Abstract
Purpose Recent study shows that blood-derived amyloid-beta (Aβ) can induce cerebral amyloidosis and is involved in the pathogenesis of Alzheimer's disease (AD). The vast majority of blood Aβ is generated from platelet. Whether blood Aβ levels are associated with the count of platelets remains unknown. Methods 58 clinically diagnosed AD patients, 18 11C-PIB-PET diagnosed AD patients, and 61 age- and gender-matched cognitively normal controls were included to analyze the correlation of plasma Aβ levels with platelet count. 13 AD patients and 40 controls with cerebrospinal fluid (CSF) samples were included to further analyze the correlation of CSF Aβ levels with platelet count. Aβ40 and Aβ42 levels in plasma and CSF were measured by ELISA kits. Results The plasma Aβ42 level was positively correlated with platelet count in both AD patients and control group, especially in AD patients with positive PIB-PET, while there was no correlation as to Aβ40. The CSF Aβ levels also had no significant correlation with platelet count. Conclusion It suggests that platelets may be involved in the pathogenesis of AD and become a potential peripheral biomarker for AD.
Highlights
Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the elderly
AD patients and controls were similar in educational level (p1=0.225, p2=0.550), and there were no significant differences in the comorbidity of hypertension, diabetes mellitus, cardiovascular disease, and hyperlipidemia
There were no correlations of cerebrospinal fluid (CSF) Aβ40 or Aβ42 levels with platelet count in either AD or control group (Figure 4). This is the first research to investigate the association between plasma and CSF Aβ levels and platelet count
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the elderly. It causes cognitive deficits and memory dysfunction that usually starts slowly and worsens over time. Recent study has shown that blood Aβ could enter brain and lead to the occurrence of AD, suggesting that AD may be a systemic disease [2]. Platelets express amyloid precursor protein (APP), β-secretase, and γ-secretase, and it can generate Aβ [3, 4]. It has been shown that almost 90% of the blood Aβ originated from platelet [5]. Platelet activation may lead to the deposition of Aβ40 in the wall of brain vessels, which results in cerebral amyloid angiopathy (CAA) [8]. We aim to investigate whether Aβ levels are correlated with the platelet count
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