Neurology 5 / Neuropathology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Via Celoria 11, 20133 Milan, Italy.
Clinical Neuropsychology, Cognitive Disorders and Adult Dyslexia Unit, Neurology, Department of Neuro-Motor Diseases, AUSL IRCCS - Ospedale Santa Maria Nuova di Reggio Emilia, Via Amendola 2, 42122 Reggio Emilia, Italy.
Neurobiol Aging. 2022 Apr;112:191-196. doi: 10.1016/j.neurobiolaging.2022.01.008. Epub 2022 Feb 4.
Mutations in presenilin 1 gene (PSEN1) are the most common causes of autosomal dominant early-onset Alzheimer's disease (EOAD). We report a novel PSEN1 mutation (I213S) that was discovered in an Italian patient with a family history of early-onset dementia, who developed a slowly progressive cognitive decline since the age of 40 years. Clinical investigations, including neuropsychological assessment, brain MRI and 18-fluorodeoxyglucose PET, as well as cerebrospinal fluid biomarkers, supported the diagnosis of EOAD. Genetic studies identified a novel missense mutation at codon 213 (I213S). Three other mutations at the same codon have been described in association with EOAD. Previous in silico, in vitro and in vivo studies indicated that these mutations affect the functional properties of γ-secretase and are most likely pathogenic. In silico algorithms suggested that even the I213S mutation has similar deleterious effects on PSEN1 structure and function. Overall, these data strongly support a role of hotspot site for the codon 213 of PSEN1, and provide evidence that the genetic variants located on this site cause EOAD.
早发性阿尔茨海默病(EOAD)的最常见病因是早老素 1 基因(PSEN1)的突变。我们报告了一例意大利 EOAD 家族史患者的新型 PSEN1 突变(I213S),该患者自 40 岁起出现进行性认知衰退。临床研究包括神经心理学评估、脑 MRI 和 18-氟脱氧葡萄糖 PET 以及脑脊液生物标志物,支持 EOAD 的诊断。基因研究在密码子 213 处发现了一个新型错义突变(I213S)。其他三个相同密码子的突变与 EOAD 有关。先前的计算机模拟、体外和体内研究表明,这些突变影响 γ-分泌酶的功能特性,很可能是致病的。计算机算法表明,即使是 I213S 突变也对 PSEN1 结构和功能具有类似的有害影响。总的来说,这些数据强烈支持 PSEN1 密码子 213 热点的作用,并提供了证据表明该位点的遗传变异导致 EOAD。