Cullen K M, Halliday G M
Department of Pathology, University of Sydney, Australia.
Neuropathol Appl Neurobiol. 1995 Aug;21(4):312-8. doi: 10.1111/j.1365-2990.1995.tb01065.x.
Magnocellular neurons in the cholinergic nucleus basalis appear to be vulnerable in a variety of pathological conditions, including chronic alcoholism. While neurofibrillary degeneration of these neurons has been noted in a number of disorders characterized by dementia, the mechanism of cell death in thiamine-deficient chronic alcoholics has not been identified. In the present post-mortem investigation, multiple brain regions of seven thiamine-deficient chronic alcoholics, three neurologically asymptomatic chronic alcoholics and seven non-alcoholic age matched controls were screened for neurofibrillary pathology using both tau-immunohistochemistry and a modified Bielschowsky silver stain. In chronic alcoholics with thiamine deficiency, neurofibrillary pathology was found in the nucleus basalis, but not any other brain region. Neurofibrillary tangles were not seen in age-matched controls and were infrequent in alcoholics without neuropathological signs of thiamine-deficiency. Neurofibrillary tangles were most numerous in those cases with cell loss in the nucleus basalis. These findings suggest that neurodegeneration of the nucleus basalis in chronic alcoholics proceeds through the formation of neurofibrillary tangles.
胆碱能基底核中的大细胞神经元在包括慢性酒精中毒在内的多种病理状况下似乎很脆弱。虽然在一些以痴呆为特征的疾病中已注意到这些神经元的神经原纤维变性,但硫胺素缺乏的慢性酒精中毒患者的细胞死亡机制尚未明确。在本次尸检研究中,使用tau免疫组织化学和改良的 Bielschowsky 银染法,对7名硫胺素缺乏的慢性酒精中毒患者、3名无神经症状的慢性酒精中毒患者以及7名年龄匹配的非酒精中毒对照者的多个脑区进行了神经原纤维病理筛查。在硫胺素缺乏的慢性酒精中毒患者中,神经原纤维病理改变见于基底核,但在其他脑区未发现。在年龄匹配的对照者中未见神经原纤维缠结,在无硫胺素缺乏神经病理体征的酒精中毒患者中也很少见。在基底核有细胞丢失的病例中,神经原纤维缠结最为多见。这些发现表明,慢性酒精中毒患者基底核的神经退行性变是通过神经原纤维缠结的形成而发生的。