🧬 BDNF Extraction Viewer

Извлечено: 997 / 997 (100.0%) Средняя confidence: 0.13
← Назад к списку

Neurobiological mechanisms of acupuncture for post-ischemic stroke comorbid insomnia and cognitive impairment: a narrative review.

PMID: 41835071 · DOI: 10.3389/fneur.2026.1696958 · Frontiers in neurology, 2026 · HuiHui Yin, Ming Liu, Ce Shi, JiaXi Liu, Xia Sun, XianFeng Ye
📄 Abstract

This narrative review systematically synthesizes recent clinical and pre-clinical evidence to elucidate the latest neurobiological mechanisms underlying acupuncture for post-stroke insomnia combined with cognitive impairment (PS-ICI). PS-ICI is characterized pathologically by a hippocampal-prefrontal circuitry-mediate "sleep-cognition vicious cycle" and clinically by concurrent cognitive decline and sleep-architecture disruption, both of which markedly impede post-stroke neurological recovery. Grounded in the Traditional Chinese Medicine (TCM) principle of "regulating Shen and re-animating the brain, "acupuncture exerts bidirectional modulation on cognition and sleep, significantly improving core functional outcomes and activities of daily living. Up-to-date studies confirm that synergistic, multi-dimensional effects are achieved through regulation of the BDNF-TrkB-PI3K/Akt signaling axis, preservation of neurovascular unit integrity, restoration of gut-brain axis homeostasis, normalization of circadian immune rhythms, and reshaping of default-mode network (DMN) plasticity. Given the high heterogeneity of included studies, a qualitative integrative approach was employed. Current evidence is nevertheless limited by small sample sizes, short follow-up durations, and substantial heterogeneity in acupuncture parameters (frequency and point selection); future work must therefore focus on dissecting inter-pathway interactions, standardizing therapeutic protocols, and integrating multi-omic technologies to propel acupuncture toward precision, evidence-based management of PS-ICI.

Confidence: 0 · 0 полей извлечено
Идентификация (6 полей)
Механизм действия (21 полей)
Mechanism
0.00
Mutations (obesity/lean)
0.00
Activity (obesity)
0.00
Activity temporal
0.00
Energy balance
0.00
Appetite
0.00
Fat metabolism
0.00
Lipolysis
0.00
Thermogenesis
0.00
Muscle metabolism
0.00
Inflammation
0.00
Glucose metabolism
0.00
AA metabolism
0.00
Hormonal pathways
0.00
Cell death
0.00
Adipocyte fibrosis
0.00
Upstream (biochem)
0.00
Upstream (physiol)
0.00
Downstream (biochem)
0.00
Downstream (physiol)
0.00
PTMs
0.00
Экспрессия (8 полей)
Tissue expression
0.00
In vitro
0.00
In vivo
0.00
In silico
0.00
Genetic association
0.00
Ex vivo
0.00
Animal model
0.00
Diet/model
0.00
Клиника (11 полей)
Drug
0.00
Indication
0.00
Patient subgroups
0.00
Safety concerns
0.00
Off-target
0.00
Trial stage
0.00
Pharma competitors
0.00
AE severity
0.00
MOA weight loss
0.00
Endpoints
0.00
Approved
0.00