ArticleNeurochemical research1999
Prothrombin concentration in the cerebrospinal fluid is not altered in Alzheimer's disease.
Article in Neurochemical research, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance.Pharmacology & therapeutics · 2022Review
- Expanding the family of extracellular chaperones: Identification of human plasma proteins with chaperone activity.Protein science : a publication of the Protein Society · 2021Article
- Markers for neural degeneration and regeneration: novel highly sensitive methods for the measurement of thrombin and activated protein C in human cerebrospinal fluid.Neural regeneration research · 2021Article
- Activation and proteolytic activity of the Treponema pallidum metalloprotease, pallilysin.PLoS pathogens · 2012Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prothrombin, known to be expressed in brain and to possess growth modulating properties, has been suggested to be involved in the pathogenesis of Alzheimer's disease (AD). We studied prothrombin concentration in lumbar CSF (L-CSF) in patients with AD (n = 25), neurologic disease controls (NDC; n = 33) covering a wide range of neurologic disorders, and subjects with Guillain-Barre syndrome (GBS; n = 4) as well as in samples of non-pathological ventricular CSF (V-CSF; n = 4). The results were evaluated with respect to CSF flow rate, as indicated by the albumin quotient (Q(Alb)). The concentrations of prothrombin in L-CSF in NDC (mean: 0.46 mg/l, range: 0.21-0.96), and AD (mean: 0.6 mg/l, range: 0.19-1.2) were in the normal range reported previously. Expectedly, prothrombin concentration in L-CSF of GBS was increased (mean: 6.3 mg/l, range: 2.3-9.7) corresponding to the increased Q(Alb) in this group (mean 54.6x10(-3), range: 17-88.1). The concentrations of both prothrombin and albumin were 5.5-fold higher in L-CSF than in V-CSF (mean Q(Alb) : 1.1x10(-3), mean concentration of prothrombin: 0.088 mg/l). In conclusion, CSF prothrombin in all conditions evaluated here is exclusively derived from blood.
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