Jian‐Zhi Wang

ORCID: 0000-0003-3569-9715
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Cholinesterase and Neurodegenerative Diseases
  • 14-3-3 protein interactions
  • Mitochondrial Function and Pathology
  • Microtubule and mitosis dynamics
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Folate and B Vitamins Research
  • Wnt/β-catenin signaling in development and cancer
  • Endoplasmic Reticulum Stress and Disease
  • Tryptophan and brain disorders
  • Protein Tyrosine Phosphatases
  • Nuclear Receptors and Signaling
  • Amino Acid Enzymes and Metabolism
  • Trace Elements in Health
  • Ubiquitin and proteasome pathways
  • Circadian rhythm and melatonin
  • Protein Kinase Regulation and GTPase Signaling
  • Cellular transport and secretion
  • Genetics and Neurodevelopmental Disorders
  • Dementia and Cognitive Impairment Research
  • Memory and Neural Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Epigenetics and DNA Methylation
  • Prion Diseases and Protein Misfolding

Huazhong University of Science and Technology
2016-2025

Nantong University
2015-2024

Jianghan University
2021-2024

Tongji Hospital
2006-2024

Wuhan Institute of Technology
2016-2024

Hunan Normal University
2023

University of South China
2023

Xinxiang Medical University
2019-2023

First Affiliated Hospital of Xinxiang Medical University
2023

Northeast Agricultural University
2023

Abstract: Microtubule‐associated protein τ is abnormally hyperphosphorylated and aggregated in affected neurons of Alzheimer disease brain. This can be dephosphorylated at some the abnormal phosphorylated sites by purified phosphatase‐1, 2A, 2B vitro. In present study, we have developed an assay to measure phosphatase activity toward τ‐1 (Ser 199 /Ser 202 ) using isolated from brain as substrate. Using this assay, identified that normal brain, phosphatase‐2A and, a lesser extent, 1 are...

10.1046/j.1471-4159.1995.65020732.x article EN Journal of Neurochemistry 1995-08-01

Intracellular accumulation of tau is a hallmark pathology in Alzheimer disease (AD) and the related tauopathies, thus targeting could be promising for drug development. Proteolysis Targeting Chimera (PROTAC) novel discovery strategy selective protein degradation from within cells.

10.7150/thno.55680 article EN cc-by Theranostics 2021-01-01

Microtubule-associated protein τ is abnormally hyperphosphorylated in the brain of patients with Alzheimer disease and this form major subunit paired helical filaments (PHF), most prominent lesion disease. In study dephosphorylation sparingly soluble PHF, PHF II-τ by phosphatase (PP)-2A1 PP-2B, resulting biochemical, biological, structural alterations were investigated. Both phosphatases dephosphorylated at sites Ser-199/Ser-202 partially it Ser-396/Ser-404; addition, was Ser-46 PP-2A1...

10.1074/jbc.270.9.4854 article EN cc-by Journal of Biological Chemistry 1995-03-01

Activation of glycogen synthase kinase-3 (GSK-3) can cause memory deficits as seen in Alzheimer's disease, the most common age-associated dementia, but mechanism is not understood. Here, we found that activation GSK-3 by wortmannin or transient overexpression wild-type GSK-3beta could suppress induction long-term potentiation (LTP) rat hippocampus, whereas simultaneous inhibition lithium SB216763 expression a dominant-negative mutant (dnGSK-3beta) preserved LTP. After high-frequency...

10.1523/jneurosci.3321-07.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-11-07

Intracellular accumulation of wild-type tau is a hallmark sporadic Alzheimer's disease (AD), but the molecular mechanisms underlying tau-induced synapse impairment and memory deficit are poorly understood. Here we found that overexpression human full-length (termed hTau) induced deficits with impairments synaptic plasticity. Both in vivo vitro data demonstrated hTau caused remarkable dephosphorylation cAMP response element binding protein (CREB) nuclear fraction. Simultaneously,...

10.1073/pnas.1604519113 article EN Proceedings of the National Academy of Sciences 2016-06-13

Brain iron deposition has been proposed to play an important role in the pathophysiology of neurodegenerative diseases. The aim this study was investigate correlation brain accumulation with severity cognitive impairment patients Alzheimer disease (AD).This approved by institutional review board Tongji Hospital (Wuhan, China) and written informed consent obtained from all participants. Fifteen AD, 15 age-and sex-matched healthy controls, 30 volunteers underwent high-resolution magnetic...

10.1148/radiol.2532082324 article EN Radiology 2009-08-27

Abstract Hyperhomocysteinemia (Hhcy) may induce memory deficits with β‐amyloid (Aβ) accumulation and tau hyperphosphorylation. Simultaneous supplement of folate vitamin B12 partially restored the plasma homocysteine level attenuated hyperphosphorylation, Aβ impairments induced by Hhcy. However, treatment have no effects on Hhcy which has methylenetetrahydrofolate reductase genotype mutation. In this study, we investigated simultaneous betaine Alzheimer‐like pathological changes in...

10.1111/jnc.12094 article EN Journal of Neurochemistry 2012-11-16

Accumulation of unfolded proteins can disturb the functions endoplasmic reticulum (ER), leading to ER-stress or protein response (UPR). Recent data have shown that activation UPR be found in postmortem brains Alzheimer's dis

10.3233/jad-2011-111037 article EN Journal of Alzheimer s Disease 2012-02-20

Collecting evidence has shown that type 2 diabetes mellitus is a high risk factor of late-onset Alzheimer's disease (AD); the energy metabolic dysfunction thought to be convergent point two diseases. However, underlying mechanisms diabetes-associated AD are still unclear. In current study, we investigated roles AMPK in diabetes-related AD-like pathologic features models intracerebroventricular-streptozotocin (ICV-STZ) animals. Rats infused with STZ (3 mg/kg, once) were followed by injection...

10.3233/jad-140564 article EN Journal of Alzheimer s Disease 2014-12-02

Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties synaptic plasticity. Recent studies have demonstrated the serum brain magnesium levels decreased in AD patients; however, exact role pathogenesis remains unclear. Here, we found intraperitoneal administration sulfate increased protected memory capacities streptozotocin-induced sporadic model rats. We also...

10.1371/journal.pone.0108645 article EN cc-by PLoS ONE 2014-09-30

10.1016/j.jtice.2016.10.004 article EN Journal of the Taiwan Institute of Chemical Engineers 2016-10-22

Glycogen synthase kinase-3β (GSK-3β) is one of the most effective kinases in promoting tau hyperphosphorylation and accumulation Alzheimer's disease (AD). However, it not clear how GSK-3β activity regulated during AD progression.We firstly used mass spectrometry to identify acetylation site GSK-3β, then established cell animal models acetylation. Next, we conducted molecular, biological behavioral tests. Finally, designed a peptide test whether blocking tau-mediated could be beneficial AD.We...

10.1016/j.ebiom.2022.103970 article EN cc-by-nc-nd EBioMedicine 2022-03-25

The unspecified impact of green innovation on corporate financial performance has made some enterprises delay investment plans, and even abandon innovation. Mitigating the economic concerns faced in process decision-making is great significance to accelerate enterprises’ transformation. Using an unbalanced panel data Chinese heavy pollution listed companies from 2008-2017, this paper investigates firm value. We further test likely channels through which can affect value, including...

10.3389/fenrg.2021.806926 article EN cc-by Frontiers in Energy Research 2022-01-20
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