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KMID : 1100220030020020115
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Dementia and Neurocognitive Disorders
2003 Volume.2 No. 2 p.115 ~ p.119
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Platelet Amyloid Precursor Protein Abnormalities in Alzheimer’s Disease
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Lee Ae-Young
Jo Eun-Kyung
Kim Kyun-Ik
Kim Sun-Kook
Sohn Eun-Hee
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Abstract
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Background: Although Alzheimer’s disease (AD) is a progressive neurodegenerative disorder without any truly effective pharmacological treatment at present, early accurate diagnosis is important for the delaying of disease progression and proper management. It would be desirable to have a peripheral biological marker to identify patients affected by AD. Amyloid β-peptide originates from a larger precursor, the amyloid precursor protein (APP), which can be seen in the platelet of its equivalent to those found in brain. To investigate if there is a correlation between level of platelet APP isoform and AD, we evaluate a cohort of subjects including patients affected by sporadic AD, vascular dementia, and controls.
Subjects & Methods: Thirty-five patients with sporadic AD diagnosed according to the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer’s Disease and Related Disorders criteria (NINCDS-ADRDA) and 26 vascular dementia patients diagnosed by the Diagnosis and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria and 12 controls were included. Blood sample were drawn from fasting state and collected into 3 mL of 3.8% sodium citrate. Platelets were collected by centrifugation at 500 g for 20 minutes and washed, and the platelet pellet was stored at -80℃ until used. APP was assessed by Western blot analysis and quantified by densitometry using Image Analyzer.
Results: In platelets obtained from patients affected by sporadic AD, the absolute level of APP quantitated by densitometer as well as the result of Western blot was higher compared with those of patients with non-Alzheimer dementia and controls. We observed statistically significant reductions in the ratio of 120 kDa to 130 kDa APP to 110 kDa APP (APPr) for patients with probable AD compared with control subjects and patients with vascular dementia. APPr levels in AD correlated with the severity of dementia measured by CDR. Accuracy levels measured by Receiver Operating Curve analysis showed that a cut-off level of 0.45 resulted in a sensitivity of 71% and a specificity of 74%, with an area under the curve of 0.793.
Conclusion: Platelet APPr allowed to differentiate AD from normal aging and vascular dementia with high sensitivity and specificity. These findings suggest that platelet APPr may be a helpful peripheral marker for diagnosis and clinical progression of Alzheimer disease.
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KEYWORD
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Alzheimer’s disease, Peripheral marker, Platelet APPr
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