Cantone Mariagiovanna, Bramanti Alessia, Lanza Giuseppe, Pennisi Manuela, Bramanti Placido, Pennisi Giovanni, Bella Rita
1 Department of Neurology IC, IRCCS " Oasi" Institute for Research on Mental Retardation and Brain Aging, Troina, Italy.
2 IRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy.
ASN Neuro. 2017 May-Jun;9(3):1759091417711512. doi: 10.1177/1759091417711512.
Neural plasticity is considered the neurophysiological correlate of learning and memory, although several studies have also noted that it plays crucial roles in a number of neurological and psychiatric diseases. Indeed, impaired brain plasticity may be one of the pathophysiological mechanisms that underlies both cognitive decline and major depression. Moreover, a degree of cognitive impairment is frequently observed throughout the clinical spectrum of mood disorders, and the relationship between depression and cognition is often bidirectional. However, most evidence for dysfunctional neural plasticity in depression has been indirect. Transcranial magnetic stimulation has emerged as a noninvasive tool for investigating several parameters of cortical excitability with the aim of exploring the functions of different neurotransmission pathways and for probing in vivo plasticity in both healthy humans and those with pathological conditions. In particular, depressed patients exhibit a significant interhemispheric difference in motor cortex excitability, an imbalanced inhibitory or excitatory intracortical neurochemical circuitry, reduced postexercise facilitation, and an impaired long-term potentiation-like response to paired-associative transcranial magnetic stimulation, and these symptoms may indicate disrupted plasticity. Research aimed at disentangling the mechanism by which neuroplasticity plays a role in the pathological processes that lead to depression and evaluating the effects of modulating neuroplasticity are needed for the field to facilitate more powerful translational research studies and identify novel therapeutic targets.
神经可塑性被认为是学习和记忆的神经生理关联,尽管多项研究也指出它在多种神经和精神疾病中起着关键作用。事实上,大脑可塑性受损可能是认知衰退和重度抑郁症共同的病理生理机制之一。此外,在情绪障碍的整个临床范围内经常观察到一定程度的认知障碍,并且抑郁与认知之间的关系通常是双向的。然而,抑郁症中神经可塑性功能失调的大多数证据都是间接的。经颅磁刺激已成为一种非侵入性工具,用于研究皮质兴奋性的几个参数,目的是探索不同神经传递途径的功能以及探究健康人和患有病理状况的人的体内可塑性。特别是,抑郁症患者在运动皮质兴奋性方面表现出明显的半球间差异、皮质内神经化学回路抑制或兴奋失衡、运动后易化降低以及对配对联想经颅磁刺激的长时程增强样反应受损,这些症状可能表明可塑性受到破坏。该领域需要开展旨在阐明神经可塑性在导致抑郁症的病理过程中发挥作用的机制并评估调节神经可塑性的效果的研究,以促进更有力的转化研究并确定新的治疗靶点。