Microstructural abnormality in white matter, regulatory T lymphocytes, and depressive symptoms after stroke.

Microstructural abnormality in white matter, regulatory T lymphocytes, and depressive symptoms after stroke.
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白质微观结构异常、调节性 T 淋巴细胞和中风后抑郁症状。

DOI:
10.1002/gps.4235
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发表时间:
2014
期刊:
影响因子:
2
通讯作者:
Nagatsuka K.
Nagatsuka K.
中科院分区:
医学4区
文献类型:
--
作者:
Yasuno F;Taguchi A;Yamamoto A;Kajimoto K;Kazui H;Kudo T;Kikuchi-Taura A;Sekiyama A;Kishimoto T;Iida H;Nagatsuka K.

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ObjectiveSeveral epidemiological studies have found a lower incidence of Alzheimer's disease in highly educated populations, but the protective mechanism of education against the disease is still unclear. Our objective was to investigate the association between education and11C‐labeled Pittsburgh Compound B (PIB) uptake with positron emission tomography in participants with normal cognitive ability.MethodsWe performed11C‐labeled PIB positron emission tomography and neuropsychological testing in 30 cognitively normal older participants. Of the participants, 16 had a period of education less than 12 years (low‐education group) and 14 had more than 13 years (high‐education group). Amyloid‐β deposition was quantified by binding potential (BPND) in several brain regions and was compared between the groups with different education levels.ResultsWe found significantly higher cortical PIB‐BPNDin the cognitively normal participants with low education compared with the ones with high education. None of the brain regions in low‐education group showed significantly lower BPNDvalues. This finding was not affected by the inclusion of possible confounding variables such as age, sex, and general intelligence. Our findings indicated a reduced amyloid pathology in highly educated, cognitively normal, participants.ConclusionsOur findings lead to the proposal that early‐life education has a negative association with Alzheimer's disease pathology. This proposal is not in opposition to the brain reserve hypothesis. People with more education might be prone to a greater inhibitory effect against amyloid‐β deposition before the preclinical stage. At the same time, they have a greater reserve capacity, and greater pathological changes are required for dementia to manifest. Copyright © 2014 John Wiley & Sons, Ltd.