Jasmin Bartl

ORCID: 0000-0002-8737-2610
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About
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Research Areas
  • Attention Deficit Hyperactivity Disorder
  • Alzheimer's disease research and treatments
  • Glioma Diagnosis and Treatment
  • Neurotransmitter Receptor Influence on Behavior
  • Parkinson's Disease Mechanisms and Treatments
  • Cancer-related molecular mechanisms research
  • Genetic Neurodegenerative Diseases
  • Nuclear Receptors and Signaling
  • Bipolar Disorder and Treatment
  • Hedgehog Signaling Pathway Studies
  • Chromatin Remodeling and Cancer
  • Circular RNAs in diseases
  • Diet and metabolism studies
  • Protein Degradation and Inhibitors
  • Ginkgo biloba and Cashew Applications
  • Dementia and Cognitive Impairment Research
  • Mitochondrial Function and Pathology
  • Acute Lymphoblastic Leukemia research
  • Tryptophan and brain disorders
  • Pluripotent Stem Cells Research
  • Autism Spectrum Disorder Research
  • Neuroscience and Neural Engineering
  • Genetics and Neurodevelopmental Disorders
  • Genomics and Chromatin Dynamics
  • Ferroptosis and cancer prognosis

Düsseldorf University Hospital
2017-2025

Heinrich Heine University Düsseldorf
2016-2025

German Cancer Research Center
2018-2024

Deutschen Konsortium für Translationale Krebsforschung
2019-2024

Universität Hamburg
2022-2024

Heidelberg University
2018-2023

University Hospital of Zurich
2013-2018

University of Zurich
2013-2018

Universitätsklinikum Würzburg
2011-2012

University of Würzburg
2007-2010

Excitatory neurotransmitter dysfunction has been discussed to be involved in the pathophysiology of Alzheimer's disease (AD). In current study we investigated gene and protein expression patterns glutamatergic receptors transporters brains AD patients various stages using chip arrays, real time PCR immunohistochemistry. We found marked impairment excitatory amino acid (EAAT1 EAAT 2) at both levels hippocampus gyrus frontalis medialis patients, already early clinical disease. The loss...

10.3233/jad-2007-11113 article EN Journal of Alzheimer s Disease 2007-03-01

Background While major advances have been made in improving the quality of life and survival children with most forms medulloblastoma (MB), those MYC-driven tumors (Grp3-MB) still suffer significant morbidity mortality. There is an urgent need to explore multimodal therapeutic regimens which are effective safe for children. Large-scale studies revealed abnormal cancer epigenomes caused by mutations structural alterations chromatin modifiers, aberrant DNA methylation, histone modification...

10.1136/jitc-2022-005871 article EN cc-by-nc Journal for ImmunoTherapy of Cancer 2023-01-01

Abstract Glioblastoma is the most common malignant primary brain tumor. To date, clinically relevant biomarkers are restricted to isocitrate dehydrogenase (IDH) gene 1 or 2 mutations and O6-methylguanine DNA methyltransferase ( MGMT ) promoter methylation. Long non-coding RNAs (lncRNAs) have been shown contribute glioblastoma pathogenesis could potentially serve as novel biomarkers. The clinical significance of HOXA Transcript Antisense RNA, Myeloid-Specific HOTAIRM1 was determined by...

10.1038/s41419-021-04146-0 article EN cc-by Cell Death and Disease 2021-09-28

Most lncRNAs display species-specific expression patterns suggesting that animal models of cancer may only incompletely recapitulate the regulatory crosstalk between and oncogenic pathways in humans. Among these pathways, Sonic Hedgehog (SHH) signaling is aberrantly activated several human entities. We unravel aberrant primate-specific lncRNA HedgeHog Interacting Protein-AntiSense 1 (HHIP-AS1) a hallmark SHH-driven tumors including medulloblastoma atypical teratoid/rhabdoid tumors. HHIP-AS1...

10.1038/s41467-022-31574-z article EN cc-by Nature Communications 2022-07-13

Alzheimer's disease (AD), the most common cause of dementia, is a progressive neurodegenerative disease. At present, diagnosis AD rather late in Therefore, we attempted to find peripheral biomarkers for early AD. We investigated profiles 33 genes, previously found by our group have altered expression postmortem brains The gene were studied via quantitative-real-time-reverse-transcription-polymerase-chain-reaction, whole blood samples (collected with PAXgene RNA system) isolated from...

10.3233/jad-2009-0996 article EN Journal of Alzheimer s Disease 2009-03-09

Sporadic Alzheimer's (AD) and Parkinson's disease (PD) are late-onset neurodegenerative diseases with tremendous impact on lives of affected individuals. There is a great probability developing concurrent Parkinsonism in AD vice-versa than would be predicted by independent prevalence each disease. We hypothesize that sporadic as well PD combination environmental effects gene expression may affect specific brain areas leading to neurodegeneration. profiled compared age matched controls...

10.3233/jad-2007-12402 article EN Journal of Alzheimer s Disease 2007-12-25

Abstract Background Intratumoral heterogeneity is crucially involved in metastasis, resistance to therapy, and cancer relapse. Amplifications of the proto-oncogene MYC display notable at single-cell level are associated with a particularly dismal prognosis high-risk medulloblastomas (MBs). The aim this study was establish relevance interclonal cross-talk between MYC-driven non-MYC-driven MB cells. Methods We used fluorescence situ hybridization, transcriptomics, immunohistochemistry, vitro...

10.1093/neuonc/noac068 article EN Neuro-Oncology 2022-03-17

The hallmarks of sporadic Alzheimer's disease (AD) are extracellular amyloid deposits, intracellular neurofibrillary tangles (NFTs), and neuronal death. Hyperphosphorylation tau is a key factor in the generation NFTs. Mitogen activated protein kinase 1 (MAPK1) C beta (PRKCB) thought to play role hyperphosphorylation, PRCKB be involved hypoxic stress vascular dysfunction, trigger MAPK phosphorylation pathways. We performed single-cell analyses neurons with different vulnerabilities AD-related...

10.3233/jad-131280 article EN Journal of Alzheimer s Disease 2014-03-10

The spontaneously hypertensive rat (SHR) has been used to model changes in the central nervous system associated with cognitive-related disorders. Recent human and animal studies indicate a possible relationship between cognitive deficits, insulin resistance hypertension. We aimed investigate whether cognitively impaired SHRs develop and/or peripheral how their performance is influenced by animal's sex age as well strains for comparison (Wistar Wistar-Kyoto/WKY).Three seven-month-old SHR,...

10.1186/s40303-015-0012-6 article EN cc-by Journal of Molecular Psychiatry 2015-06-03

Abstract Methylphenidate (Ritalin) is the most commonly prescribed drug in treatment of attention-deficit hyperactivity disorder. It suggested that vivo, methylphenidate supports cortical maturation, however, molecular and cellular mechanisms are not well understood. This study aimed to explore potential effect on cell proliferation maturation various models, hypothesizing its interaction with Wnt-signaling. The termination concomitant neuronal following was observed all cell-models tested:...

10.1038/s41398-018-0096-8 article EN cc-by Translational Psychiatry 2018-02-28

Objectives. Although Alzheimer's disease (AD) is the most common form of dementia in elderly, its aetiology remains mostly unknown. A potential pathophysiological mechanism for AD arises from knowledge that insulin also synthesized independently central nervous system and involved regulation memory formation. may represent a brain-specific resistance. Methods. We used immunohistochemistry to investigate numbers cells expressing receptor β-subunit (IRβ) phosphorylated PPARγ (PPARγ(p)) human...

10.3109/15622975.2011.650204 article EN The World Journal of Biological Psychiatry 2012-02-14

The psychostimulant methylphenidate (MPH) is the first choice of drug treatment in Attention-Deficit/Hyperactivity Disorder (ADHD). Since therapy often begins at a time when brain still developing and long-term consequences MPH are not fully clarified, we examined influences an acute with on differentiation proliferation murine neural stem cells (mNSC).We found that enhanced neuronal inhibited proliferation.

10.1186/2049-9256-1-5 article EN cc-by Journal of Molecular Psychiatry 2013-01-01
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