Sevush S, Jy W, Horstman L L, Mao W W, Kolodny L, Ahn Y S
Department of Psychiatry, University of Miami School of Medicine, Fla 33136, USA.
Arch Neurol. 1998 Apr;55(4):530-6. doi: 10.1001/archneur.55.4.530.
In light of recent reports of diminished platelet serotonin concentration and increased plasma serotonin levels in patients with Alzheimer disease (AD), we hypothesized that a state of heightened platelet activation might be present in AD.
To compare baseline activation of unstimulated platelets in patients with AD with that in control subjects.
Flow cytometry was used to measure platelet activation in 91 patients with probable AD and 40 age-matched control subjects. Groups were compared for percentage of circulating platelet aggregates, expression of CD62p, formation of leukocyte-platelet complexes, and presence of circulating platelet microparticles, controlling for effects of demographic, clinical, physiological, and logistical factors.
Multiple analysis of covariance on ranked data revealed a 39.5% increase in percentage of platelet aggregates (P=.0001), a 59.3% increase in expression of CD62p (P=.001), and a 53.3% increase in leukocyte-platelet complexes (P=.0001) in the group with AD but no differences in the number of platelet microparticles, overall platelet count, plasma fibrinogen level, or plasma platelet factor 3. Activation was weakly correlated with sex, but was independent of age, severity of disease, duration of disease, depression, agitation, and family history of dementia.
Platelets of patients with AD exhibit greater unstimulated activation than those of controls. Potential causes of such activation include possible stimulation of platelets by damaged cerebral endothelial cells or platelet activation induced by membrane abnormalities previously reported to be present in platelets of patients with AD. In light of recent evidence that platelets are the principal source of both amyloid precursor protein and beta-amyloid peptide in human blood, it is possible that AD platelet activation may reflect or even contribute to the pathogenesis of the disease.
鉴于近期有报道称阿尔茨海默病（AD）患者血小板5-羟色胺浓度降低而血浆5-羟色胺水平升高，我们推测AD患者可能存在血小板活化增强的状态。
比较AD患者与对照者未受刺激血小板的基线活化情况。
采用流式细胞术检测91例可能患有AD的患者和40例年龄匹配的对照者的血小板活化情况。比较两组循环血小板聚集体的百分比、CD62p的表达、白细胞-血小板复合物的形成以及循环血小板微粒的存在情况，并对人口统计学、临床、生理和后勤因素的影响进行控制。
对排序数据进行的多因素协方差分析显示，AD组血小板聚集体百分比增加39.5%（P = 0.0001），CD62p表达增加59.3%（P = 0.001），白细胞-血小板复合物增加53.3%（P = 0.0001），但血小板微粒数量、血小板总数、血浆纤维蛋白原水平或血浆血小板因子3无差异。活化与性别呈弱相关，但与年龄、疾病严重程度、病程、抑郁、激越和痴呆家族史无关。
AD患者的血小板比对照者表现出更强的未受刺激活化。这种活化的潜在原因可能包括受损的脑内皮细胞对血小板的可能刺激或先前报道的AD患者血小板中存在的膜异常诱导的血小板活化。鉴于最近有证据表明血小板是人体血液中淀粉样前体蛋白和β-淀粉样肽的主要来源，AD血小板活化可能反映甚至促成该疾病的发病机制。
