From the Helen Wills Neuroscience Institute (S.V., M.W., C.M.M., N.A., W.J.J.), University of California, Berkeley; Department of Neurology (B.R.R., D.M., C.D.), University of California, Davis; School of Education and Social Policy (C.M.H.), Northwestern University; Departments of Preventive Medicine (W.M.) and Neurology (H.C.C.), University of Southern California; Center for Imaging of Neurodegenerative Diseases (M.W.W.), University of California, San Francisco.
Neurology. 2014 Mar 4;82(9):761-7. doi: 10.1212/WNL.0000000000000170. Epub 2014 Jan 31.
To investigate the associations among β-amyloid (Aβ), cortical thickness, and episodic memory in a cohort of cognitively normal to mildly impaired individuals at increased risk of vascular disease.
In 67 subjects specifically recruited to span a continuum of cognitive function and vascular risk, we measured brain Aβ deposition using [(11)C] Pittsburgh compound B-PET imaging and cortical thickness using MRI. Episodic memory was tested using a standardized composite score of verbal memory, and vascular risk was quantified using the Framingham Coronary Risk Profile index.
Increased Aβ was associated with cortical thinning, notably in frontoparietal regions. This relationship was strongest in persons with high Aβ deposition. Increased Aβ was also associated with lower episodic memory performance. Cortical thickness was found to mediate the relationship between Aβ and memory performance. While age had a marginal effect on these associations, the relationship between Aβ and cortical thickness was eliminated after controlling for vascular risk except when examined in only Pittsburgh compound B-positive subjects, in whom Aβ remained associated with thinner cortex in precuneus and occipital lobe. In addition, only the precuneus was found to mediate the relationship between Aβ and memory after controlling for vascular risk.
These results suggest strong links among Aβ, cortical thickness, and memory. They highlight that, in individuals without dementia, vascular risk also contributes to cortical thickness and influences the relationships among Aβ, cortical thickness, and memory.
在认知正常至轻度受损、血管疾病风险增加的队列中，研究β-淀粉样蛋白（Aβ）、皮质厚度和情景记忆之间的关系。
在专门招募的 67 名受试者中，我们使用 [(11)C]匹兹堡化合物 B-PET 成像测量脑内 Aβ沉积，使用 MRI 测量皮质厚度。情景记忆通过使用言语记忆的标准化综合评分进行测试，血管风险通过弗雷明汉冠心病风险评分指数进行量化。
Aβ 增加与皮质变薄有关，特别是在前顶叶区域。这种关系在 Aβ 沉积高的人群中最强。Aβ 增加还与情景记忆表现降低有关。皮质厚度被发现介导了 Aβ 与记忆表现之间的关系。虽然年龄对这些关联有一定影响，但在控制血管风险后，Aβ 与皮质厚度之间的关系被消除，除非仅在匹兹堡化合物 B 阳性受试者中进行检查，在这些受试者中，Aβ 仍然与扣带回和枕叶皮质变薄有关。此外，仅在扣带后发现 Aβ 与记忆之间的关系在控制血管风险后具有介导作用。
这些结果表明 Aβ、皮质厚度和记忆之间存在紧密联系。它们强调，在没有痴呆的个体中，血管风险也会影响皮质厚度，并影响 Aβ、皮质厚度和记忆之间的关系。
