Decreased CSF-ß-amyloid 42 in Alzheimer's disease and amyotrophic lateral sclerosis may reflect mismetabolism of ß-amyloid induced by disparate mechanisms

Sjogren, M.Sjögren, M., Institute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden, Institute of Clinical Neuroscience, Section Psychiatry, Göteborg University at Sahlgrenska Universitetssjukhuset/Mölndal, SE-43180 Mölndal, Sweden (author)

Both tau and ß-amyloid 42 (Aß42) have been implicated in Alzheimer's disease (AD) and tau alone in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). These proteins can be measured in the cerebrospinal fluid (CSF), differences from normal CSF levels may reflect pathophysiological mechanisms. Using ELISAs, we investigated the levels of total CSF-tau (here referred to as tau), phosphorylated CSF-tau (phospho-tau), and Aß42 in patients with AD (n = 19), FTD (n = 14), ALS (n = 11) and Parkinson's disease (PD, n = 15) and in age-matched controls (n = 17). Both CSF-tau and CSF-phosphotau were increased in AD compared with FTD (p < 0.001), ALS (p < 0.001), PD (p < 0.001) and controls (p < 0.001). CSF-Aß42 was markedly decreased in AD and ALS (both p < 0.001) and slightly decreased in FTD (p < 0.01) and PD (p < 0.05) compared with controls. Using CSF-phosphotau may improve the differentiation of AD from FTD and ALS in clinical praxis. Furthermore, decreased CSF-Aß42 levels may be common in neurode-generative disorders possibly reflecting changes in the metabolism of ß-amyloid or axonal degeneration. Copyright © 2002 S. Karger AG, Basel.

Davidsson, P.Institute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden (author)
Wallin, A.Institute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden (author)
Granerus, Ann-KathrineÖstergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Geriatrik,Geriatriska kliniken(Swepub:liu)anngr79 (author)
Grundstrom, E.Grundström, E., Department of Neuroscience, Neurology, University Hospital, Uppsala, Sweden (author)
Askmark, H.Department of Neuroscience, Neurology, University Hospital, Uppsala, Sweden (author)
Vanmechelen, E.Innogenetics, Ghent, Belgium (author)
Blennow, K.Institute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden, Medical Research Council, Sweden (author)
Sjögren, M., Institute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden, Institute of Clinical Neuroscience, Section Psychiatry, Göteborg University at Sahlgrenska Universitetssjukhuset/Mölndal, SE-43180 Mölndal, SwedenInstitute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden (creator_code:org_t)

In:Dementia and Geriatric Cognitive Disorders: S. Karger AG13:2, s. 112-1181420-80081421-9824

By the author/editor: Sjogren, M.; Davidsson, P.; Wallin, A.; Granerus, Ann-Ka ...; Grundstrom, E.; Askmark, H.; show more...; Vanmechelen, E.; Blennow, K.; show less...

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