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Ellen Kanter

Researcher at Columbia University Medical Center

Publications -  18
Citations -  2780

Ellen Kanter is an academic researcher from Columbia University Medical Center. The author has contributed to research in topics: Dopaminergic & Epitope. The author has an hindex of 11, co-authored 14 publications receiving 2115 citations. Previous affiliations of Ellen Kanter include Columbia University.

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Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits

TL;DR: This work reports increased dendritic spine density with reduced developmental spine pruning in layer V pyramidal neurons in postmortem ASD temporal lobe and suggests that mTOR-regulated autophagy is required for developmental spinePruning, and activation of neuronal Autophagy corrects synaptic pathology and social behavior deficits in ASD models with hyperactivated mTOR.
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Interplay between Cytosolic Dopamine, Calcium, and α-Synuclein Causes Selective Death of Substantia Nigra Neurons

TL;DR: Using intracellular patch electrochemistry to directly measure cytosolic dopamine in cultured midbrain neurons, it is confirmed that elevated DA(cyt) and its metabolites are neurotoxic and that genetic and pharmacological interventions that decrease DA(Cyt) provide neuroprotection.
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MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration

TL;DR: Evidence is provided from immunolabel, RNA expression, and mass spectrometry analysis of postmortem samples that human catecholaminergic substantia nigra and locus coeruleus neurons express MHC-I, and that this molecule is inducible in human stem cell derived dopamine (DA) neurons.
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Mitochondrial dysfunction and mitophagy defect triggered by heterozygous GBA mutations

TL;DR: It is shown that in GbaL444P/WT knockin mice, the L444P heterozygous Gba mutation triggers mitochondrial dysfunction by inhibiting autophagy and mitochondrial priming, two steps critical for the selective removal of dysfunctional mitochondria by Autophagy, a process known as mitophagy.