Jinhua Zhong

ORCID: 0000-0002-5313-1413
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Nerve injury and regeneration
  • Neurogenesis and neuroplasticity mechanisms
  • Chronic Lymphocytic Leukemia Research
  • Alzheimer's disease research and treatments
  • Chronic Myeloid Leukemia Treatments
  • Signaling Pathways in Disease
  • Pain Mechanisms and Treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Spinal Cord Injury Research
  • Lymphoma Diagnosis and Treatment
  • Bayesian Methods and Mixture Models
  • Cellular transport and secretion
  • Curcumin's Biomedical Applications
  • Census and Population Estimation
  • Biochemical effects in animals
  • RNA Interference and Gene Delivery
  • Mitochondrial Function and Pathology
  • Botulinum Toxin and Related Neurological Disorders
  • Schizophrenia research and treatment
  • Electroconvulsive Therapy Studies
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • 14-3-3 protein interactions
  • Prion Diseases and Protein Misfolding
  • Statistical Methods and Bayesian Inference
  • Treatment of Major Depression

BeiGene (China)
2020-2025

Shenzhen Bioeasy Biotechnology (China)
2021

GlaxoSmithKline (China)
2018-2020

University of South Australia
2012-2018

Shanghai University of Finance and Economics
2013-2014

Flinders University
2003-2012

Xiamen Tobacco Industry (China)
2010

Chinese Academy of Medical Sciences & Peking Union Medical College
2004

Peking Union Medical College Hospital
2004

Abstract Injury to a peripheral nerve induces in the dorsal root ganglia (DRG) sprouting of sympathetic and peptidergic terminals around large‐diameter sensory neurons that project damaged nerve. This pathological change may be implicated chronic pain syndromes seen some patients with injury. The mechanisms underlying are not known. Using situ hybridization immunohistochemical techniques, we have now found growth factor (NGF) neurotrophin‐3 (NT3) synthesis is upregulated satellite cells...

10.1046/j.1460-9568.1999.00589.x article EN European Journal of Neuroscience 1999-05-01

Significance Alzheimer’s disease (AD) is a devastating that results in the progressive cognitive deficits of elderly and has become one major social economic burdens worldwide. There no effective drug or therapy to prevent halt dysfunctions due complex mechanisms such as accumulation amyloid-β (Aβ), increase oxidative stress, formation neurofibrillary tangle drive development disease. We found here Edaravone, been used for ischemic stroke, able treat AD by targeting multiple pathways...

10.1073/pnas.1422998112 article EN Proceedings of the National Academy of Sciences 2015-04-06

Background Neurons extend their dendrites and axons to build functional neural circuits, which are regulated by both positive negative signals during development. Brain-derived neurotrophic factor (BDNF) is a regulator for neurite outgrowth neuronal survival but the functions of its precursor (proBDNF) less characterized. Methodology/Principal Findings Here we show that proBDNF collapses in murine dorsal root ganglion (DRG) neurons cortical activating RhoA via p75 neurotrophin receptor...

10.1371/journal.pone.0035883 article EN cc-by PLoS ONE 2012-04-27

BackgroundThe blood brain barrier (BBB) and truncated trkB receptor on astrocytes prevent the penetration of derived neurotrophic factor (BDNF) applied into peripheral (PNS) central nervous system (CNS) thus restrict its application in treatment diseases. As BDNF is anterogradely transported by axons, we propose that peripherally and/or may act regeneration axons ascending sensory neurons.Methodology/Principal FindingsThe present study aimed to test hypothesis using conditioning lesion...

10.1371/journal.pone.0001707 article EN cc-by PLoS ONE 2008-03-04

Accumulation of toxic amyloid-β (Aβ) in the cerebral cortex and hippocampus is a major pathological feature Alzheimer's disease (AD). The neurotrophin receptor p75NTR has been proposed to mediate Aβ-induced neurotoxicity; however, its role development AD remains be clarified. p75NTR/ExonIII−/− mice APPSwe/PS1dE9 were crossed generate transgenic with deletion gene. In mice, expression was localized basal forebrain neurons degenerative neurites neocortex, increased aging, further activated by...

10.1523/jneurosci.2733-10.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-02-09

The neurotrophin receptor p75NTR is the coreceptor for Nogo receptor, mediating growth cone collapse in vitro by MAG, myelin oligodendrocyte glycoprotein (Omgp), and Nogo. Whether plays any role failure of nerve regeneration vivo not known. Immunohistochemical data showed that was expressed only a very small subset ascending sensory axons but corticospinal dorsal column either normal or injured spinal cord. Using p75NTR-deficient mice, we depletion functional did promote descending tract...

10.1523/jneurosci.4281-03.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-01-14

Abstract The precursors for neurotrophins are proteolytically cleaved to form biologically active mature molecules which activate their receptors p75NTR and trks. A recent study showed that the precursor nerve growth factor (NGF) can bind with a high affinity induces apoptosis of neurons in vitro . Mutation Val66Met brain‐derived neurotrophic (BDNF) results reduction hippocampal function learning dysfunction intracellular BDNF sorting secretion. To examine functions pro‐neurotrophins vivo ,...

10.1111/j.1471-4159.2004.02775.x article EN Journal of Neurochemistry 2004-10-05

Abstract Remyelination is an important aspect of nerve regeneration after injury but the underlying mechanisms are not fully understood. The neurotrophin receptor, p75 NTR , in activated Schwann cells Wallerian degenerated up‐regulated and may play a role remyelination regenerating peripheral nerves. In present study, sciatic was investigated mutant mice. Histological results showed that number myelinated axons thickness myelin sheath injured nerves were reduced mice compared with wild‐type...

10.1111/j.1471-4159.2005.03564.x article EN Journal of Neurochemistry 2005-11-29

Mature brain-derived neurotrophic factor (mBDNF) plays a vital role in the nervous system, whereas proBDNF elicits neurodegeneration and neuronal apoptosis. Although current enzyme-linked immunosorbent assay (ELISA) has been widely used to measure BDNF levels, it cannot differentiate mBDNF from proBDNF. As function of differs mBDNF, is necessary establish an ELISA specific for detection mBDNF. Therefore, we aimed new mBDNF-specific sandwich ELISA. In this study, have screened found...

10.1111/jnc.13108 article EN Journal of Neurochemistry 2015-04-01

Abstract Purpose: Although Bruton tyrosine kinase (BTK) inhibitors have demonstrated promising efficacy in patients with Waldenström macroglobulinemia (WM), data Asian populations are scarce. This trial is the first to investigate effect of a BTK inhibitor Chinese relapsed/refractory (R/R) WM. Patients and Methods: R/R WM at least one prior regimen were enrolled into this single-arm, multicenter, phase II study (NCT03332173) received zanubrutinib 160 mg twice daily until disease progression...

10.1158/1078-0432.ccr-21-0539 article EN cc-by-nc-nd Clinical Cancer Research 2021-07-12

Sortilin, a Golgi sorting protein and member of the VPS10P family, is co-receptor for proneurotrophins, regulates trafficking, targets proteins to lysosomes, low density lipoprotein metabolism. The aim this study was investigate expression regulation sortilin in Alzheimer's disease (AD). A significantly increased level found human AD brain brains 6-month-old swedish-amyloid precursor protein/PS1dE9 transgenic mice. Aβ₄₂ enhanced mRNA levels dose- time-dependent manner SH-SY5Y cells, but had...

10.1111/jnc.12383 article EN Journal of Neurochemistry 2013-07-30

J. Neurochem . (2012) 122 , 1010–1022. Abstract Amyloid precursor protein (APP) is involved in the pathogenesis of Alzheimer’s disease. It axonally transported, endocytosed and sorted to different cellular compartments where amyloid beta (Aβ) produced. However, mechanism APP trafficking remains unclear. We present evidence that huntingtin associated 1 (HAP1) may reduce Aβ production by regulating non‐amyloidogenic pathway. HAP1 are highly colocalized a number brain regions, with similar...

10.1111/j.1471-4159.2012.07845.x article EN Journal of Neurochemistry 2012-06-25

The processing of Amyloid precursor protein (APP) is multifaceted, comprising transport, internalization and sequential proteolysis. However, the exact mechanism APP intracellular trafficking distribution remains unclear. To determine interaction between sortilin effect on processing, we studied binding site its function by mapping experiments, colocalization, coimmunoprecipitation sucrose gradient fractionation. We identified for first time that interacts with at both N- C-terminal regions....

10.1371/journal.pone.0063049 article EN cc-by PLoS ONE 2013-05-21

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive deposition of amyloid beta (Aβ) and dysregulation neurotrophic signaling, causing synaptic dysfunction, loss memory, cell death. The expression p75 neurotrophin receptor elevated in the brain AD patients, suggesting its involvement this disease. However, exact mechanism action not yet clear. Here, we show that interacts with beta-site precursor protein cleaving enzyme-1 (BACE1), interaction enhanced...

10.1111/jnc.14206 article EN Journal of Neurochemistry 2017-09-04
Coming Soon ...