Xin Wang

ORCID: 0000-0001-7440-3150
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Cholinesterase and Neurodegenerative Diseases
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Mitochondrial Function and Pathology
  • Epigenetics and DNA Methylation
  • Sleep and Wakefulness Research
  • Tryptophan and brain disorders
  • Autophagy in Disease and Therapy
  • Neurological Disease Mechanisms and Treatments
  • Neuroscience of respiration and sleep
  • Genetics and Neurodevelopmental Disorders
  • Cancer, Hypoxia, and Metabolism
  • Diet and metabolism studies
  • Obstructive Sleep Apnea Research
  • Ubiquitin and proteasome pathways
  • Neurotransmitter Receptor Influence on Behavior
  • Dementia and Cognitive Impairment Research
  • Neuroblastoma Research and Treatments
  • Nutrition and Health in Aging
  • Stress Responses and Cortisol
  • Regulation of Appetite and Obesity
  • Nuclear Receptors and Signaling
  • Neuroendocrine regulation and behavior

Xiamen University
2018-2025

Huazhong University of Science and Technology
2015-2024

Shenzhen University
2024

First Affiliated Hospital of Xiamen University
2024

Union Hospital
2024

Jinan City People's Hospital
2024

Shandong First Medical University
2024

Nantong University
2023-2024

Chinese PLA General Hospital
2024

University of Toledo
2018-2023

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

Abstract The basolateral amygdala (BLA) and ventral hippocampal CA1 (vCA1) are cellularly functionally diverse along their anterior–posterior superficial-deep axes. Here, we find that anterior BLA (aBLA) posterior (pBLA) innervate deep-layer calbindin1-negative (Calb1−) superficial-layer calbindin1-positive neurons (Calb1+) in vCA1, respectively. Photostimulation of pBLA–vCA1 inputs has an anxiolytic effect mice, promoting approach behaviours during conflict exploratory tasks. By contrast,...

10.1038/s41467-019-13919-3 article EN cc-by Nature Communications 2020-01-10

Abstract Different emotional states lead to distinct behavioural consequences even when faced with the same challenging events. Emotions affect learning and memory capacities, but underlying neurobiological mechanisms remain elusive. Here we establish models of learned helplessness (LHL) hopefulness (LHF) by exposing animals inescapable foot shocks or anticipated avoidance trainings. The LHF show spatial potentiation excitatory monosynaptic upscaling between posterior basolateral amygdale...

10.1038/ncomms11935 article EN cc-by Nature Communications 2016-07-14

Trimethylamine-N-oxide (TMAO), a metabolite of gut microbiota, has been implicated in the pathogenesis Alzheimer's disease (AD). However, mechanisms by which TMAO influence cognitive and pathological processes AD have not investigated. In this study, we found that circulating levels displayed an age-related increase both WT APP/PS1 mice association with AD-like behavioral profile. Reduced 3,3-Dimethyl-1-butanol (DMB) treatment ameliorated deterioration long-term potentiation (LTP) mice....

10.18632/aging.102352 article EN cc-by Aging 2019-10-14

Increased tau acetylation at K274 and K281 has been observed in the brains of Alzheimer's disease (AD) patients animal models, mitochondrial dysfunction are noticeable early features AD. However, effect acetylated on mitochondria unclear until now. Here, we constructed three type forms, mutant by mutating its K274/K281 into Glutamine (TauKQ) to mimic disease-associated lysine acetylation, non-acetylation Arginine (TauKR) wild-type human full-length (TauWT). By overexpression these forms vivo...

10.1016/j.redox.2023.102697 article EN cc-by-nc-nd Redox Biology 2023-04-06

Abstract Impaired brain glucose metabolism is an early indicator of Alzheimer’s disease (AD); however, the fundamental mechanism unknown. In this study, we found a substantial decline in isocitrate dehydrogenase 3β (IDH3β) levels, critical tricarboxylic acid cycle enzyme, AD patients and AD-transgenic mice’s brains. Further investigations demonstrated that knockdown IDH3β induced oxidation-phosphorylation uncoupling, leading to reduced energy lactate accumulation. The resulting increased...

10.1038/s41392-024-01812-5 article EN cc-by Signal Transduction and Targeted Therapy 2024-04-28

The probiotic Escherichia coli Nissle (EcN) is an exceptional strain that has attracted significant attention not only for its clinical efficacy in the treatment and prevention of gastrointestinal disorders but also as a burgeoning microbial chassis living therapeutic applications. However, there immediate necessity to develop conditional expression systems confine activity EcN specifically tract, avoid influencing environment. Here, we constructed two genetically encoded interchangeable...

10.1021/acssynbio.4c00747 article EN ACS Synthetic Biology 2025-01-08

Abstract Generalization is a fundamental cognitive ability of organisms to deal with the uncertainty in real-world situations. Excessive fear generalization and impaired reward are closely related many psychiatric disorders. However, neural circuit mechanism for its role anxiety-like behaviours remain elusive. Here, we found robust activation calbindin 1-neurons (Calb 1) posterior basolateral amygdala (pBLA), simultaneous an ambiguous cue after conditioning mice. We identify infralimbic...

10.1038/s41467-022-33139-6 article EN cc-by Nature Communications 2022-09-17

Abstract Background Episodic memory loss is a prominent clinical manifestation of Alzheimer’s disease (AD), which closely related to tau pathology and hippocampal impairment. Due the heterogeneity brain neurons, specific roles different neurons in terms their sensitivity accumulation contribution AD-like social remain unclear. Therefore, further investigation necessary. Methods We investigated effects by Tandem mass tag proteomic phosphoproteomic analysis, behavioural tests,...

10.1186/s40779-024-00512-z article EN cc-by Military Medical Research 2024-03-11

BackgroundBoth type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) are common age-associated disorders T2DM patients show an increased risk to suffer from AD, however, there is currently no marker identify who in populations will develop AD. Since glycogen synthase kinase-3β (GSK-3β) activity, ApoE genotypes olfactory function involved both AD pathogenesis, we investigate whether alterations of these factors can cognitive impairment patients.MethodsThe ability was evaluated using...

10.1016/j.ebiom.2016.02.014 article EN cc-by-nc-nd EBioMedicine 2016-02-07

It has been suggested that excessive reactive oxygen species (ROS) and oxidative stress play an important role in ethanol-induced damage to both the developing mature central nervous system (CNS). The mechanisms underlying neuronal ROS, however, remain unclear. In this study, we investigated of NADPH oxidase (NOX) ROS generation. We demonstrated ethanol activated NOX inhibition reduced ethanol-promoted Ethanol significantly increased expression p47phox p67phox, essential subunits for...

10.1371/journal.pone.0038075 article EN cc-by PLoS ONE 2012-05-25

Abstract Abnormal aggregation of pathological tau protein is a neuropathological feature Alzheimer’s disease (AD). In the AD patients, abnormal accumulation first appeared in entorhinal cortex (EC) and then propagated to hippocampus with microglia activation inflammation, but mechanism elusive. Here, we studied role mechanisms underlying periphery inflammation on brain transmission. By intraperitoneal injection lipopolysaccharide (LPS) medial (MEC)-specific overexpressing P301L human...

10.1042/bsr20193629 article EN Bioscience Reports 2020-02-01

Respiratory depression is the main cause of morbidity and mortality associated with opioids. Obesity increases opioid-related mortality, which mostly related to comorbid obstructive sleep apnea. Naloxone, a μ-opioid receptor blocker, an effective antidote, but it reverses analgesia. Like humans obesity, mice diet-induced obesity hypoventilate during develop apnea, can be treated intranasal leptin. We hypothesized that leptin opioid-induced sleep-disordered breathing in obese without...

10.1165/rcmb.2020-0117oc article EN American Journal of Respiratory Cell and Molecular Biology 2020-06-30

Abstract Cholinergic impairments and tau accumulation are hallmark pathologies in sporadic Alzheimer’s disease (AD), however, the intrinsic link between cholinergic deficits is missing. Here, we found that overexpression of human wild-type full-length (termed hTau) induced a significant reduction α4 subunit nicotinic acetylcholine receptors (nAChRs) with an increased cleavage receptor producing ~55kDa fragment primary hippocampal neurons rat brains, meanwhile, nAChR currents decreased....

10.1038/srep27283 article EN cc-by Scientific Reports 2016-06-09

Abstract Abnormal tau accumulation and spatial memory loss constitute characteristic pathology symptoms of Alzheimer disease (AD). Yet, the intrinsic connections mechanism between them are not fully understood. In current study, we observed a prominent AD‐like hyperphosphorylated truncated (hTau N368) proteins in hippocampal dentate gyrus (DG) mossy cells 3xTg‐AD mice. Further investigation demonstrated that ventral DG (vDG) cell‐specific overexpressing hTau for 3 months induced cognitive...

10.1111/acel.13600 article EN cc-by Aging Cell 2022-03-31

Abstract In tauopathies, memory impairment positively strongly correlates with the amount of abnormal tau aggregates; however, how accumulation induces synapse is unclear. Recently, we found that human activated Signal Transduction and Activator Transcription-1 (STAT1) to inhibit transcription synaptic N-methyl-D-aspartate receptors (NMDARs). Here, overexpressing P301L mutant (P301L-hTau) increased phosphorylated level Transcription-3 (STAT3) at Tyr705 by JAK2, which would promote STAT3...

10.1038/s41392-020-00290-9 article EN cc-by Signal Transduction and Targeted Therapy 2020-12-26

To investigate the characteristics of three-dimensional distribution subchondral fracture lines on surface osteonecrosis femoral head, and to discuss underlying mechanisms that contribute its collapse. We retrospectively analyzed computed tomography (CT) images from 75 patients (comprising a total 77 heads) diagnosed with Association Research Circulation Osseous (ARCO) stage IIIA or IIIB head necrosis. The structures both line were reconstructed subsequently fitted into normal model. A heat...

10.1016/j.jot.2024.06.004 article EN cc-by-nc-nd Journal of Orthopaedic Translation 2024-06-20
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