对亨廷顿病的大脑和认知储备的批判性评价。
A critical review of brain and cognitive reserve in Huntington's disease.
机构信息
School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Melbourne, Victoria 3800, Australia.
School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Melbourne, Victoria 3800, Australia; Monash Biomedical Imaging, 770 Blackburn Road, Melbourne, Victoria 3800, Australia; Australian Research Council Centre of Excellence for Integrative Brain Function, Melbourne, Victoria, Australia.
出版信息
Neurosci Biobehav Rev. 2018 May;88:155-169. doi: 10.1016/j.neubiorev.2018.03.003. Epub 2018 Mar 11.
The 'reserve' hypothesis posits that the brain undergoes structural and functional reorganisation to actively cope with brain damage or disease. Consistent with passive and active components of 'reserve', the brain moderates its biological substrates (brain reserve) and differentially changes the level of neural activity in tasks-specific networks and/or by recruiting additional non-task related brain regions (cognitive reserve) to optimise behavioural performance. How the 'reserve' hypothesis applies in neurodegenerative disorders such as Huntington's disease (HD) remains unknown. We postulate that unless the 'reserve' hypothesis is tested empirically, it is impossible to draw firm conclusions about how task-related neural activity is providing a neuroplastic change in HD and possibly other neurodegenerative disorders. We conclude that there is a pressing need to operationalise cognitive reserve, as well as incorporate different biological substrates into a model of 'reserve'. We suggest that it is important to identify and embed potential neuroprotective modulating factors of 'reserve' in randomised controlled multi-domain non-pharmaceutical interventions to potentially enhance 'reserve' and thus preserve cognitive and psychosocial functioning in HD patients.
“储备”假说认为，大脑会发生结构和功能重组，以主动应对脑损伤或疾病。与“储备”的被动和主动成分一致，大脑会调节其生物基质（大脑储备），并通过招募额外的与任务无关的大脑区域（认知储备）来优化行为表现，从而改变特定任务网络中的神经活动水平。“储备”假说在亨廷顿病（HD）等神经退行性疾病中的应用尚不清楚。我们假设，除非通过实证检验“储备”假说，否则不可能得出关于任务相关神经活动如何在 HD 及其他可能的神经退行性疾病中提供神经可塑性变化的确切结论。我们得出的结论是，迫切需要将认知储备付诸实践，并将不同的生物基质纳入“储备”模型。我们认为，确定并嵌入“储备”的潜在神经保护调节因素非常重要，以便在随机对照多领域非药物干预中增强“储备”，从而保护 HD 患者的认知和社会心理功能。
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