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Sialic acid and sialidase activity in acute stroke
L Nanetti1, A Vignini, F Raffaelli
1Department of Neurological Science, Faculty of Medicine, Marche Polytechnic University, Italy. L.nanetti@hotmail.com
Disease Markers
|December 20, 2008
Summary
Erythrocyte sialic acid levels are decreased in stroke patients, while plasma levels and sialidase activity are elevated. These changes correlate with stroke severity, suggesting potential new biomarkers for ischemic stroke.
Area of Science:
- Biochemistry
- Neurology
- Hematology
Background:
- Stroke is a complex neurological condition involving disrupted cerebral blood flow.
- Erythrocytes, rich in sialic acid, may offer insights into stroke-related biochemical changes.
- Sialic acid and sialidase activity are implicated in various physiological and pathological processes.
Purpose of the Study:
- To investigate the relationship between erythrocyte membrane, plasma, and sialic acid content in stroke patients.
- To evaluate the impact of sialic acid content and sialidase activity on stroke severity.
- To identify potential biochemical markers for ischemic stroke.
Main Methods:
- Compared sialic acid content and sialidase activity in 54 first-stroke patients and 53 healthy controls.
- Measured total bound sialic acid in erythrocytes and plasma.
- Assessed neurological deficit severity using the National Institute of Health Stroke Scale (NIHSS).
Main Results:
- Total bound sialic acid was significantly decreased in erythrocytes of stroke patients.
- Elevated sialidase activity showed a significant correlation with higher NIHSS scores (stroke severity).
- Stroke patients exhibited lower erythrocyte sialic acid and higher plasma sialic acid levels alongside increased sialidase activity.
Conclusions:
- Low erythrocyte sialic acid, high plasma sialic acid, and elevated sialidase activity may serve as markers for ischemic stroke.
- These biochemical alterations could play a role in the development and progression of cerebral ischemic damage.
- Further research is warranted to elucidate the precise mechanisms linking these findings to stroke pathophysiology.

