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Insulin resistance (IR) is a risk factor for metabolic disorders and neurodegeneration. Peroxisome proliferator-activated receptor (PPAR) agonists have been proven to mitigate the neuronal pathology associated with IR. However, the synergetic efficacy of these agonists is yet to be fully described. Hence, we aimed to investigate the efficacy of PPARα/γ agonists (fenofibrate and pioglitazone) on a high-fat diet (HFD) and streptozotocin (STZ)-induced hippocampal neurodegeneration. Male Wistar rats (200 ± 25 mg/body weight [BW]) were divided into five groups. The experimental groups were fed on an HFD for 12 weeks coupled with 5 days of an STZ injection (30 mg/kg/BW, i.p) to induce IR. Fenofibrate (FEN; 100 mg/kg/BW, orally), pioglitazone (PIO; 20 mg/kg/BW, orally), and their combination were administered for 2 weeks postinduction. Behavioral tests were conducted, and blood was collected to determine insulin sensitivity after treatment. Animals were killed for assessment of oxidative stress, cellular morphology characterization, and astrocytic evaluation. HFD/STZ-induced IR increased malondialdehyde (MDA) levels and decreased glutathione (GSH) levels. Evidence of cellular alterations and overexpression of astrocytic protein was observed in the hippocampus. By contrast, monotherapy of FEN and PIO increased the GSH level (p < 0.05), decreased the MDA level (p < 0.05), and improved cellular morphology and astrocytic expression. Furthermore, the combined treatment led to improved therapeutic activities compared to monotherapies. In conclusion, FEN and PIO exerted a therapeutic synergistic effect on HFD/STZ-induced IR in the hippocampus.

Autoscopic phenomena or an “invisible doppelgänger” refer to the illusory reduplication of one's own body. Body image disorder involves distorted perception or decreased body awareness. In the literature, feeling of presence (FOP) is rarely presented with a circumscribed cerebral pathology due to acute vascular lesions, and concomitant FOP and disorders of the body image or the body schema (BIBS) have rarely been reported. We present three cases of both FOP and BIBS disorders. All patients reported the two types of symptoms almost simultaneously: The first patient had the symptom of somatoparaphrenia characterized by deny ownership of the hand and feeling that it does not belong to her, the second patient had the sign of fading limb presented with misuse of his left hand when it was not under visual control and could not mentally represent and locate this part of the body in space, and the third patient had autotopagnosia; he was unable to localize any touched area below the elbow and knee. All patients had right parietal ischemic lesions involving the superior parietal lobule, and two patients had an adjacent additional precuneal involvement. Based on the cases presented here, it is plausible that BIBS may develop in addition to FOP, especially in lesions involving the superior parietal lobule and precuneus.

To explore the effect of electroacupuncture on spinal cord injury (SCI) involving immune-related factors and regeneration-related factors in rats. The model of spinal cord contusion was established by PCI 3000 instrument. Two types of acupuncture points were selected for electroacupuncture treatment on rats. The rats were tested once a week, and the fiber remodeling was detected by magnetic resonance imaging. Transcriptome sequencing was performed on spinal scar samples. Using Python to write code, statistical analysis and bioinformatics analysis of the correlation between transcriptome sequencing data and fiber reconstruction results are carried out. Lastly, the expression of CD4 and brain-derived neurotrophic factor (BDNF) in spinal cord scar was verified by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Electroacupuncture exhibited a positive effect on the recovery of motor function in rats after SCI. Bioinformatics analysis found a direct interaction between CD4 and BDNF. Transcriptome sequencing and PCR results verified that electroacupuncture significantly reduced the expression of CD4, and increased significantly the expression of BDNF, simultaneously corresponding to nerve regeneration in rats with SCI. Our results showed that electroacupuncture intervention in SCI rats improves neural behavior via inhibiting the expression of CD4 and increasing the expression of BDNF.

Neonatal hypoxic-ischemic encephalopathy (NHIE) is one of the major diseases in newborns during the perinatal stage, which globally is the main reason for children's morbidity and mortality. However, the mechanism of NHIE still remains poorly clear. In this study, the 7-day-old rats were subjected to hypoxic-ischemia (HI), then brain damage was detected. Afterward, the expression of eva-1 homolog C (EVA1C) was measured in vitro by establishing the oxygen-glucose deprivation (OGD) model in SHSY5Y cells and human fetal neurons. Subsequently, the potential function and mechanism of EVA1C were explored by silencing EVA1C and alternative splicing prediction. As a result, obvious neurobehavioral impairment and brain infarction were detected through Zea-Longa score and TTC staining; meanwhile, neuron injury was tested by HE and Nissl staining post HI. Moreover, it was found that the expression of EVA1C was notably upregulated in SHSY5Y cells and human fetal neurons after OGD. In addition, cell survival and growth were increased after silencing EVA1C, which might be associated with alternative splicing. In conclusion, EVA1C interference exhibited potential in promoting neuron survival and growth, associated with exon skipping with the alternative splicing site in 34613318:34687258, which may provide the basis for the therapeutic target and mechanism research of NHIE.

Optimal exercise can promote the development of cognitive functions. Nevertheless, mechanisms that elicit these positive effects of exercise still need to be elucidated. Insulin-like growth factor 2 (IGF2) is known to act as a potent enhancer of memory and cognitive functions, whereas the mechanism by which IGF2 regulates cognitive functions in terms of moderate treadmill exercise remains largely vague. In the study, rats were subjected to low-, moderate-, and high-intensity treadmill training for 6 weeks. Then, the Morris water maze test was used to investigate spatial learning and memory ability in rats subjected to treadmill exercises of different intensities. Subsequently, gene chip and bioinformatics analyses were used to explore IGF2 and predict target microRNAs (miRNAs). Quantitative real-time polymerase chain reaction, western blot, and immunofluorescence analysis were performed to detect the levels of IGF2. Furthermore, IGF2-small interfering RNA, the miRNA-483-mimic, and the miRNA-483-inhibitor were transfected to determine the role of IGF2 and miRNA-483 in the growth of hippocampal neurons. The results of the Morris water maze test showed that moderate-intensity treadmill training enhanced cognitive functions; meanwhile, the expression of IGF2 was significantly upregulated in the hippocampus after moderate-intensity treadmill exercise. From databases, miRNA-483 was screened and predicted as the target gene of IGF2. Moreover, silencing IGF2 inhibited neurite growth in the hippocampus of rats, the miRNA-483-inhibitor ameliorated silencing IGF2 induced impairment of hippocampal neurons. These findings suggested that treadmill training could enhance cognitive functions, wherein the underlying mechanism involved an increase in the expression of IGF2 and downregulation of miRNA-483.

To investigate the changes in neuromuscular function of anterior approach combined with subtotal vertebral body resection and titanium mesh cage (TMC) internal fixation for the old fracture-dislocated lower cervical spine. A 56-year-old female was admitted to the hospital with neck pain and numbness of the left upper extremity for 3 years due to a fall injury from a height, which worsened for 20 days. Although 3 years had passed, the patient still had significant left limb numbness and decreased muscle strength. Eventually, the patient was diagnosed with the old fracture-dislocation type injury of C6 and C7. C6 was II-degree anterior dislocation and the bilateral joint process was locked, C7 was burst fracture, and C5 was spinal cord segment injury. Then, the operation of the anterior approach combined with subtotal vertebral body resection and TMC internal fixation was performed under general anesthesia. Postoperative symptoms were significantly improved. And during five-year of follow-up, no adverse reactions and complications were reported. Although cervical fracture and dislocation combined with cervical spinal cord injury had persisted for many years, surgical treatment was necessary. The anterior approach combined with subtotal vertebral body resection and TMC internal fixation was desirable to improve neuromuscular function for the old fracture-dislocation of the lower cervical spine, which has some guiding effects on the clinical treatment.

Neonatal hypoxic-ischemic encephalopathy (NHIE) causes devastating cerebral damage and neurological deficits that seldom have effective therapies. This study aimed to explore the mechanisms underlying the therapeutic efficacy of Scutellarin in NHIE. NHIE models were successfully established. Zea-longa score and triphenyte-trazoliumchloride (TTC) staining demonstrated that hypoxia and ischemia (HI) insult induced prominent neurological dysfunctions and brain infarction. Protein microarray was applied to detect the differentially expressed genes in the cortex, hippocampus, and lung tissues of HI rats, which revealed the downregulation of vascular endothelial growth factor (VEGF) in these tissues. Additionally, double immunostaining uncovered VEGF expression was localized in the neurons. Besides, VEGF was decreasingly expressed in oxygen-glucose deprivation (OGD) neurons, which was intriguingly reversed by Scutellarin treatment. Moreover, VEGF silencing increased OGD-induced neuronal apoptosis and attenuated neurite outgrowth, which was enhanced by Scutellarin administration. GeneMANIA predicted a close correlation of VEGF with caspase 3, caspase 7, and interleukin (IL)-1β, and qRT-PCR revealed that Scutellarin treatment depressed the expression levels of them elevated in OGD neurons, but the Scutellarin-depressed levels of these factors were prominently increased after VEGF silencing. Our findings suggested that Scutellarin exerted neuroprotective effects in NHIE potentially through mediating VEGF-targeted inactivation of caspase 3, caspase 7, and IL-1β.

Autism in a broader sense is a neurodevelopmental disorder, which frequently occurs during early childhood and can last for a lifetime. This condition is primarily defined by difficulties with social engagement, with individuals displaying repetitive and stereotyped behaviors. Numerous neuroanatomical investigations on autistic children have revealed that their brains grow atypically, resulting in atypical neurogenesis, neuronal migration, maturation, differentiation, and degeneration. Special education programs, speech therapy, and occupational therapy have all been used to address autism-related behavioral problems. While widely prescribed antidepressant drugs, antipsychotics, anticonvulsants, and stimulants have demonstrated response in autistic individuals. However, these medications do not fully reverse the core symptoms associated with autism spectrum disorder (ASD). The adverse reactions of ASD medicines and an increased risk of developing various other problems, such as obesity, dyslipidemia, diabetes mellitus, and thyroid disorders, prompted the researchers to investigate herbal medicines for the treatment of autistic individuals. Clinical trials are now being done to establish the efficacy of alternative techniques based on natural substances and to understand better the context in which they may be used to treat autism. This review of literature will look at crucial natural compounds derived from animals and plants that have shown promise as safe and effective autism treatment strategies.

The aim of this article was to analyze the clinical and genetic characteristics of a patient with Huntington's disease and her family. We analyzed the clinical data of a patient with Huntington's disease and her family members in the Department of Neurology of our hospital, drew the genetic pedigree, and used gene fragment analysis to detect and analyze the genes of three people in the family according to the principle of informed consent. The genetic pedigree of the family was consistent with that of autosomal dominant diseases. A total of five people in this family developed the disease, two died, and the main clinical manifestations were dystonia, ataxia, and cognitive impairment. Three people in this family underwent genetic testing, and two exhibited normal genotypes. The cytosine-adenine-guanine trinucleotide (CAG) repeats of the proband were abnormally amplified, and the number of repeats reached 43. The main clinical features of the patient included chronic obscure onset, obvious positive family genetic history, clinical features of involuntary limb movement with cognitive impairment, rapid disease progression, poor treatment effect, and abnormal amplification of CAG repeats as shown through genetic testing. All the above features met the diagnostic criteria of Huntington's disease.

Spinal cord injury (SCI) is a severe disabling disease, which mainly manifests as impairments of sensory and motor functions, sexual function, bladder and intestinal functions, respiratory and cardiac functions below the injury plane. In addition, the condition has a profound effect on the mental health of patients, which often results in severe sequelae. Some patients may be paraplegic for life or even die, which places a huge burden on the family and society. There is still no effective treatment for SCI. Studies have confirmed that endogenous neural stem cells (ENSCs), as multipotent neural stem cells, which are located in the ependymal region of the central canal of the adult mammalian spinal cord, are activated after SCI and then differentiate into various nerve cells to promote endogenous repair and regeneration. However, the central canal of the spinal cord is often occluded to varying degrees in adults, and residual ependymal cells cannot be activated and do not proliferate after SCI. Besides, the destruction of the microenvironment after SCI is also an important factor that affects the proliferation and differentiation of ENSCs and spinal cord repair. Therefore, this review describes the role of ENSCs in SCI, in terms of the origin, transformation, treatment, and influencing factors, to provide new ideas for clinical treatment of SCI.