Francis P T, Webster M T, Chessell I P, Holmes C, Stratmann G C, Procter A W, Cross A J, Green A R, Bowen D M
Miriam Marks Department of Neurochemistry, Institute of Neurology, London, United Kingdom.
Ann N Y Acad Sci. 1993 Sep 24;695:19-26. doi: 10.1111/j.1749-6632.1993.tb23021.x.
A substantial loss of cortical cholinergic nerve endings, along with a much more circumscribed cortical degeneration of pyramidal neurons, almost certainly causes glutamatergic hypoactivity in live Alzheimer's patients. These selective pathologies are discussed in terms of therapy. An additional effect of some proposed treatments is emerging as there is evidence that processing pathways for beta-amyloid precursor proteins in cortical pyramidal neurons, a target cell for acetylcholine, are affected by neuronal activity.
皮质胆碱能神经末梢的大量丧失,以及更为局限的锥体神经元皮质变性,几乎可以肯定会导致活体阿尔茨海默病患者谷氨酸能活性低下。这些选择性病变将从治疗角度进行讨论。随着有证据表明皮质锥体神经元(乙酰胆碱的靶细胞)中β-淀粉样前体蛋白的加工途径受神经元活动影响,一些提议治疗方法的额外效果正在显现。