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HIV相关痴呆是AIDS指征性疾病之一,表现为运动和认知功能障碍。尸检发现皮质萎缩和广泛的神经元细胞丢失,其发病机制还不十分清楚。目前发现HIV蛋白Tat和gp120具有直接和间接的神经毒性。谷氨酸、NO、钙、氧化应激、凋亡和小胶质细胞都参与了HIV相关神经变性的致病过程。本文综述了HIV相关神经毒性致病理论的最新进展,展示了阻止神经丢失和运动/认知功能衰退的潜在治疗干预途径。
HIV-related dementia is one of the AIDS-degenerative diseases, manifested as motor and cognitive dysfunction. Autopsy revealed cortical atrophy and extensive neuronal cell loss, the pathogenesis is not yet clear. It has been found that HIV proteins Tat and gp120 have both direct and indirect neurotoxicity. Glutamate, NO, calcium, oxidative stress, apoptosis and microglia are all involved in the pathogenesis of HIV-associated neurodegeneration. This review summarizes recent advances in the pathogenesis of HIV-related neurotoxicity and demonstrates potential therapeutic interventions to prevent neurological loss and motor / cognitive decline.