BACKGROUND Major prevention trials for Alzheimer's disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. METHODS A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. RESULTS In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. CONCLUSIONS In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression.

中文翻译：

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淀粉样蛋白和 tau 病理学与散发性和常染色体显性阿尔茨海默病临床前阶段的人格特征、神经精神症状和认知生活方式相关

背景 阿尔茨海默病 (AD) 的主要预防试验现在集中在多领域的生活方式干预上。然而，与 AD 病理学相关的行为因素的确切组合仍不清楚。在 2 个有 AD 风险的认知未受损个体队列中，我们检查了哪些人格特征、神经精神症状和认知生活方式（受教育年限或终生认知活动）与 AD、淀粉样蛋白-β 和 tau 沉积物的病理特征相关的组合. 方法 共有 115 名父母或多兄弟姐妹有散发性 AD 家族史的老年人（PREVENT-AD [AD 的实验性或新疗法的症状评估] 队列）接受了淀粉样蛋白和 tau 正电子发射断层扫描，并回答了几份相关的问卷调查。到行为属性。分别地，我们使用淀粉样蛋白正电子发射断层扫描和行为数据研究了来自 DIAN（显性遗传阿尔茨海默病网络）研究组队列的 117 名突变携带者。使用偏最小二乘法分析，我们确定了与淀粉样蛋白或 tau 病理学与人格特征、神经精神症状和认知生活方式的组合相关的潜在变量。结果 在 PREVENT-AD 中，较低的神经质、神经精神负担和较高的教育与较少的淀粉样蛋白沉积相关 (p = .014)。较低的神经质和神经精神特征，以及较高的开放性和外向性，与较少的 tau 沉积有关 (p = .006)。在 DIAN，较低的神经精神负担和较高的教育也与较少的淀粉样蛋白相关（p = .005）。这些因素的组合占 AD 病理学的 14%。结论 在散发性和常染色体显性 AD 的临床前阶段，多种行为特征与 AD 病理学相关。这些结果可能表明多领域干预可能有助于延缓 AD 发作或进展的潜在途径。