阿茲海默症與創傷性腦損傷關係的研究進展

Research Progress on the Relationship between Alzheimer's Disease and Traumatic Brain Injury

10.6202/THJ.202212_(18).0001

車土玲(Che Tu-ling)；蘇裕盛(Su Yu-sheng)

阿茲海默症 ； 創傷性腦損傷 ； Aβ ； Tau蛋白 ； Alzheimer's disease ； Traumatic brain injury ； Aβ ； Tau

慈惠學報

18期（2022 / 12 / 01）

1 - 16

繁體中文;英文

阿茲海默症（Alzheimer's disease, AD）是一種神經退行性疾病，主要表現為認知障礙，且是一種不可逆轉的疾病。儘管近年來對AD發病機制的研究取得許多成就，但始終沒有研發出能根治AD的藥物。有研究發現創傷性腦損傷（Traumatic brain injury ,TBI）是罹患AD的一個風險因素。經歷TBI後會對大腦海馬區產生不利影響，而大腦海馬區又是人類長期學習與記憶的重要區域。大腦海馬區對AD的發病有至關重要的作用，海馬體中斑塊和纏結的存在與認知能力下降密切相關，這將會導致AD的發生。從預防的角度來看，減少或阻止TBI的發生，就有可能降低AD的患病風險。有研究通過對AD發病炎症因子β-澱粉樣蛋白（Amyloid β-protein，Aβ）、Tau蛋白的兩種假說與TBI後產生的Aβ、Tau蛋白沉積之間的關係，來證實AD與TBI之間的聯繫。AD的發病與Aβ的神經毒性以及與Tau異常纏結沉積有關。研究發現TBI後也會產生Aβ、Tau兩種蛋白並且與AD中的兩種蛋白有相似之處，從而懷疑TBI與AD之間存在著某種聯繫。TBI後產生Aβ、Tau蛋白會加重其病理進程，大腦中的Aβ、Tau蛋白之間相互作用，沉積過多後將進一步引發AD等疾病。TBI和AD之間有一個共同的神經解剖模式，通過減少或阻止TBI的發生，將會減少Aβ、Tau蛋白的產生與積累。此時，也將會降低Aβ、Tau蛋白對人類大腦的影響，可在一定程度預防AD的發生。

Alzheimer's disease (AD) is a Neurodegeneration disorder characterized by cognitive impairment that is irreversible. Although many achievements have been made in the study of the pathogenesis of AD in recent years, no drug has been developed to cure AD. Traumatic brain injury (TBI) has been found to be a risk factor for AD. After TBI, the brain will have adverse effects on the hippocampus, which is an important area of long-term learning and memory. The hippocampus plays an important role in the pathogenesis of AD. The existence of plaques and tangles in the hippocampus is closely related to the decline of cognitive ability, which will lead to the occurrence of AD. From the perspective of prevention, reducing or preventing the occurrence of TBI may reduce the risk of AD. In order to confirm the relationship between AD and TBI, two hypotheses of the pathogenesis of AD, Amyloid β-protein (Aβ) and Tau, and the deposition of Aβ and Tau after TBI were studied. The pathogenesis of AD is related to the neurotoxicity of Aβ and the abnormal tangles of Tau. It was found that TBI also produced Aβ and Tau proteins, which were similar to those in AD, suggesting a possible link between TBI and AD. After TBI, the production of Aβ and Tau protein will aggravate the pathological process, and the interaction between Aβ and Tau protein in the brain will further lead to AD and other diseases after excessive deposition. There is a common neuroanatomical pattern between TBI and AD. By reducing or preventing the occurrence of TBI, the production and accumulation of Aβ and Tau proteins will be reduced. At this time, it will also reduce the impact of Aβ and Tau protein on the human brain, which can prevent the occurrence of AD to a certain extent.

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