Marc Dörner, Anthony Tyndall, Nicolin Hainc, Roland von Känel, Katja Neumann, Sebastian Euler, Frank Schreiber, Philipp Arndt, Erelle Fuchs, Cornelia Garz, Wenzel Glanz, Michaela Butryn, Jan Ben Schulze, Sarah Lavinia Florence Schiebler, Anna-Charlotte John, Annkatrin Hildebrand, Andreas B Hofmann, Lena Machetanz, Johannes Kirchebner, Pawel Tacik, Alexander Grimm, Robin Jansen, Marc Pawlitzki, Solveig Henneicke, Jose Bernal, Valentina Perosa, Emrah Düzel, Sven G Meuth, Stefan Vielhaber, Hendrik Mattern, Stefanie Schreiber
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Since NPS are associated with functional impairment, faster cognitive decline and faster progression to death, replication studies in more diverse settings and samples are warranted.</p><p><strong>Methods: </strong>We prospectively recruited n = 69 CAA patients and n = 18 cognitively normal controls (NC). The number and severity of NPS were assessed using the Alzheimer's Disease (AD) Assessment Scale's (ADAS) noncognitive subscale. We applied different regression models exploring associations between NPS number or severity and group status (CAA vs. NC), CAA severity assessed with magnetic resonance imaging (MRI) or cognitive function (Mini-Mental State Examination (MMSE), ADAS cognitive subscale), adjusting for age, sex, years of education, arterial hypertension, AD pathology, and apolipoprotein E status. Mediation analyses were performed to test indirect effects of lifelong mental activities on CAA severity and NPS.</p><p><strong>Results: </strong>Patients with CAA had 4.86 times (95% CI 2.20-10.73) more NPS and 3.56 units (95% CI 1.94-5.19) higher expected NPS severity than NC. Higher total CAA severity on MRI predicted 1.14 times (95% CI 1.01.-1.27) more NPS and 0.57 units (95% CI 0.19-0.95) higher expected NPS severity. More severe white matter hyperintensities were associated with 1.21 times more NPS (95% CI 1.05-1.39) and 0.63 units (95% CI 0.19-1.08) more severe NPS. NPS number (MMSE mean difference - 1.15, 95% CI -1.67 to -0.63; ADAS cognitive mean difference 1.91, 95% CI 1.26-2.56) and severity (MMSE - 0.55, 95% CI -0.80 to -0.30; ADAS cognitive mean difference 0.89, 95% CI 0.57-1.21) predicted lower cognitive function. Greater lifelong mental activities partially mediated the relationship between CAA severity and NPS (indirect effect 0.05, 95% CI 0.0007-0.13), and greater lifelong mental activities led to less pronounced CAA severity and thus to less NPS (indirect effect - 0.08, 95% CI -0.22 to -0.002).</p><p><strong>Discussion: </strong>This study suggests that NPS are common in CAA, and that this relationship may be driven by CAA severity. Furthermore, NPS seem to be tied to lower cognitive function. However, lifelong mental activities might mitigate the impact of NPS in CAA.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":null,"pages":null},"PeriodicalIF":7.9000,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11375846/pdf/","citationCount":"0","resultStr":"{\"title\":\"Neuropsychiatric symptoms and lifelong mental activities in cerebral amyloid angiopathy - a cross-sectional study.\",\"authors\":\"Marc Dörner, Anthony Tyndall, Nicolin Hainc, Roland von Känel, Katja Neumann, Sebastian Euler, Frank Schreiber, Philipp Arndt, Erelle Fuchs, Cornelia Garz, Wenzel Glanz, Michaela Butryn, Jan Ben Schulze, Sarah Lavinia Florence Schiebler, Anna-Charlotte John, Annkatrin Hildebrand, Andreas B Hofmann, Lena Machetanz, Johannes Kirchebner, Pawel Tacik, Alexander Grimm, Robin Jansen, Marc Pawlitzki, Solveig Henneicke, Jose Bernal, Valentina Perosa, Emrah Düzel, Sven G Meuth, Stefan Vielhaber, Hendrik Mattern, Stefanie Schreiber\",\"doi\":\"10.1186/s13195-024-01519-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>While several studies in cerebral amyloid angiopathy (CAA) focus on cognitive function, data on neuropsychiatric symptoms (NPS) and lifelong mental activities in these patients are scarce. Since NPS are associated with functional impairment, faster cognitive decline and faster progression to death, replication studies in more diverse settings and samples are warranted.</p><p><strong>Methods: </strong>We prospectively recruited n = 69 CAA patients and n = 18 cognitively normal controls (NC). The number and severity of NPS were assessed using the Alzheimer's Disease (AD) Assessment Scale's (ADAS) noncognitive subscale. We applied different regression models exploring associations between NPS number or severity and group status (CAA vs. NC), CAA severity assessed with magnetic resonance imaging (MRI) or cognitive function (Mini-Mental State Examination (MMSE), ADAS cognitive subscale), adjusting for age, sex, years of education, arterial hypertension, AD pathology, and apolipoprotein E status. Mediation analyses were performed to test indirect effects of lifelong mental activities on CAA severity and NPS.</p><p><strong>Results: </strong>Patients with CAA had 4.86 times (95% CI 2.20-10.73) more NPS and 3.56 units (95% CI 1.94-5.19) higher expected NPS severity than NC. Higher total CAA severity on MRI predicted 1.14 times (95% CI 1.01.-1.27) more NPS and 0.57 units (95% CI 0.19-0.95) higher expected NPS severity. More severe white matter hyperintensities were associated with 1.21 times more NPS (95% CI 1.05-1.39) and 0.63 units (95% CI 0.19-1.08) more severe NPS. NPS number (MMSE mean difference - 1.15, 95% CI -1.67 to -0.63; ADAS cognitive mean difference 1.91, 95% CI 1.26-2.56) and severity (MMSE - 0.55, 95% CI -0.80 to -0.30; ADAS cognitive mean difference 0.89, 95% CI 0.57-1.21) predicted lower cognitive function. Greater lifelong mental activities partially mediated the relationship between CAA severity and NPS (indirect effect 0.05, 95% CI 0.0007-0.13), and greater lifelong mental activities led to less pronounced CAA severity and thus to less NPS (indirect effect - 0.08, 95% CI -0.22 to -0.002).</p><p><strong>Discussion: </strong>This study suggests that NPS are common in CAA, and that this relationship may be driven by CAA severity. Furthermore, NPS seem to be tied to lower cognitive function. 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引用次数: 0
摘要
背景：尽管对脑淀粉样血管病（CAA）的一些研究侧重于认知功能，但有关这些患者的神经精神症状（NPS）和终生精神活动的数据却很少。由于神经精神症状与功能障碍、认知功能衰退加快和死亡进展加快有关，因此有必要在更多样化的环境和样本中进行重复研究：我们前瞻性地招募了 n = 69 名 CAA 患者和 n = 18 名认知功能正常的对照组（NC）。使用阿尔茨海默病（AD）评估量表（ADAS）的非认知子量表评估非认知功能障碍的数量和严重程度。我们采用了不同的回归模型来探索 NPS 数量或严重程度与群体状况（CAA 与 NC）、磁共振成像（MRI）评估的 CAA 严重程度或认知功能（迷你精神状态检查（MMSE）、ADAS 认知分量表）之间的关联，并对年龄、性别、受教育年限、动脉高血压、AD 病理和载脂蛋白 E 状态进行了调整。进行了中介分析，以检验终生心理活动对CAA严重程度和NPS的间接影响：与 NC 相比，CAA 患者的 NPS 增加了 4.86 倍（95% CI 2.20-10.73），预期 NPS 严重程度增加了 3.56 个单位（95% CI 1.94-5.19）。MRI 上总 CAA 严重程度越高，NPS 预测值越高 1.14 倍（95% CI 1.01.-1.27），预期 NPS 严重程度越高 0.57 个单位（95% CI 0.19-0.95）。更严重的白质高密度与 1.21 倍的 NPS（95% CI 1.05-1.39）和 0.63 个单位（95% CI 0.19-1.08）的更严重 NPS 相关。NPS数量（MMSE平均差异-1.15，95% CI-1.67至-0.63；ADAS认知平均差异1.91，95% CI 1.26至2.56）和严重程度（MMSE-0.55，95% CI-0.80至-0.30；ADAS认知平均差异0.89，95% CI 0.57至1.21）预示着认知功能较低。更多的终生心理活动部分调解了CAA严重程度与NPS之间的关系（间接效应为0.05，95% CI为0.0007-0.13），更多的终生心理活动导致CAA严重程度不那么明显，从而导致NPS较低（间接效应为-0.08，95% CI为-0.22至-0.002）：本研究表明，NPS 在 CAA 中很常见，而这种关系可能是由 CAA 的严重程度所决定的。此外，NPS 似乎与认知功能低下有关。然而，终生的心理活动可能会减轻 NPS 对 CAA 的影响。
Neuropsychiatric symptoms and lifelong mental activities in cerebral amyloid angiopathy - a cross-sectional study.
Background: While several studies in cerebral amyloid angiopathy (CAA) focus on cognitive function, data on neuropsychiatric symptoms (NPS) and lifelong mental activities in these patients are scarce. Since NPS are associated with functional impairment, faster cognitive decline and faster progression to death, replication studies in more diverse settings and samples are warranted.
Methods: We prospectively recruited n = 69 CAA patients and n = 18 cognitively normal controls (NC). The number and severity of NPS were assessed using the Alzheimer's Disease (AD) Assessment Scale's (ADAS) noncognitive subscale. We applied different regression models exploring associations between NPS number or severity and group status (CAA vs. NC), CAA severity assessed with magnetic resonance imaging (MRI) or cognitive function (Mini-Mental State Examination (MMSE), ADAS cognitive subscale), adjusting for age, sex, years of education, arterial hypertension, AD pathology, and apolipoprotein E status. Mediation analyses were performed to test indirect effects of lifelong mental activities on CAA severity and NPS.
Results: Patients with CAA had 4.86 times (95% CI 2.20-10.73) more NPS and 3.56 units (95% CI 1.94-5.19) higher expected NPS severity than NC. Higher total CAA severity on MRI predicted 1.14 times (95% CI 1.01.-1.27) more NPS and 0.57 units (95% CI 0.19-0.95) higher expected NPS severity. More severe white matter hyperintensities were associated with 1.21 times more NPS (95% CI 1.05-1.39) and 0.63 units (95% CI 0.19-1.08) more severe NPS. NPS number (MMSE mean difference - 1.15, 95% CI -1.67 to -0.63; ADAS cognitive mean difference 1.91, 95% CI 1.26-2.56) and severity (MMSE - 0.55, 95% CI -0.80 to -0.30; ADAS cognitive mean difference 0.89, 95% CI 0.57-1.21) predicted lower cognitive function. Greater lifelong mental activities partially mediated the relationship between CAA severity and NPS (indirect effect 0.05, 95% CI 0.0007-0.13), and greater lifelong mental activities led to less pronounced CAA severity and thus to less NPS (indirect effect - 0.08, 95% CI -0.22 to -0.002).
Discussion: This study suggests that NPS are common in CAA, and that this relationship may be driven by CAA severity. Furthermore, NPS seem to be tied to lower cognitive function. However, lifelong mental activities might mitigate the impact of NPS in CAA.
期刊介绍：
Alzheimer's Research & Therapy is an international peer-reviewed journal that focuses on translational research into Alzheimer's disease and other neurodegenerative diseases. It publishes open-access basic research, clinical trials, drug discovery and development studies, and epidemiologic studies. The journal also includes reviews, viewpoints, commentaries, debates, and reports. All articles published in Alzheimer's Research & Therapy are included in several reputable databases such as CAS, Current contents, DOAJ, Embase, Journal Citation Reports/Science Edition, MEDLINE, PubMed, PubMed Central, Science Citation Index Expanded (Web of Science) and Scopus.
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