脑老化组织形态学特征:脑淀粉样血管病的不同类型及脑实质中淀粉样β蛋白沉积

Histomorphological features of brain aging: different types of cerebral amyloid angiopathy and beta-amyloid protein disposition in brain parenchyma

目的:观察脑老化中淀粉样β蛋白(β-Amyloidprotein,Aβ)在脑中沉积情况,探讨脑淀粉样血管病的不同类型以及脑实质中Aβ沉积的特点。方法:应用甲苯胺蓝、LFB染色及Aβ免疫组化方法,观察28例正常增龄病例犤23～100岁,平均(65.75±22.78)岁,男∶女=23∶5犦尸检脑标本的额叶、枕叶、壳核、海马及6例阿尔茨海默病(Alzheimerdis-ease,AD)病例犤76～94岁,平均(83.33±7.74)岁,男∶女=5∶1犦的海马标本。结果:正常增龄病例中,部分70岁以上病例脑中出现Aβ沉积,未出现Aβ沉积者年龄最高为90岁。7例正常老年病例出现脑淀粉样血管病(cerebralamyloidangiopathy,CAA),分别表现为嗜刚果红血管病(congophilicangiopathy,CA)、斑样血管病(plaque-likeangiopathy,PA)及混合型。8例正常老年病例脑中可见老年斑(senileplaque,SP),额叶最常受累,海马最少受累及,其中2例白质中也出现类似于终末斑的Aβ沉积。AD患者在海马及海马旁回出现大量Aβ沉积,表现为SP和CA及PA,其数量和严重程度均远远超过正常老年人。结论:Aβ沉积是脑老化的重要组织形态改变之一,但并非其必然结果。脑老化中斑块样Aβ沉积并不局限于灰质,白质内也可出现。不同类型的CAA可能存在不同的发病机制。

AIM: To observe the disposition of beta-amyloid protein(Aβ) in brain aging, and investigate the different types of cerebral amyloid angiopathy (CAA) and the characteristics of Aβdeposition in brain parenchyma. METHODS: Twenty-eight brains of subjects[aged from 23 to 100 years old, mean age was(65.75±22.78) years old, the ratio of male to female was 23 to 5]who died without clinical or pathological involvement of nervous system and 6 brains of patients with Alzheimer disease(AD)(aged from 76 to 94 years old, mean age(83.33±7.74) years old, the ratio of male to female was 5 to 1) were obtained at autopsy. Sections from frontal lobe, occipital lobe, putamen and hippocampus of the normal subjects and those from hippocampus of the AD patients were observed by using the toluidine blue and LFB staining and Aβimmunohistochemistry. RESULTS: Among the normal aging subjects, Aβdepositions were observed in some cases over 70 years old, and the oldest case without Aβdeposition was 90 years old. Seven nomal aging subjects had CAA, manifested by congophilic angiopathy(CA), plaque-like angiopathy (PA) and the mixed pattern. Senile plaque(SP) was observed in the brain of 8 nomal aging subjects, with the most frequently involvement of frontal lobe and the least frequently involvement of hippocampus, and burn-out plaque like Aβdepositions were also found in the white matter of 2 cases. Numerous Aβdepositions were found in the hippocampus and subiculum pippocampi of the AD patients, including SP, CA and CAA, the number and severity were significantly suppassed those in the normal aging subjects. CONCLUSION: Aβdeposition is one of the important histomorphological changes of brain aging but is not its necessary result. Plaque-like Aβdisposition is not only limited in the gray matter, but also in the white matter. Different mechanisms may be involved in the development of different patterns of CAA.