Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Magdeburg, Germany.
Neuropathol Appl Neurobiol. 2020 Apr;46(3):219-239. doi: 10.1111/nan.12576. Epub 2019 Sep 11.
Deep perforator arteriopathy (DPA) and cerebral amyloid angiopathy (CAA) are the commonest known cerebral small vessel diseases (CSVD), which cause ischaemic stroke, intracebral haemorrhage (ICH) and vascular cognitive impairment (VCI). While thus far mainly considered as separate entities, we here propose that DPA and CAA share similarities, overlap and interact, so that 'pure' DPA or CAA are extremes along a continuum of age-related small vessel pathologies. We suggest blood-brain barrier (BBB) breakdown, endothelial damage and impaired perivascular β-amyloid (Aβ) drainage are hallmark common mechanisms connecting DPA and CAA. We also suggest a need for new biomarkers (e.g. high-resolution imaging) to deepen understanding of the complex relationships between DPA and CAA.
深穿支动脉病 (DPA) 和脑淀粉样血管病 (CAA) 是最常见的已知脑小血管疾病 (CSVD)，可引起缺血性脑卒中、脑实质内出血 (ICH) 和血管性认知障碍 (VCI)。虽然迄今为止主要被认为是两种独立的疾病实体，但我们在此提出 DPA 和 CAA 具有相似性、重叠和相互作用，因此“纯”DPA 或 CAA 是沿着与年龄相关的小血管病变连续体的两个极端。我们认为血脑屏障 (BBB) 破坏、内皮损伤和受损的血管周β-淀粉样蛋白 (Aβ) 引流是连接 DPA 和 CAA 的共同标志性机制。我们还建议需要新的生物标志物（例如高分辨率成像）来加深对 DPA 和 CAA 之间复杂关系的理解。
