The phenomenon of clasmatodendrosis.

The phenomenon of clasmatodendrosis.
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DOI:
10.1016/j.heliyon.2021.e07605
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发表时间:
2021-07
期刊:
影响因子:
4
通讯作者:
Torre M
Torre M
中科院分区:
综合性期刊4区
文献类型:
--
作者:
Balaban D;Miyawaki EK;Bhattacharyya S;Torre M

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Clasmatodendrosis源自希腊语的片段(klasma),树(dendron)和条件(- osis)。Cajal在1913年首次使用该术语:他观察到星形胶质细胞远端细胞突起的解体,沿着靠近星形胶质细胞细胞体的近端突起的碎片或串珠。在当代临床和实验报道中,在脑缺血和癫痫发作(包括癫痫持续状态)模型、老年脑、白色物质疾病、与淀粉样斑块相关的海马模型和细胞培养物、头部创伤、毒性暴露、脱髓鞘疾病、脑炎和感染相关性脑病以及使用免疫效应细胞治疗癌症中观察到了枝梗病。我们研究证据来支持一个说法,即clasmatodendrotic星形胶质细胞过程明显珠(截断)作为一个形态学标志正在进行的损害死前。在灰色和白色物质中,通常与血管腔相关,当在适当的高倍镜下检查标本时,通过胶质细胞酸性蛋白的免疫组化染色,串珠变得明显,但远端星形胶质细胞突起丢失的证明可能需要额外的标记物研究和成像。提出的clammatodendritic变化的机制已经检查了缺氧缺血,脱髓鞘和自噬模型。在这些模型中,以及在神经病理学报告,实质肿胀,血管壁渗漏,或干扰清除毒素可以发生与clasmatodendrosis。Clasmatodendric功能可以作为急性或慢性神经胶质血管失调的标志。我们回顾了与星形胶质细胞结构变化相关的血脑屏障(BBB)功能障碍的相关证据,并关注内皮细胞、周细胞和星形胶质细胞终足之间的相互作用。树突状细胞,星形胶质细胞,尾足,血脑屏障,内皮细胞,周细胞
Clasmatodendrosis derives from the Greek for fragment (klasma), tree (dendron), and condition (- osis). Cajal first used the term in 1913: he observed disintegration of the distal cell processes of astrocytes, along with a fragmentation or beading of proximal processes closer to the astrocyte cell body. In contemporary clinical and experimental reports, clasmatodendrosis has been observed in models of cerebral ischemia and seizures (including status epilepticus), in elderly brains, in white matter disease, in hippocampal models and cell cultures associated with amyloid plaques, in head trauma, toxic exposures, demyelinating diseases, encephalitides and infection-associated encephalopathies, and in the treatment of cancer using immune effector cells. We examine evidence to support a claim that clasmatodendrotic astrocyte cell processes overtly bead (truncate) as a morphological sign of ongoing damage premortem. In grey and white matter and often in relationship to vascular lumina, beading becomes apparent with immunohistochemical staining of glial fibrillary acidic protein when specimens are examined at reasonably high magnification, but demonstration of distal astrocytic loss of processes may require additional marker study and imaging. Proposed mechanisms for clasmatodendrotic change have examined hypoxic-ischemic, osmotic-demyelinating, and autophagic models. In these models as well as in neuropathological reports, parenchymal swelling, vessel-wall leakage, or disturbed clearance of toxins can occur in association with clasmatodendrosis. Clasmatodendrotic features may serve as a marker for gliovascular dysregulation either acutely or chronically. We review correlative evidence for blood-brain barrier (BBB) dysfunction associated with astrocytic structural change, with attention to interactions between endothelial cells, pericytes, and astrocytic endfeet. Clasmatodendrosis, Astrocyte, Endfoot, Blood-brain barrier, Endothelial cell, Pericyte
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