Jie Zhang

ORCID: 0000-0003-1040-5848
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Microtubule and mitosis dynamics
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Mitochondrial Function and Pathology
  • Tryptophan and brain disorders
  • Cancer-related Molecular Pathways
  • Ubiquitin and proteasome pathways
  • Amino Acid Enzymes and Metabolism
  • Memory and Neural Mechanisms
  • Trace Elements in Health
  • Cholinesterase and Neurodegenerative Diseases
  • Adipose Tissue and Metabolism
  • Medicinal Plants and Neuroprotection
  • Sirtuins and Resveratrol in Medicine
  • Circadian rhythm and melatonin
  • Stress Responses and Cortisol
  • Genetic Neurodegenerative Diseases
  • Microbial metabolism and enzyme function
  • Telomeres, Telomerase, and Senescence
  • Aluminum toxicity and tolerance in plants and animals
  • Machine Learning in Bioinformatics
  • Tuberous Sclerosis Complex Research
  • Adenosine and Purinergic Signaling
  • Chromatin Remodeling and Cancer

Xiamen University
2012-2025

Hebei Medical University
2024-2025

Fujian Medical University
2022-2025

First Affiliated Hospital of Xiamen University
2023-2024

Union Hospital
2023

Indiana University – Purdue University Indianapolis
2022

Indiana University School of Medicine
2022

First Affiliated Hospital of Nanchang University
2020

Nanchang University
2020

First People's Hospital of Yunnan Province
2020

Hyperglycemia accelerates Alzheimer's disease (AD) progression, yet the role of monosaccharides remains unclear. Here, it is demonstrated that mannose, a hexose, closely correlates with pathological characteristics AD, as confirmed by measuring mannose levels in brains and serum AD mice, well patients. mice are given intra-cerebroventricular injection (ICV) or drinking water to investigate effects on cognition progression. Chronic overload increases β-amyloid (Aβ) burdens exacerbates...

10.1002/advs.202409105 article EN cc-by Advanced Science 2025-01-14

Cerebral energy metabolism in Alzheimer disease (AD) has recently been given increasing attention. This study focuses on the alterations of cerebral lactate double-transgenic amyloid precursor protein/presenilin 1 (APP/PS1) mouse model AD. Immunofluorescence staining and Western blotting analysis were used to identify content transporters (MCT1, MCT2, MCT4) APP/PS1 brains, which display beta plaques, reduced amounts neurons oligodendrocytes, increased quantity astrocytes. We found that...

10.1093/jnen/nly102 article EN Journal of Neuropathology & Experimental Neurology 2018-11-01

Significance CDK5 and GSK3β are recognized as interrelated kinases; they share a strong structural resemblance, both known tau kinases that contribute to the etiology of Alzheimer’s disease. We report here p25 but not p35, normal cyclin-like activator CDK5, unexpectedly binds in AXIN-binding region. The binding increases activity alters its substrate specificity. Results, vivo vitro, suggest many effects previously assumed be due hyperactivation must now reexamined for potential role altered...

10.1073/pnas.1402627111 article EN Proceedings of the National Academy of Sciences 2014-10-20

Abstract Background Nuclear acetyl-CoA pools govern histone acetylation that controls synaptic plasticity and contributes to cognitive deterioration in patients with Alzheimer’s disease (AD). are generated partially from local acetate is metabolized by synthetase 2 (ACSS2). However, the underlying mechanism of dysregulation AD remains poorly understood. Methods We detected ACSS2 expression levels brains 5 × FAD mice. When we altered injecting adeno-associated virus into dorsal hippocampus...

10.1186/s13024-023-00625-4 article EN cc-by Molecular Neurodegeneration 2023-07-12

Aging is a systemic process, which risk factor for impaired physiological functions, and finally death. The molecular mechanisms driving aging process the associated cognitive decline are not fully understood. hypothalamus acts as arbiter that orchestrates through neuroinflammatory signaling. Our recent findings revealed Menin plays important roles in neuroinflammation brain development. Here, we found hypothalamic signaling diminished aged mice, correlates with deficits. Restoring...

10.1371/journal.pbio.3002033 article EN cc-by PLoS Biology 2023-03-16

Objective This study aimed to evaluate the effects of intermittent energy restriction (IER; only for 2‐3 d/wk) versus continuous (CER) on weight loss and metabolic outcomes in adults with overweight or obesity. Methods included searching databases from last decade December 18, 2019, randomized controlled trials (RCTs) that assessed IER CER. RevMan version 5.3 software was used statistical analysis data. The effect sizes were expressed as mean differences 95% CI. Results review 11 RCTs ( n =...

10.1002/oby.23023 article EN Obesity 2020-12-21

Bile acids (BAs) metabolism has a significant impact on the pathogenesis of Alzheimer’s disease (AD). We found that deoxycholic acid (DCA) increased in brains AD mice at an early stage. The enhanced production DCA induces up-regulation bile receptor Takeda G protein-coupled (TGR5), which is also specifically neurons mouse accumulation exogenous impairs cognitive function wild-type mice, but not TGR5 knockout mice. This suggests primary mediating these effects DCA. Furthermore, excitatory...

10.1126/sciadv.ado1855 article EN cc-by-nc Science Advances 2024-06-28

Abstract Dysregulation of mitochondrial dynamics is a key contributor to the pathogenesis Parkinson's disease (PD). Aberrant fission induced by dynamin‐related protein 1 (DRP1) causes dysfunction in dopaminergic (DA) neurons. However, mechanism DRP1 activation and its role PD progression remain unclear. In this study, Mass spectrometry analysis performed identified significant increased acetylation at lysine residue 711 (K711) mitochondria under oxidative stress. Enhanced K711 facilitated...

10.1002/advs.202411235 article EN cc-by Advanced Science 2025-02-20

In a variety of neurodegenerative disease, despite the frequent correlation neuronal cell cycle and death in same populations, mechanistic pathway linking two remains undefined. One possible link is atypical cyclin dependent kinase, Cdk5. Cdk5 exerts double protective function neurons, first by suppressing nucleus second cytoplasm. transport between cytoplasm serves to regulate balance these events. nuclear localization relies on its interaction with p27, suppression activity achieved direct...

10.4161/cc.10.8.15328 article EN Cell Cycle 2011-04-15

10.1074/jbc.m112.343152 article EN cc-by Journal of Biological Chemistry 2012-06-01

Synaptic protein dyshomeostasis and functional loss is an early invariant feature of Alzheimer's disease (AD), yet the unifying etiological pathway remains largely unknown. Knowing that cyclin-dependent kinase 5 (CDK5) plays critical roles in synaptic formation degeneration, its phosphorylation targets were reexamined search candidates with direct global impacts on dynamics, associated regulatory network was also analyzed.

10.1016/j.biopsych.2019.11.013 article EN cc-by-nc-nd Biological Psychiatry 2019-11-21

The accumulation of amyloid-β protein precursor (AβPP) is related to the pathogenesis Alzheimer's disease (AD); however, underlying mechanism still unclear. abnormal interactions AβPP with metal ions such as iron are implicated in process oxidative stress AD brains. In this study, we found that overexpression wild-type human AβPP695 decreased content and increased neuroblastoma SH-SY5Y cells. catalase activity stably transfected cells overexpressing (AβPP cells) was significantly lower than...

10.3233/jad-2012-111169 article EN Journal of Alzheimer s Disease 2012-06-04

Vincamine is a plant alkaloid used clinically as peripheral vasodilator that increases cerebral blood flow and oxygen glucose utilization by neural tissue to combat the effect of aging. The main purpose present study investigate influence vincamine on amyloid-β 25-35 (Aβ25-35) induced cytotoxicity, gain better understanding neuroprotective effects this anti-Alzheimer's disease drug.Oxidative stress was assessed measuring malondialdehyde, glutathione, superoxide dismutase (SOD) levels. Cell...

10.4103/0973-1296.196309 article EN Pharmacognosy Magazine 2016-12-20

Abstract Dysfunction of parvalbumin (PV) neurons is closely involved in depression, however, the detailed mechanism remains unclear. Based on previous finding that multiple endocrine neoplasia type 1 (Protein: Menin; Gene: Men1 ) mutation (G503D) associated with a higher risk Menin‐G503D mouse model generated exhibits heritable depressive‐like phenotypes and increases PV expression brain. This study generates screens serial neuronal specific deletion mice, found interneuron mice (PcKO)...

10.1002/advs.202305659 article EN cc-by Advanced Science 2023-12-03

Abstract FOXG1 syndrome is a developmental encephalopathy caused by (Forkhead box G1) mutations, resulting in high phenotypic variability. However, the upstream transcriptional regulation of Foxg1 expression remains unclear. This report demonstrates that both deficiency and overexpression Men1 (protein: menin, pathogenic gene MEN1 known as multiple endocrine neoplasia type 1) lead to autism‐like behaviors, such social defects, increased repetitive cognitive impairments. Multifaceted...

10.1002/advs.202307953 article EN cc-by Advanced Science 2024-04-06
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