中国科技核心期刊
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Neural Injury and Functional Reconstruction

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  • 2026 Volume 21 Issue 3
    Published: 25 March 2026
      
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  • Platelet Factor 4 Promotes Amyloid-β Clearance through Regulating Microglia Polarizationvia Trem2 in AD Cell Models
    SENG Xixi1,2a ，LI Min2b,3 ，SONG Chenran2b,3 ，YE Chengchen1,2b ，WANG Yuchen1,2a ，HUANG Shengjie1,2a ，CHENG Yong2a
    2026, 21(3): 125-130. https://doi.org/10.16780/j.cnki.sjssgncj.20251364
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    To investigate the potential impact of platelet factor 4 (PF4) on the M1/M2 polarization of microglia in an Alzheimer's disease (AD) cell model and its possible molecular mechanisms. Methods: An AD cell model was induced by treating BV2 microglial cells with A β 1-42, followed by PF4 intervention. Furthermore, Trem2 expression was knocked down in BV2 cells through Trem2-siRNA transfection. Cell viability was assessed using the CCK8 assay; levels of TNF-α, IL-6, and IL-1β were measured by ELISA; the expressions of Trem2, iNOS, and Arg1 were detected via double-label immunofluorescence and Western blot analyses; mRNA levels of Trem2, iNOS, Arg1, TNF-α, and IL-10 were determined by RT-qPCR; and phagocytic function was evaluated using flow cytometry. Results: Compared with the control group, the A β 1-42 group exhibited significantly elevated expression levels of M1 phenotype markers (iNOS, TNF-α, IL-1 β) and IL-6, along with markedly decreased expression of M2 phenotype markers (Arg1, IL-10) and Trem2. In contrast, the (A β1-42+PF4) group showed reduced expression of M1 phenotype markers (iNOS, TNF-α, IL-1β) and IL-6, increased expression of M2 phenotype markers (Arg1, IL-10) and Trem2, and enhanced phagocytic capacity for A β 1-42 compared with the Aβ1-42 group. However, compared with the (Trem2-siRNA+Aβ1-42) group, PF4 failed to exert the aforementioned effects in BV2 cells in the (Trem2-siRNA+Aβ1-42+PF4) group. Conclusion: PF4 can regulate microglial polarization via Trem2, alleviate AD-related neuroinflammation, and promote the clearance of Aβ1-42.
  • Exploring the Neuroprotective Effect of the mTOR Inhibitor KU-0063794 on Ischemic StrokeBased on Bioinformatics
    ZHU Xiaoming, GUO Zhaoyan, ZHANG Chenxi
    2026, 21(3): 131-137. https://doi.org/10.16780/j.cnki.sjssgncj.20240229
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    To employ bioinformatics to screen for neuroprotective drugs for cerebral ischemia and evaluate them in an animal transient Middle Cerebral Artery Occlusion (tMCAO) model. Methods: Two datasets from the Gene Expression Omnibus (GEO) database, representing the 6 h and 12 h time points after MCAO, were obtained and subjected to differential gene analysis. The biological processes and signaling pathways of the differentially expressed genes were enriched using DAVID and Metascape. Key genes were identified using Cytoscape and validated in a mouse tMCAO model. The Connectivity Map (Cmap) online tool was used to predict potential therapeutic drugs for cerebral ischemia, and the autophagy inhibitor KU-0063794 was selected to investigate its neuroprotective effect on tMCAO mice. Results: A total of 289 common differentially expressed genes were identified between the two datasets. Enrichment analysis revealed that the differentially expressed genes were primarily enriched in biological processes such as regulation of synaptic transmission, lipid biosynthesis, and apoptosis during the acute phase of ischemic stroke. Real-time PCR results showed that the mRNA levels of Hmox1, Serpine1, Ptgs2, and Timp1 in the peri-infarct cortex increased 12 h after tMCAO. Western blotting results indicated that the expression level of Hmox1 increased from 6 to 24 h after ischemic injury. KU-0063794 significantly reduced cerebral infarct volume in tMCAO mice, mitigated oxidative stress and neuronal apoptosis by activating the Nrf2/Hmox1 pathway, and behavioral tests demonstrated that KU-0063794 significantly improved motor dysfunction in tMCAO mice. Conclusion: KU-0063794 exerts neuroprotective effects by reducing oxidative stress and neuronal apoptosis.
  • Efficacy of Motor Imagery Therapy on Post-stroke Motor Dysfunction: an Overview ofSystematic Reviews
    FENG Luye1,2 ，ZHOU Shanshan1 ，YANG Yuanyuan1 ，WANG Dehua1 ，YANG Rong1 ，TANG Jiqin1,3
    2026, 21(3): 138-144. https://doi.org/10.16780/j.cnki.sjssgncj.20240971
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    To conduct a systematic re-evaluation of systematic reviews (SR) or Meta-analyses on the efficacy of motor imagery therapy (MIT) in treating post-stroke motor dysfunction. Methods: A computerized search was conducted in domestic and international databases for SR/Meta-analyses on MIT for post-stroke motor dysfunction, with the search period spanning from the establishment of the databases to September 2023. The AMSTAR 2 tool, PRISMA 2020 guidelines, and GRADE system were employed to evaluate the quality of the included studies in terms of literature quality and evidence quality. Results: Ultimately, 11 studies were included. According to the AMSTAR 2 assessment, there were 2 studies of moderate quality (18.18%), 2 studies of low quality (18.18%), and 7 studies of very low quality (63.64%). The PRISMA 2020 guidelines indicated that 3 studies (27.27% ) had relatively complete reporting, while 8 studies (72.73% ) had certain reporting deficiencies. The GRADE evidence grading revealed a total of 49 outcome indicators, among which 2 were of moderate quality (4.08% ), 24 were of low quality (48.98% ), and 23 were of very low quality evidence (63.64% ). Conclusion: MIT contributes to the recovery of limb motor function, balance function, and activities of daily living in post-stroke patients.
  • Effect of Repetitive Transcranial Magnetic Stimulation Combined with TizanidineHydrochloride in the Treatment of Upper Limb Flexor Spasm after Stroke
    TIAN Peia ，YU Yia ，FAN Rongfub
    2026, 21(3): 145-149. https://doi.org/10.16780/j.cnki.sjssgncj.20240459
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    To investigate the clinical effectiveness of the combined therapy of low-frequency repetitive transcranial magnetic stimulation (rTMS) and Tizanidine Hydrochloride in alleviating upper limb flexor spasticity symptoms in stroke patients. Methods: Clinical data were collected from 60 patients with upper limb flexor spasticity following stroke who received rehabilitation treatment at Beijing Boai Hospital from December 2020 to December 2023. These patients were divided into a control group and an observation group, with 30 patients in each group, according to different treatment methods. The control group was treated with oral Tizanidine Hydrochloride, while the observation group received a combination of Tizanidine Hydrochloride and low-frequency rTMS. Both groups of patients received secondary stroke prevention treatment and conventional rehabilitation training. Before treatment initiation and at the end of the 4th week of treatment, the Modified Ashworth Spasm Scale (MAS) was used to measure the degree of spasticity in the upper limb elbow flexors. The Upper Limb Fugl-Meyer Assessment (UFMA) was employed to evaluate the recovery of upper limb motor function, and the Modified Barthel Index (MBI) was applied to quantify the level of activities of daily living (ADL) in patients. Additionally, the occurrence of adverse reactions in both groups was recorded. Results: Prior to treatment, there were no statistically significant differences in MAS, UFMA, and MBI scores between the two groups (P>0.05). At the end of the 4th week of treatment, all three scores in both groups improved compared to those before treatment. The observation group showed superior performance to the control group in terms of the increase in UFMA and MBI scores and the decrease in MAS score, with all differences being statistically significant (P<0.05). Adverse reactions in both groups were infrequent and mild, with an incidence rate of 6.67% in each group, primarily manifested as drowsiness and dizziness. Conclusion: Compared to the use of Tizanidine Hydrochloride alone, the combination of low-frequency rTMS and Tizanidine Hydrochloride is effective in reducing the muscle tone of the upper limb flexors on the hemiplegic side, improving upper limb motor function, enhancing patients' quality of life, and demonstrating good safety in the treatment of upper limb flexor spasticity after stroke.
  • Evidence based on Mendelian Randomization: Causality between Mitochondria and Epilepsy
    LI Jun1 ，XU Litao1 ，HUANG Yan1 ，ZHAO Qichao1 ，ZHANG Yongquan2
    2026, 21(3): 150-155. https://doi.org/10.16780/j.cnki.sjssgncj.20241073
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    To explore the causal relationship between mitochondria and epilepsy using Mendelian randomization (MR). Methods: Single nucleotide polymorphisms (SNPs) significantly associated with mitochondrial abundance across 66 traits were utilized as instrumental variables. The inverse variance weighted (IVW) method, MR Egger regression, and weighted median approach were employed to determine the causal relationship between exposure factors and the onset of epilepsy. Additionally, Cochran’s Q test, leave-one-out analysis, and MR-PRESSO were used to assess the robustness of the results. Results: Significant causal relationships were identified between three datasets and generalized epilepsy. The IVW results indicated that [pyruvate dehydrogenase (lipoamide) kinase isozyme 1] was associated with an increased risk of generalized epilepsy (OR=1.275, 95%CI=1.056～1.540, PIVW=0.011, PFDR=0.017), rRNA methyltransferase 3 was also linked to a heightened risk of generalized epilepsy (OR=1.158, 95% CI=1.002～1.338, PIVW=0.047, PFDR=0.047), while the essential MCU regulator was associated with a reduced risk of generalized epilepsy (OR=0.727, 95% CI= 0.578～0.915, PIVW=0.007, PFDR=0.020). Five datasets exhibited significant causal relationships with focal epilepsy. The IVW results revealed that ribosome recycling factor was associated with an increased risk of focal epilepsy (OR=1.085, 95% CI=1.000～1.178, PIVW=0.049, PFDR=0.061), protein lysine deacylase Sirtuin 5 was also linked to a heightened risk of focal epilepsy (OR=1.080, 95% CI=1.001～1.167, PIVW=0.048, PFDR=0.079), complement component 1 Q subcomponent-binding protein was associated with a reduced risk of focal epilepsy (OR=0.917, 95% CI=0.861～0.977, PIVW=0.007, PFDR=0.018), serine--tRNA ligase was also linked to a decreased risk of focal epilepsy (OR=0.852, 95% CI=0.779～0.934, PIVW=0.001, PFDR=0.003), and NFU1 iron-sulfur cluster scaffold homolog was associated with an increased risk of focal epilepsy (OR=1.098, 95% CI=1.000～1.204, PIVW=0.049, PFDR=0.049). Sensitivity tests confirmed the robustness of the findings (all P>0.05). Conclusion: A causal relationship between mitochondria and epilepsy has been established.
  • Research Progress on the Involvement of the Glial-Vascular Unit in Cortical SpreadingDepression
    YANG Xiao, YAO Di, WANG Minghuan
    2026, 21(3): 156-161. https://doi.org/10.16780/j.cnki.sjssgncj.20251375
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    Cortical spreading depression (CSD) is a key pathological event in various neurological disorders such as migraine and cerebral ischemia. Recent research reveals that the glial-vascular unit (GVU) serves as a central platform regulating the CSD process. This review systematically elucidates the dynamic roles and mechanisms of GVU components in CSD: the dual functions of astrocytes as central hubs; microglia acting as one of initiating cells potentially involved in both damaging and reparative effects; abnormal post-CSD contraction of pericytes mediating sustained capillary hypoperfusion; while functional alterations in the perivascular space and glymphatic system may represent potential factors influencing CSD initiation and recovery. These findings establish the GVU as the core regulatory platform for CSD, whose internal synergy and conflicts determine disease progression. This shifts the research focus from individual components to the entire GVU, providing novel perspectives for comprehensively understanding CSD pathophysiology and developing multi-target synergistic therapeutic strategies.
  • Research Progress on Nose-to-Brain Delivery for Treating Central Nervous SystemDemyelinating Diseases
    MAO Jialing, WANG Manxia.
    2026, 21(3): 162-167. https://doi.org/10.16780/j.cnki.sjssgncj.20251485
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    Central nervous system demyelinating diseases, represent a group of chronic autoimmune conditions requiring long-term intervention. Traditional systemic administration methods face limitations due to the blood-brain barrier, resulting in issues such as low central nervous system delivery efficiency, high systemic exposure, and significant interindividual pharmacokinetic variability. These factors compromise treatment precision and patient compliance. The Nose-to-Brain (N2B) route bypasses the blood-brain barrier via the olfactory and trigeminal pathways, enabling direct central drug delivery with advantages including non-invasiveness, high targeting specificity, and minimal systemic side effects. This study systematically reviews the dual-pathway delivery mechanism of this route, along with recent advances in reducing neuroinflammation, promoting myelin regeneration, and neuroprotective delivery strategies. It also analyzes current challenges in clinical translation.
  • Clinical Application of Magnetoencephalography in Neurodegenerative Diseases
    LIU Yawen1 ，YANG Mengyu1 ，TIAN Shulei1 ，WANG Yingxuan1 ，WANG Xuezhen2 ，ZHAO Xiumin3
    2026, 21(3): 168-172. https://doi.org/10.16780/j.cnki.sjssgncj.20241167
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    Neurodegenerative diseases are structural damage to the nervous system caused by the loss of neurons and/or their myelin sheaths, which progressively worsens over time, leading to dysfunction. Magnetoencephalography (MEG) is a record of the spontaneous neural magnetic field of brain tissue, which is a completely non-invasive and non-damaging brain function detection technology with good temporal and spatial resolution, and has been gradually applied to the early diagnosis of neurodegenerative diseases. This review mainly describes the clinical application of MEG in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Multiple sclerosis, Dementia with Lewy bodies, Frontotemporal dementia and Amyotrophic lateral sclerosis.