Kril J J
Department of Anatomical Pathology, Royal Prince Alfred Hospital, Camperdown, Australia.
Metab Brain Dis. 1995 Mar;10(1):9-16. doi: 10.1007/BF01991778.
The relative roles of alcohol toxicity, thiamine deficiency and cirrhosis of the liver in the pathogenesis of alcohol-related brain damage are unclear. Brain shrinkage and neuronal loss from four regions of the cortex was determined in 22 alcoholics with the Wernicke-Korsakoff Syndrome (WKS), cirrhosis of the liver or neither of these complications and compared to 22 age-matched non-alcoholic controls. Brain shrinkage was most marked in those alcoholics with WKS. Neuronal loss occurred only from the superior cortex and was of equal magnitude in all alcoholic subgroups. In an animal model of alcohol abuse and thiamine deficiency, neuronal loss from the cerebral cortex occurred in a time-dependent manner. Furthermore, those cells which contained the calcium-binding protein parvalbumin appeared to be preferentially damaged in this model.
酒精毒性、硫胺素缺乏和肝硬化在酒精相关脑损伤发病机制中的相对作用尚不清楚。对22名患有韦尼克-科萨科夫综合征（WKS）、肝硬化或无这些并发症的酗酒者，测定了其大脑皮质四个区域的脑萎缩和神经元丢失情况，并与22名年龄匹配的非酗酒对照者进行比较。脑萎缩在患有WKS的酗酒者中最为明显。神经元丢失仅发生在大脑皮质上层，且在所有酗酒亚组中程度相同。在酒精滥用和硫胺素缺乏的动物模型中，大脑皮质的神经元丢失呈时间依赖性。此外，在该模型中，含有钙结合蛋白小白蛋白的细胞似乎更容易受损。
