Cerebral pericytes are an integral component of the neurovascular unit, which governs the blood–brain barrier. There is paucity of knowledge on cortical pericytes across different dementias. We quantified cortical pericytes in capillaries in 124 post-mortem brains from subjects with post-stroke dementia (PSD), vascular dementia (VaD), Alzheimer’s disease (AD) and AD-VaD (Mixed) and, post-stroke non-demented (PSND) stroke survivors as well as normal ageing controls. Collagen 4 (COL4)-positive nucleated pericyte soma were identified as protrusions on capillaries of the frontal cortex. The COL4-positive somata or nodule-like cell bodies were also verified by platelet derived growth factor receptor-β (PDGFR-β) immunohistochemistry. The mean (± SEM) pericyte somata in frontal cortical capillaries in normal young controls (46–65 years of age) was estimated as 5.2 ± 0.2 per mm capillary length. This number was reduced by 45% in older controls (> 78 years) to 2.9 ± 0.1 per mm capillary length (P < 0.001). We further found that the numbers of pericyte cell bodies per COL4 mm2 area or per mm capillary length were not decreased but rather preserved or increased in PSD, AD and Mixed dementia groups compared to similar age older controls (P < 0.01). Consistent with this, we noted that capillary length densities identified by the endothelial marker glucose transporter 1 or COL4 were not different across the dementias compared to older controls. There was a negative correlation with age (P < 0.001) suggesting fewer pericyte somata in older age, although the % COL4 immunoreactive capillary area was increased in older controls compared to young controls. Using a proven reliable method to quantify COL4-positive nucleated pericytes, our observations demonstrate ageing related loss but mostly preserved pericytes in the frontal cortex of vascular and AD dementias. We suggest there is differential regulation of capillary pericytes in the frontal lobe between the cortex and white matter in ageing-related dementias.

中文翻译：

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中风后痴呆、血管性痴呆和阿尔茨海默病中额叶皮质毛细血管周细胞随年龄增长而丧失但保留

脑周细胞是控制血脑屏障的神经血管单元的一个组成部分。关于不同痴呆症的皮质周细胞的知识很少。我们量化了来自卒中后痴呆 (PSD)、血管性痴呆 (VaD)、阿尔茨海默病 (AD) 和 AD-VaD (混合) 以及卒中后非痴呆受试者的 124 个死后大脑中毛细血管的皮层周细胞。 PSND) 中风幸存者以及正常的老化对照。胶原 4 (COL4) 阳性有核周细胞体被确定为额叶皮层毛细血管上的突起。COL4 阳性胞体或结节样细胞体也通过血小板衍生生长因子受体-β (PDGFR-β) 免疫组织化学验证。在正常年轻对照（46-65 岁）中，额叶皮层毛细血管中的平均 (± SEM) 周细胞体估计为每毫米毛细血管长度 5.2 ± 0.2。在老年对照（> 78 岁）中，这一数字减少了 45%，至每毫米毛细管长度 2.9 ± 0.1（P < 0.001）。我们进一步发现，与年龄相似的老年对照组相比，PSD、AD 和混合性痴呆组中每 COL4 mm2 面积或每 mm 毛细血管长度的周细胞体数量并未减少，而是保持或增加（P < 0.01）。与此一致，我们注意到内皮标记葡萄糖转运蛋白 1 或 COL4 确定的毛细血管长度密度与老年对照组相比在痴呆症中没有差异。与年龄呈负相关（P < 0.001），表明年龄较大的周细胞体细胞较少，尽管与年轻对照相比，年长对照的 COL4 免疫反应性毛细血管面积增加。使用一种经过验证的可靠方法来量化 COL4 阳性有核周细胞，我们的观察结果表明与衰老相关的损失，但主要保留了血管和 AD 痴呆额叶皮层中的周细胞。我们认为在衰老相关性痴呆中，皮质和白质之间的额叶毛细血管周细胞存在差异调节。