Publications by authors named "Xin-fu Zhou"

Alzheimer's disease (AD) is a common cause of dementia characterized by the presence of two proteinaceous deposits in the brain. These pathologies may be a consequence of complex interactions between neurons and glia before the onset of cognitive impairments. Curcumin, a bioactive compound found in turmeric, is a promising candidate for AD because it alleviates neuropathologies in mouse models of the disease.

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  • * Treatment with oral edaravone, which is known for scavenging free radicals, effectively reduced oxidative stress and improved cognitive function in these mice, also decreasing neuroinflammation and restoring neural stem cells in the hippocampus.
  • * The study highlights the importance of oxidative stress and suggests that edaravone could be a promising therapeutic option for addressing cognitive deficits associated with chronic high-altitude hypoxia.
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  • A study introduced a recombinant fusion protein called p75ECD-Fc, which combines the extracellular domain of p75 and the Fc fragment of human IgG1, to promote neuronal growth and restore brain function in rats with neonatal hypoxic-ischemic encephalopathy (NHIE).
  • In vitro tests showed that p75ECD-Fc significantly improves cell viability and neurite outgrowth under oxygen-glucose deprivation conditions.
  • In vivo results revealed that p75ECD-Fc reduced brain damage and neurological issues more effectively than hypothermia, while also enhancing neuronal survival and shifting glial cell phenotypes, suggesting its potential as a therapeutic option for NHIE.
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Autism spectrum disorder (ASD) is neurodevelopmental disorder with a high incidence rate, characterized by social deficits and repetitive behaviors. There is currently no effective management available to treat the core symptoms of ASD; however, oxidative stress has been implicated in its pathogenesis. Edaravone (EDA), a free-radical scavenger, is used to treat amyotrophic lateral sclerosis (ALS) and acute ischemic stroke (AIS).

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  • The global rise in aging populations is linked to a higher incidence of Alzheimer's disease (AD) and its socioeconomic impacts, driven largely by abnormal amyloid-β (Aβ) metabolism.
  • Current treatments focusing on Aβ removal have shown limited cognitive benefits, highlighting the complexity of AD's causes, which include a range of factors like tau accumulation, neuroinflammation, and vascular dysfunction.
  • To effectively treat AD, extensive research is needed on neurodegeneration mechanisms, identifying intervention targets, and developing combinatorial treatment strategies, with the overarching goal of reversing cognitive decline through the Alzheimer's Disease Neuroprotection Research Initiative.
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Introduction: Self-repair of spinal cord injury (SCI) has been found in humans and experimental animals with partial recovery of neurological functions. However, the regulatory mechanisms underlying the spontaneous locomotion recovery after SCI are elusive.

Aims: This study was aimed at evaluating the pathological changes in injured spinal cord and exploring the possible mechanism related to the spontaneous recovery.

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  • ProBDNF is a precursor to BDNF, and its levels, along with p75 neurotrophic receptors, were found to be elevated in individuals with major depressive disorder (MDD), pointing to a potential link between these proteins and depression.
  • The study analyzed blood samples from MDD patients and normal donors, revealing that proBDNF and p75NTR were primarily present in specific immune cells (CD4 and CD8 T cells) and showed significant increases in MDD patients.
  • Additionally, inflammatory cytokines were correlated with depressive symptoms, with specific cytokines showing positive or negative relationships with depression scores, indicating a complex interplay between immune response and mood disorders.
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  • - Alzheimer's disease (AD) is a progressive brain disorder characterized by the accumulation of amyloid-β (Aβ) peptide plaques, which are seen as a major focus for developing treatments.
  • - Despite past clinical trial failures targeting Aβ clearance, recent successful trials of lecanemab and donanemab support Aβ's role in AD and the potential for these therapies.
  • - The analysis emphasizes the need for effective treatment strategies, including early intervention, sufficient Aβ removal, longer treatment durations, and possible combination therapies to improve cognitive outcomes in future AD trials.
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Anxiety and depressive disorders are closely associated; however, the pathophysiology of these disorders remains poorly understood. Further exploration of the mechanisms involved in anxiety and depression such as the stress response may provide new knowledge that will contribute to our understanding of these disorders. Fifty-eight 8-12-week-old C57BL6 mice were separated into experimental groups by sex as follows: male controls ( = 14), male restraint stress ( = 14), female controls ( = 15) and female restraint stress ( = 15).

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The early transition to Alzheimer's disease is characterized by a period of accelerated brain atrophy that exceeds normal ageing. Identifying the molecular basis of this atrophy could facilitate the discovery of novel drug targets. The precursor of brain-derived neurotrophic factor, a well characterized neurotrophin, is increased in the hippocampus of aged rodents, while its mature isoform is relatively stable.

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Poorer mental health is common in undergraduate students due to academic stress. An interplay between stress and diet exists, with stress influencing food choices. Nutritional interventions may be effective in preventing mental health decline due to complex bidirectional interactions between the brain, the gut and the gut microbiota.

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The interaction of neurotrophins with their receptors is involved in the pathogenesis and progression of various neurological diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, spinal cord injury and acute and chronic cerebral damage. The p75 neurotrophin receptor (p75NTR) plays a pivotal role in the development of neurological dysfunctions as a result of its high expression, abnormal processing and signalling. Therefore, p75NTR represents as a vital therapeutic target for the treatment of neurodegeneration, neuropsychiatric disorders and cerebrovascular insufficiency.

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The major hallmark of Parkinson's disease (PD) is the degeneration of dopaminergic neurons in the substantia nigra (SN), which is responsible for the core motor symptoms of PD. Currently, there is no cure for PD, and its prevalence is increasing, prompting the search for novel neuroprotective treatments. Neuroinflammation is a core pathological process in PD, evident by increased inflammatory biomarkers in the SN and cerebrospinal fluid.

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Most Alzheimer disease (AD) patients present as sporadic late onset AD, with metabolic factors playing an important role in the occurrence and development of AD. Given the link between peripheral insulin resistance and tau pathology in streptozotocin-injected and db/db mouse models of diabetes, we fed high fat diet (HFD) to pR5 mice expressing P301L mutant human tau, with the aim of developing a new model with characteristics of obesity, T2DM and AD to mimic AD patients exacerbated by obesity and T2DM, an increasing trend in modern society. In our study, pR5 and C57BL/6 (WT) mice were randomly allocated to a standard diet (STD) or HFD for 30 weeks starting at 8 weeks of age.

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Edaravone has been widely used in the treatment of acute ischemic stroke. However, there has been no oral preparation of edaravone in the clinic. In this study, we assessed the effect and possible mechanisms of oral edaravone on the middle cerebral artery occlusion (MCAO) model in rats.

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Oxidative stress plays a crucial role in the pathophysiology of diastolic dysfunction associated with diabetic cardiomyopathy. Novel oral edaravone (OED) alleviates oxidative stress by scavenging free radicals and may be suitable for the treatment of chronic diseases such as diabetic cardiomyopathy. Oral administration of OED to type 2 diabetic rats (induced by high-sugar/high-fat diet and intraperitoneal injection of streptozotocin) for 4 w decreased malondialdehyde and increased superoxide dismutase.

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Induced neural stem cells (iNSCs) reprogrammed from somatic cells hold great potentials for drug discovery, disease modelling and the treatment of neurological diseases. Although studies have shown that human somatic cells can be converted into iNSCs by introducing transcription factors, these iNSCs are unlikely to be used for clinical application due to the safety concern of using exogenous genes and viral transduction vectors. Here, we report the successful conversion of human fibroblasts into iNSCs using a cocktail of small molecules.

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P75 pan-neurotrophin receptor (p75NTR) is an important receptor for the role of neurotrophins in survival and death of neurons during development and after nerve injury. Our previous research found that the precursor of brain-derived neurotrophic factor (proBDNF) regulates pain as an inflammatory mediator. The current understanding of the role of proBDNF/p75NTR signaling pathway in inflammatory arthritis pain and rheumatoid arthritis (RA) is unclear.

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Stress hormones such as cortisol play a critical role in depressive disorders. Therefore, corticosterone has been used to develop a depression model in animals. Our previous studies found that the precursor of brain-derived neurotrophic factor (proBDNF) and its receptors are upregulated in depression in human and animal models.

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Inappropriate expansion of antibody-secreting cells (ASCs) is typical of systemic lupus erythematosus (SLE), but the regulatory signaling of pathogenic ASCs is unclear. The present study shows that brain-derived neurotrophic factor precursor (proBDNF) and its high-affinity pan-75 neurotrophin receptor (p75) are highly expressed in CD19CD27CD38 ASCs in patients with SLE and in CD19CD44CD138 ASCs in lupus-like mice. The increased proBDNF ASCs were positively correlated with clinical symptoms and higher titers of autoantibodies in SLE.

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Alzheimer's disease is a neurodegenerative condition that is potentially mediated by synaptic dysfunction before the onset of cognitive impairments. The disease mostly affects elderly people and there is currently no therapeutic which halts its progression. One therapeutic strategy for Alzheimer's disease is to regenerate lost synapses by targeting mechanisms involved in synaptic plasticity.

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Neurological disorders are big public health challenges that are afflicting hundreds of millions of people around the world. Although many conventional pharmacological therapies have been tested in patients, their therapeutic efficacies to alleviate their symptoms and slow down the course of the diseases are usually limited. Cell therapy has attracted the interest of many researchers in the last several decades and has brought new hope for treating neurological disorders.

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