The Implications of Microglial Regulation in Neuroplasticity-Dependent Stroke Recovery

Abstract

Stroke causes varying degrees of neurological deficits, leading to corresponding dysfunctions. There are different therapeutic principles for each stage of pathological development. Neuroprotection is the main treatment in the acute phase, and functional recovery becomes primary in the subacute and chronic phases. Neuroplasticity is considered the basis of functional restoration and neurological rehabilitation after stroke, including the remodeling of dendrites and dendritic spines, axonal sprouting, myelin regeneration, synapse shaping, and neurogenesis. Spatiotemporal development affects the spontaneous rewiring of neural circuits and brain networks. Microglia are resident immune cells in the brain that contribute to homeostasis under physiological conditions. Microglia are activated immediately after stroke, and phenotypic polarization changes and phagocytic function are crucial for regulating focal and global brain inflammation and neurological recovery. We have previously shown that the development of neuroplasticity is spatiotemporally consistent with microglial activation, suggesting that microglia may have a profound impact on neuroplasticity after stroke and may be a key therapeutic target for post-stroke rehabilitation. In this review, we explore the impact of neuroplasticity on post-stroke restoration as well as the functions and mechanisms of microglial activation, polarization, and phagocytosis. This is followed by a summary of microglia-targeted rehabilitative interventions that influence neuroplasticity and promote stroke recovery.

Influencing factors of corticomuscular coherence in stroke patients

“…The selection of target muscles in stroke patients is critical as brain damage can lead to irregularities in neuromuscular regulation and muscle activity response, resulting in impaired signaling of brain-muscle control and feedback pathways, ultimately leading to limb motor dysfunction ( Qiao et al, 2023 ). Based on the principle of cortical topography, the human hand and upper arm represent a significant portion of projections in the sensorimotor region ( Penfield and Boldrey, 1937 ), making them more susceptible to functional impairment due to brain damage in stroke patients.…”

Treg Cells in Ischemic Stroke: A Small Key to a Great Orchestrion

“…На мышах с экспериментальным инсультом показано, что при инфузии экзогенных Treg их количество увеличивается в период с первого дня до второй недели и сохраняется в течение месяца, объективно наблюдается уменьшение объёма инсульта и долгосрочное функциональное восстановление [16]. В связи с этим очевидна важность определения молекулярных и клеточных механизмов регуляции Treg-клетками иммунного ответа в ходе развития ишемического инсульта [35]. Успешное клиническое применение трансплантации аутологичных Treg в качестве терапевтического инструмента при рассеянном склерозе [8], а также данные о снижении уровня и дисфункции Treg при инсульте [36] позволяют надеяться, что они найдут клиническое применение и при ишемическом инсульте [34].…”