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Reduced levels of amyloid-beta-binding proteins in cerebrospinal fluid from Alzheimer's disease patients.

Artikel i vetenskaplig tidskrift
Författare Sarah Hansson
Ulf Andreasson
Mariann Wall
Ingmar Skoog
Niels Andreasen
Anders Wallin
Henrik Zetterberg
Kaj Blennow
Publicerad i Journal of Alzheimer's disease : JAD
Volym 16
Nummer/häfte 2
Sidor 389-97
ISSN 1387-2877
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 389-97
Språk en
Länkar dx.doi.org/10.3233/JAD-2009-0966
Ämnesord Aged, Aged, 80 and over, Alzheimer Disease, cerebrospinal fluid, Amyloid beta-Protein, cerebrospinal fluid, Cystatin C, cerebrospinal fluid, Dementia, cerebrospinal fluid, Electrochemistry, Female, Humans, Intramolecular Oxidoreductases, cerebrospinal fluid, Linear Models, Lipocalins, cerebrospinal fluid, Male, Nephelometry and Turbidimetry, methods, Peptide Fragments, cerebrospinal fluid, Prealbumin, cerebrospinal fluid, Statistics, Nonparametric, alpha 1-Antitrypsin, cerebrospinal fluid
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Amyloid-beta(Abeta) aggregation is a major hallmark of Alzheimer's disease (AD). Previous studies have suggested that only unbound Abeta can take part in the aggregation process. Therefore, endogenous Abeta-binding proteins may have an important role in preventing AD. Here, we analyzed cerebrospinal fluid (CSF) samples from 35 subjects with AD, 18 subjects with frontotemporal dementia (FTD) and 29 non-demented controls to test if reduced Abeta-binding capacity in CSF is a specific feature of AD. A panel of known Abeta-binding CSF proteins, including beta-trace/prostaglandin D2 synthase (beta-trace), transthyretin (TTR), cystatin C (CysC) and alpha(1)-antitrypsin (AAT), were quantified and related to diagnosis and CSF levels of Abeta(1-38), Abeta(1-40) and Abeta(1-42). AD patients displayed a mild reduction in the CSF levels of beta-trace (p=0.020), CysC (p=0.017), AAT (p=0.019) and TTR (p=0.012) compared with controls. While the reductions in AAT and TTR were AD-specific, the levels of beta-trace and CysC were also reduced in FTD. As expected, CSF Abeta(1-42) was reduced in AD compared with controls (p=0.00005) and with FTD patients (p=0.015). Positive correlations between Abeta(1-42) and beta-trace, CysC and TTR, respectively, were seen only in the AD group, suggesting that deficient Abeta-binding capacity in CSF may contribute to the amyloidogenic process in AD.

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