Arnon Rosenthal

ORCID: 0000-0003-1885-3880
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About
Contact & Profiles
Research Areas
  • Nerve injury and regeneration
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Developmental Biology and Gene Regulation
  • Hedgehog Signaling Pathway Studies
  • Alzheimer's disease research and treatments
  • Zebrafish Biomedical Research Applications
  • Nuclear Receptors and Signaling
  • Inflammation biomarkers and pathways
  • Signaling Pathways in Disease
  • Parkinson's Disease Mechanisms and Treatments
  • Pluripotent Stem Cells Research
  • Autism Spectrum Disorder Research
  • RNA Interference and Gene Delivery
  • Glycosylation and Glycoproteins Research
  • Wnt/β-catenin signaling in development and cancer
  • Axon Guidance and Neuronal Signaling
  • Neurological Disease Mechanisms and Treatments
  • Viral Infectious Diseases and Gene Expression in Insects
  • Amyotrophic Lateral Sclerosis Research
  • Epigenetics and DNA Methylation
  • Tryptophan and brain disorders
  • Virus-based gene therapy research
  • Immune cells in cancer
  • Neurological disorders and treatments

Alector (United States)
2014-2024

Cofactor Genomics (United States)
2022

Annexon Biosciences (United States)
2013-2016

University of California, San Francisco
2016

Posit Science (United States)
2002-2011

Pfizer (United States)
2007-2009

Stanford University
1991-2004

Molecular Oncology (United States)
1998-2001

Genentech
1990-2000

Palmetto Hematology Oncology
1998

Too much cleaning up The complement system and microglia seek out destroy unwanted cellular debris for the peripheral immune as well excess synapses in developing brain. Hong et al. now show how may go haywire adults early progression toward Alzheimer's disease (AD). Aberrant synapse loss is an feature of correlates with cognitive decline. In mice susceptible to AD, was associated synapses, microglial function required loss. authors speculate that aberrant activation this “trash disposal”...

10.1126/science.aad8373 article EN Science 2016-04-01

For survival, embryonic motoneurons in vertebrates depend on as yet undefined neurotrophic factors present the limb bud. Members of neurotrophin family are currently best candidates for such factors, but inactivation their receptor genes leads to only partial loss motoneurons, which suggests that other involved. Glial cell line-derived factor (GDNF), originally identified a trophic specific dopaminergic neurons, was found be 75-fold more potent than neurotrophins supporting survival purified...

10.1126/science.7973664 article EN Science 1994-11-11

Recombinant human brain-derived neurotrophic factor (rhBDNF) and neurotrophin 3 (rhNT-3), two recently cloned molecules closely related to nerve growth (NGF), were produced from cDNA expressed in embryonic kidney cells. The recombinant proteins tested cultures of dissociated fetal rat brain cells containing basal forebrain cholinergic neurons. rhBDNF stimulated the differentiation neurons, similar NGF, which is well established as a for these However, was particularly effective during first...

10.1073/pnas.88.3.961 article EN Proceedings of the National Academy of Sciences 1991-02-01

Brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) are homologs of the well-known nerve growth factor. The three members this family display distinct patterns target specificity. To examine distribution in brain messenger RNA for these molecules, situ hybridization was performed. Cells hybridizing intensely to antisense BDNF probe were located throughout major targets rat basal forebrain cholinergic system, that is, hippocampus, amygdala, neocortex. Strongly cells also...

10.1126/science.1688328 article EN Science 1990-10-12

Midbrain dopaminergic neurons, whose loss in adults results Parkinson's disease, can be specified during embryonic development by a contact-dependent signal from floor plate cells. Here we show that the amino-terminal product of Sonic hedgehog autoproteolysis (SHH-N), an inductive expressed cells, induce neurons vitro. We further manipulations to increase activity cyclic AMP-dependent protein kinase A, which is known antagonize signaling, block neuron induction Our and those other studies...

10.1016/0896-6273(95)90062-4 article EN cc-by-nc-nd Neuron 1995-07-01

Cardiotrophin-1 (CT-1) is a newly isolated cytokine that was identified based on its ability to induce cardiac myocyte hypertrophy. It member of the family cytokines includes interleukins-6 and −11, leukemia inhibitory factor (LIF), ciliary neurotrophic factor, oncostatin M. These pleiotropic set growth differentiation activities via receptors use common signaling subunit, gp130. In this work we determine activity CT-1 in six vitro biological assays examine composition cell surface receptor....

10.1074/jbc.270.18.10915 article EN cc-by Journal of Biological Chemistry 1995-05-01

TREM2 is a receptor for lipids expressed in microglia. The R47H variant of human impairs ligand binding and increases Alzheimer's disease (AD) risk. In mouse models amyloid β (Aβ) accumulation, defective function affects microglial response to Aβ plaques, exacerbating tissue damage, whereas overexpression attenuates pathology. Thus, AD may benefit from activation. Here, we examined the impact an anti-human agonistic mAb, AL002c, model expressing either common (CV) or TREM2. Single-cell...

10.1084/jem.20200785 article EN cc-by-nc-sa The Journal of Experimental Medicine 2020-06-24

Anti-Aβ immunotherapy in transgenic mice reduces both diffuse and compact amyloid deposits, improves memory function clears early-stage phospho-tau aggregates. As most Alzheimer disease cases occur well past midlife, the current study examined adoptive transfer of anti-Aβ antibodies to 19- 23-month old APP-transgenic mice. We investigated effects weekly antibody treatment on radial-arm water-maze performance, parenchymal vascular loads, presence microhemorrhage brain. 19-month-old were...

10.1186/1742-2094-1-24 article EN cc-by Journal of Neuroinflammation 2004-01-01
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