The normal equilibrium between CSF and plasma amyloid beta levels is disrupted in Alzheimer's disease

脑脊液 内科学 阿尔茨海默病 淀粉样蛋白(真菌学) 内分泌学 β淀粉样蛋白 退行性疾病 疾病 BETA(编程语言) 医学 病理 化学 计算机科学 程序设计语言
作者
Vilmantas Giedraitis,Johan Sundelöf,Michael C. Irizarry,Nina Gårevik,Bradley T. Hyman,Lars‐Olof Wahlund,Martin Ingelsson,Lars Lannfelt
出处
期刊:Neuroscience Letters [Elsevier BV]
卷期号:427 (3): 127-131 被引量:113
标识
DOI:10.1016/j.neulet.2007.09.023
摘要

Amyloid-beta (Abeta) with 40 (Abeta40) and 42 (Abeta42) amino acids, the main components of amyloid plaques in the Alzheimer's disease (AD) brain, can be measured in human cerebrospinal fluid (CSF) and plasma. Whereas CSF Abeta42 is decreased in AD, some studies have reported changed plasma Abeta levels in AD and in subjects with mild cognitive impairment (MCI). To this date it is unclear if and how CSF and plasma levels of Abeta correlate with each other in healthy individuals, albeit earlier studies on AD patients found no correlation between CSF and plasma Abeta. We have measured Abeta40 and Abeta42 in paired CSF and plasma samples from patients with AD (n=39), MCI (n=29) and healthy control subjects (n=18). We observed a clear correlation between CSF and plasma levels for both Abeta40 and Abeta42 in healthy individuals, whereas no such correlation could be seen for AD or MCI cases. Similarly to other studies we also found low levels of Abeta42 in AD CSF, whereas there were no significant differences in plasma Abeta levels between the diagnostic groups. Our findings suggest that the normal equilibrium between CSF and plasma Abeta may be disrupted with the initiation of amyloid deposition in the brain.

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