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- Kern, M A, et al.
(författare)
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Amyotrophic lateral sclerosis : Evidence for intact hepatocyte growth factor/MET signalling axis
- 2001
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Ingår i: Cytokine. - : W B SAUNDERS CO. - 1043-4666 .- 1096-0023. ; 15:6, s. 315-319
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Tidskriftsartikel (refereegranskat)abstract
- Hepatocyte growth factor (HGF) is a secreted cytokine which is expressed in the central nervous system (CNS) together with its specific receptor MET. Since HGF exerts strong neurotrophic activity including motoneurons, we have further analysed whether the HGF/MET axis is defective in patients with amyotrophic lateral sclerosis (ALS). Intrathecal HGF-secretion was measured in cerebrospinal fluid (CSF) from patients with amyotrophic lateral sclerosis and in controls without neurological diseases using a specific sandwich immunoassay (ELISA). MET-expression was analysed by immunohistology in spinal cord cross-sections of ALS patients and unaffected controls. The HGF concentrations in CSF were moderately but significantly increased in ALS patients compared to healthy controls (580 pg/ml vs 348 pg/ml). MET-protein was detectable in spinal cord motoneurons of patients with ALS as well as unaffected controls. The data demonstrate that ALS does not show a lack of the trophic signalling axis, HGF/MET, suggesting that the signalling system itself is not affected. The moderate increase in HGF-secretion may represent a compensatory effect.
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| 5. |
- Sjogren, M., et al.
(författare)
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Decreased CSF-ß-amyloid 42 in Alzheimer's disease and amyotrophic lateral sclerosis may reflect mismetabolism of ß-amyloid induced by disparate mechanisms
- 2002
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 13:2, s. 112-118
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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