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Ghazaleh Ashrafi

Researcher at Cornell University

Publications -  11
Citations -  2224

Ghazaleh Ashrafi is an academic researcher from Cornell University. The author has contributed to research in topics: Parkin & Mitochondrion. The author has an hindex of 8, co-authored 9 publications receiving 1466 citations. Previous affiliations of Ghazaleh Ashrafi include Boston Children's Hospital.

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Journal ArticleDOI

The pathways of mitophagy for quality control and clearance of mitochondria.

TL;DR: The relevance of these pathways in neurons where defects in mitophagy have been implicated in neurodegeneration are discussed, in addition to the importance of identifying specific regulators ofMitophagy that ensure selective sequestration of mitochondria as cargo.
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SynGO : An Evidence-Based, Expert-Curated Knowledge Base for the Synapse

Frank Koopmans, +78 more
- 17 Jul 2019 - 
TL;DR: It is shown that synaptic genes are exceptionally well conserved and less tolerant to mutations than other genes, and among de novo variants associated with neurodevelopmental disorders, including schizophrenia.
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GLUT4 Mobilization Supports Energetic Demands of Active Synapses

TL;DR: There is strong evidence that during action potential (AP) firing, nerve terminals rely on the glucose transporter GLUT4 as a glycolytic regulatory system to meet the activity-driven increase in energy demands.
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Parkinson Sac Domain Mutation in Synaptojanin 1 Impairs Clathrin Uncoating at Synapses and Triggers Dystrophic Changes in Dopaminergic Axons

TL;DR: It is shown that mice carrying a homozygous mutation in its Sac domain developed neurological manifestations similar to those of human patients, strengthening evidence for a link between synaptic endocytic dysfunction and Parkinson's disease.
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Molecular Tuning of the Axonal Mitochondrial Ca2+ Uniporter Ensures Metabolic Flexibility of Neurotransmission.

TL;DR: It is shown that synapses can switch from glycolytic to oxidative metabolism, but to do so, they rely on activity-driven presynaptic mitochondrial Ca2+ uptake to accelerate ATP production, and the brain-specific protein MICU3 is identified as a critical driver of this tuning of Ca 2+ sensitivity.