Institute of Pathology, Department of Neuropathology, University of Wuerzburg, 97080 Wuerzburg, Germany.
Department of Medical Physiology, University of Nairobi, P.O. Box 30197, Nairobi 00100, Kenya.
Cells. 2024 Sep 10;13(18):1511. doi: 10.3390/cells13181511.
Postencephalitic parkinsonism (PEP) is suggested to show a virus-induced pathology, which is different from classical idiopathic Parkinson's disease (PD) as there is no α-synuclein/Lewy body pathology. However, PEP shows a typical clinical representation of motor disturbances. In addition, compared to PD, there is no iron-induced pathology. The aim of this preliminary study was to compare PEP with PD regarding iron-induced pathology, using histochemistry methods on paraffin-embedded post-mortem brain tissue. In the PEP group, iron was not seen, except for one case with sparse perivascular depositions. Rather, PEP offers a pathology related to tau-protein/neurofibrillary tangles, with mild to moderate memory deficits only. It is assumed that this virus-induced pathology is due to immunological dysfunctions causing (neuro)inflammation-induced neuronal network disturbances as events that trigger clinical parkinsonism. The absence of iron deposits implies that PEP cannot be treated with iron chelators. The therapy with L-Dopa is also not an option, as L-Dopa only leads to an initial slight improvement in symptoms in isolated cases.
脑炎后帕金森病(PEP)被认为表现出病毒诱导的病理学,与经典的特发性帕金森病(PD)不同,因为没有α-突触核蛋白/路易体病理学。然而,PEP 表现出典型的运动障碍临床表现。此外,与 PD 相比,没有铁诱导的病理学。本初步研究的目的是使用石蜡包埋的死后脑组织的组织化学方法,比较 PEP 与 PD 之间的铁诱导病理学。在 PEP 组中,除了一例稀疏的血管周围沉积外,没有发现铁。相反,PEP 提供了与 tau 蛋白/神经原纤维缠结相关的病理学,仅有轻度至中度的记忆缺陷。据推测,这种病毒诱导的病理学是由于免疫功能障碍导致(神经)炎症引起的神经元网络紊乱,这些事件引发了临床帕金森病。没有铁沉积物意味着 PEP 不能用铁螯合剂治疗。L-Dopa 的治疗也不是一个选择,因为 L-Dopa 仅在少数情况下导致症状的初始轻微改善。