Cacabelos R, Fernández-Novoa L, Pérez-Trullén J M, Franco-Maside A, Alvarez X A
Department of Human Physiology, Complutense University Medical School, Madrid, Spain.
Methods Find Exp Clin Pharmacol. 1992 Nov;14(9):711-5.
Recent data indicate that a neuroimmune reaction might be responsible in part for neuronal death and cognitive deterioration in senile dementia. The potential involvement of brain histamine (HA) and interleukin-1 (IL-1) in this process has been previously documented. We have studied the concentration of serum HA in patients with Alzheimer's disease (AD) or multi-infarct dementia (MID) and in age-matched control subjects. Serum HA levels were significantly higher in AD (10.935 +/- 5.692 nM) and MID (8.521 +/- 3.44 nM) than in controls (5.533 +/- 2.567 nM) and correlated with mental performance as evaluated with the Mini-Mental State Examination (MMSE) (r = +0.493, p < 0.009). No correlation was found with cardiovascular parameters, cerebrovascular risk factors or age. Hyperactivation of the histaminergic system in AD at central and peripheral levels might reflect a neuroimmune reaction to brain tissue damage, a neurotrophic response, and/or a reactive process to regulate the IL-1 induced amyloid precursor protein (APP) overproduction.
近期数据表明，神经免疫反应可能在一定程度上导致了老年痴呆症中的神经元死亡和认知衰退。此前已有文献记载，脑组胺（HA）和白细胞介素-1（IL-1）可能参与了这一过程。我们研究了阿尔茨海默病（AD）或多发梗死性痴呆（MID）患者以及年龄匹配的对照受试者血清HA的浓度。AD患者（10.935±5.692 nM）和MID患者（8.521±3.44 nM）的血清HA水平显著高于对照组（5.533±2.567 nM），且与简易精神状态检查表（MMSE）评估的精神表现相关（r = +0.493，p < 0.009）。未发现与心血管参数、脑血管危险因素或年龄相关。AD患者中枢和外周组胺能系统的过度激活可能反映了对脑组织损伤的神经免疫反应、神经营养反应和/或对调节IL-1诱导的淀粉样前体蛋白（APP）过度产生的反应过程。
