Association of platelet-derived soluble glycoprotein VI in plasma with Alzheimer's disease
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Published on: July 26, 2011
Christoph Laske1, Thomas Leyhe, Elke Stransky
1Department of Psychiatry and Psychotherapy, University of Tuebingen, Osianderstrasse 24, D-72076 Tuebingen, Germany. christoph.laske@med.uni-tuebingen.de
Accumulating evidence from epidemiological, clinical and experimental studies suggests that vascular risk factors and angiopathic mechanisms are involved in the pathogenesis of Alzheimer's disease (AD). Platelets could be the missing link between AD and the vasculature. Soluble glycoprotein VI (sGPVI) and beta-thromboglobulin (beta-TG) plasma and cerebrospinal fluid (CSF) levels as markers of platelet activity were measured in 30 AD patients and 20 age-matched healthy elderly controls by ELISA. The severity of dementia was assessed by mini-mental state examination (MMSE). We found in AD patients significantly decreased sGPVI plasma levels (0.55+/-0.18ng/ml) as compared to healthy controls (0.75+/-0.43ng/ml; p=0.033). In AD patients, sGPVI levels were positively correlated with beta-TG plasma levels (r=0.244, p=0.05) and with cognitive status as measured by MMSE score (r=0.271; p=0.048). In unconcentrated CSF samples, levels of beta-TG and sGPVI were below the detection limit of the assays in AD patients and healthy controls. Our results suggest an association of sGPVI with the pathogenesis of AD. These findings encourage future research into whether sGPVI plasma levels may reflect or even mediate neuroprotective mechanisms in AD.
Accumulating evidence from epidemiological, clinical and experimental studies suggests that vascular risk factors and angiopathic mechanisms are involved in the pathogenesis of Alzheimer's disease (AD). Platelets could be the missing link between AD and the vasculature. Soluble glycoprotein VI (sGPVI) and beta-thromboglobulin (beta-TG) plasma and cerebrospinal fluid (CSF) levels as markers of platelet activity were measured in 30 AD patients and 20 age-matched healthy elderly controls by ELISA. The severity of dementia was assessed by mini-mental state examination (MMSE). We found in AD patients significantly decreased sGPVI plasma levels (0.55+/-0.18ng/ml) as compared to healthy controls (0.75+/-0.43ng/ml; p=0.033). In AD patients, sGPVI levels were positively correlated with beta-TG plasma levels (r=0.244, p=0.05) and with cognitive status as measured by MMSE score (r=0.271; p=0.048). In unconcentrated CSF samples, levels of beta-TG and sGPVI were below the detection limit of the assays in AD patients and healthy controls. Our results suggest an association of sGPVI with the pathogenesis of AD. These findings encourage future research into whether sGPVI plasma levels may reflect or even mediate neuroprotective mechanisms in AD.
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