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。 單獨(dú)應(yīng)用對(duì) PD無治療作用 , 主要與左旋多巴按一 定比例制成復(fù)方左旋多巴制劑供臨床應(yīng)用,可增加 血和腦內(nèi) Ldopa達(dá) 3 ~ 4倍。 信尼麥 ( sinemet, 心寧美 ) 左旋多巴 : 卡比多巴 =10 : 1( 100mg : 10mg) 復(fù)方芐絲肼 ( 美多巴 , Madopar) 左旋多巴 : 芐絲肼 =4∶ 1( 100mg∶ 25mg) 聯(lián)合用藥主要優(yōu)點(diǎn) 提高左旋多巴療效 ( 增效 ) 減少外周副作用 ( 減毒 ) 減少左旋多巴用量 ( 70 ~ 80%) 3. COMT抑制劑 Ldopa代謝有兩條途徑: Ldopa DA 3OMD( 3O甲基多巴) 而 3OMD又可與 Ldopa競爭轉(zhuǎn)運(yùn)載體而影響 Ldopa的吸收和進(jìn)入腦組織(生物利用度降低) co2 COMT 硝替卡朋( nitecapone) 托 卡 朋( tocapone) 安托卡朋( entocapone) 可增加紋狀體中 Ldopa和 DA。當(dāng)與卡比多巴合用時(shí),只抑制外周 COMT,增加 Ldopa生物利用度,而不影響腦內(nèi) COMT(不易通過血腦屏障)。 抗老年性癡呆藥 Downsized Target A tiny protein called ADDL could be the key to Alzheimer39。s Scientific American 2023 Scientists have long suspected that the protein clumps and tangles identified by Alois Alzheimer in 1907 somehow cause the disease that bears his name, probably by killing neurons. Now some researchers are blaming a much smaller form of protein, one that apparently produces memory deficits merely by binding to neurons and disrupting their ability to transmit signals. The search has begun for an antibody that would destroy these tiny proteinsor ADDLsthereby preventing the onset of Alzheimer39。s disease and possibly even reversing the early symptoms. The discovery of ADDLs explains glaring anomalies in the conventional thinking about Alzheimer39。s, which holds that fragments of amyloid precursor protein, produced by normal neurons, aggregate into sticky, insoluble plaques that damage neurons. The problem with this theory is that virtually every older person carries some amyloid pla