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The normal equilibrium between CSF and plasma amyloid beta levels is disrupted in Alzheimer's disease
Authors:Giedraitis Vilmantas  Sundelöf Johan  Irizarry Michael C  Gårevik Nina  Hyman Bradley T  Wahlund Lars-Olof  Ingelsson Martin  Lannfelt Lars
Affiliation:Department of Public Health/Geriatrics, Uppsala University, Uppsala, Sweden. vilmantas.giedraitis@pubcare.uu.se
Abstract:
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.
Keywords:Alzheimer's disease   Mild cognitive impairment (MCI)   Cerebrospinal fluid   Case control studies   Amyloid beta   APOE
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