Department of Psychiatry, Washington University in St. Louis, St. Louis, MO, USA.
Department of Neurology, Washington University in St. Louis, St. Louis, MO, USA.
Neuropsychopharmacology. 2024 Nov;50(1):124-136. doi: 10.1038/s41386-024-01947-7. Epub 2024 Aug 5.
Neuroplasticity during sensitive periods, the molecular and cellular process of enduring neural change in response to external stimuli during windows of high environmental sensitivity, is crucial for adaptation to expected environments and has implications for psychiatry. Animal research has characterized the developmental sequence and neurobiological mechanisms that govern neuroplasticity, yet gaps in our ability to measure neuroplasticity in humans limit the clinical translation of these principles. Here, we present a roadmap for the development and validation of neuroimaging and electrophysiology measures that index neuroplasticity to begin to address these gaps. We argue that validation of measures to track neuroplasticity in humans will elucidate the etiology of mental illness and inform the type and timing of mental health interventions to optimize effectiveness. We outline criteria for evaluating putative neuroimaging measures of plasticity in humans including links to neurobiological mechanisms shown to govern plasticity in animal models, developmental change that reflects heightened early life plasticity, and prediction of neural and/or behavior change. These criteria are applied to three putative measures of neuroplasticity using electroencephalography (gamma oscillations, aperiodic exponent of power/frequency) or functional magnetic resonance imaging (amplitude of low frequency fluctuations). We discuss the use of these markers in psychiatry, envision future uses for clinical and developmental translation, and suggest steps to address the limitations of the current putative neuroimaging measures of plasticity. With additional work, we expect these markers will significantly impact mental health and be used to characterize mechanisms, devise new interventions, and optimize developmental trajectories to reduce psychopathology risk.
神经可塑性在敏感时期,即对外界刺激在高环境敏感性窗口内做出持久神经变化的分子和细胞过程,对于适应预期环境至关重要,并且对精神病学具有重要意义。动物研究已经描述了控制神经可塑性的发育顺序和神经生物学机制,但我们在人类中测量神经可塑性的能力存在差距,限制了这些原则的临床转化。在这里,我们提出了一个开发和验证神经影像学和电生理学测量指标的路线图,以开始解决这些差距。我们认为,验证用于追踪人类神经可塑性的测量方法将阐明精神疾病的病因,并为优化心理健康干预的类型和时间提供信息,以提高其有效性。我们概述了评估人类可塑性的潜在神经影像学测量方法的标准,包括与已证明可控制动物模型可塑性的神经生物学机制的联系、反映早期生活中可塑性增强的发育变化,以及对神经和/或行为变化的预测。这些标准适用于使用脑电图(伽马振荡、功率/频率的无周期指数)或功能磁共振成像(低频波动幅度)的三种潜在的神经可塑性测量方法。我们讨论了这些标记物在精神病学中的应用,设想了它们在临床和发育转化中的未来用途,并提出了一些步骤来解决当前潜在的神经影像学可塑性测量方法的局限性。随着进一步的研究,我们预计这些标记物将对心理健康产生重大影响,并用于描述机制、设计新的干预措施和优化发育轨迹以降低精神病理学风险。