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@ARTICLE{Bhattarai:145133,
author = {Bhattarai, Prabesh and Cosacak, Mehmet Ilyas and
Mashkaryan, Violeta and Demir, Sevgican and Popova,
Stanislava Dimitrova and Govindarajan, Nambirajan and
Brandt, Kerstin and Zhang, Yixin and Chang, Weipang and
Ampatzis, Konstantinos and Kizil, Caghan},
title = {{N}euron-glia interaction through {S}erotonin-{BDNF}-{NGFR}
axis enables regenerative neurogenesis in {A}lzheimer's
model of adult zebrafish brain.},
journal = {PLoS biology},
volume = {18},
number = {1},
issn = {1545-7885},
address = {Lawrence, KS},
publisher = {PLoS},
reportid = {DZNE-2020-00492},
pages = {e3000585},
year = {2020},
abstract = {It was recently suggested that supplying the brain with new
neurons could counteract Alzheimer's disease (AD). This
provocative idea requires further testing in experimental
models in which the molecular basis of disease-induced
neuronal regeneration could be investigated. We previously
found that zebrafish stimulates neural stem cell (NSC)
plasticity and neurogenesis in AD and could help to
understand the mechanisms to be harnessed for developing new
neurons in diseased mammalian brains. Here, by performing
single-cell transcriptomics, we found that amyloid
toxicity-induced interleukin-4 (IL4) promotes NSC
proliferation and neurogenesis by suppressing the tryptophan
metabolism and reducing the production of serotonin. NSC
proliferation was suppressed by serotonin via
down-regulation of brain-derived neurotrophic factor
(BDNF)-expression in serotonin-responsive periventricular
neurons. BDNF enhances NSC plasticity and neurogenesis via
nerve growth factor receptor A (NGFRA)/ nuclear factor
'kappa-light-chain-enhancer' of activated B-cells (NFkB)
signaling in zebrafish but not in rodents. Collectively, our
results suggest a complex neuron-glia interaction that
regulates regenerative neurogenesis after AD conditions in
zebrafish.},
keywords = {Age Factors / Alzheimer Disease: genetics / Alzheimer
Disease: pathology / Alzheimer Disease: physiopathology /
Animals / Animals, Genetically Modified / Brain: metabolism
/ Brain: physiology / Brain-Derived Neurotrophic Factor:
genetics / Brain-Derived Neurotrophic Factor: metabolism /
Cell Communication: physiology / Disease Models, Animal /
Male / Mice / Mice, Transgenic / Nerve Regeneration:
genetics / Nerve Regeneration: physiology / Neural Stem
Cells: pathology / Neural Stem Cells: physiology /
Neurogenesis: physiology / Neuroglia: physiology /
Neuroimmunomodulation: physiology / Neuronal Plasticity:
physiology / Neurons: physiology / Receptors, Nerve Growth
Factor: genetics / Receptors, Nerve Growth Factor:
metabolism / Serotonin: genetics / Serotonin: metabolism /
Signal Transduction: genetics / Zebrafish / Zebrafish
Proteins: genetics / Zebrafish Proteins: metabolism /
Brain-Derived Neurotrophic Factor (NLM Chemicals) /
Receptors, Nerve Growth Factor (NLM Chemicals) / Zebrafish
Proteins (NLM Chemicals) / Serotonin (NLM Chemicals)},
cin = {AG Kizil / AG Kempermann 1 / Dresden Pre 2020 / AG Fischer
1},
ddc = {610},
cid = {I:(DE-2719)1710007 / I:(DE-2719)1710001 /
I:(DE-2719)6000013 / I:(DE-2719)1410002},
pnm = {341 - Molecular Signaling (POF3-341) / 342 - Disease
Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31905199},
pmc = {pmc:PMC6964913},
doi = {10.1371/journal.pbio.3000585},
url = {https://pub.dzne.de/record/145133},
}