protection against synaptic protein loss and synaptic plasticity impairment. The results also demonstrate that the therapeutic time window is an important consideration in efficacy studies of drugs that modulate glia biological responses involved in pathology progression and suggest that such paradigms should be considered in the development of new therapeutic regimens that seek to delay the onset or slow the progression of AD.
