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脉络丛门和褪黑素缺乏可以解释阿尔茨海默病的神经病理学。

Choroid plexus portals and a deficiency of melatonin can explain the neuropathology of Alzheimer's disease.

出版信息

Med Hypotheses. 2010 Jun;74(6):1059-66. doi: 10.1016/j.mehy.2009.12.026. Epub 2010 Jan 13.

DOI:10.1016/j.mehy.2009.12.026
PMID:20074864
Abstract

Presently, the textbook description of cerebrospinal fluid absorption is through the arachnoid granules into the superior sagittal sinus. The theory is based on non-physiologic experiments and fails to explain multiple observations. Photographs and microphotographs of choroid plexus portals are included. Evidence is presented that cerebrospinal fluid is moved from the choroid fissure into the ventricular system. The deposition pattern of corpora amylacea demonstrates the bulk flow of cerebrospinal fluid. Melatonin is found in higher concentration in the cerebrospinal fluid than in simultaneously sampled blood. Melatonin is a potent antioxidant and the loss of its protection in the cerebrospinal fluid in Alzheimer's disease can explain the pattern of cell destruction. Challenges of the embedded dogma of the arachnoid granule absorption of cerebrospinal fluid have been ignored; however this old faulty theory must be abandoned in order to understand the pathophysiology of Alzheimer's disease.

摘要

目前,教科书对脑脊液吸收的描述是通过蛛网膜颗粒进入上矢状窦。该理论基于非生理实验,无法解释多种观察结果。本文包含脉络丛门的照片和显微照片。有证据表明脑脊液从脉络裂进入脑室系统。淀粉样体的沉积模式表明脑脊液呈大体流动。脑脊液中的褪黑素浓度明显高于同时采集的血液中的褪黑素浓度。褪黑素是一种有效的抗氧化剂,在阿尔茨海默病中脑脊液中褪黑素保护作用的丧失可以解释细胞破坏的模式。蛛网膜颗粒吸收脑脊液这一既定教条的挑战被忽视了;然而,为了理解阿尔茨海默病的病理生理学,必须摒弃这一陈旧而错误的理论。

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