Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA.
J Alzheimers Dis. 2010;19(3):761-80. doi: 10.3233/JAD-2010-1274.
In and of itself, late-onset Alzheimer's disease (AD) can be a devastating illness. However, a sub-group of AD patients develop psychosis as the disease progresses. These patients have an added burden of greater cognitive impairment, higher rates of institutionalization, and higher mortality than AD patients without psychosis. While the etiopathogenesis such as psychosis in AD (AD+P) is not known, mounting evidence accrued over the past ten years indicates that AD+P represents a distinct phenotype with a genetic basis. Elucidating the genetic mechanism of AD+P is crucial if better pharmaceutical treatments are to be developed for these patients. The goal of this review is to summarize what is currently known regarding the genetic basis of psychosis in AD. Specific attention is given to familial aggregation and heritability, linkage to chromosomal loci, and associations of candidate genes of APOE and the monoamine neurotransmitter system.
迟发性阿尔茨海默病(AD)本身就是一种毁灭性的疾病。然而,AD 患者亚组在疾病进展过程中会出现精神病。与没有精神病的 AD 患者相比,这些患者认知障碍更严重,住院率更高,死亡率更高。虽然 AD 中精神病的发病机制(AD+P)尚不清楚,但过去十年积累的越来越多的证据表明,AD+P 代表一种具有遗传基础的独特表型。阐明 AD+P 的遗传机制对于为这些患者开发更好的药物治疗方法至关重要。本综述的目的是总结目前已知的 AD 中精神病的遗传基础。特别关注家族聚集和遗传性、与染色体基因座的连锁以及 APOE 和单胺神经递质系统候选基因的关联。