Author
Grace E. Stutzmann
Rosalind Franklin University of Medicine and ScienceORCID 0000-0003-2841-8532Unclaimed ORCID profile · follow to get notified of new preprints
Biology Disciplines
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2022-2025 · peak 2/yrCo-Author Collaboration Network
10 top collaborators · 20 mutual co-author links5 papers
Recent·Most cited
- NeurosciencebioRxivPreprint
Mitochondrial Dysfunction in Alzheimer's Disease Is Driven By Excess ER-Calcium Release in Patient-Derived Neurons
Sarah Mustaly-Kalimi, Wacey Gallegos, Robert A. Marr…·Grace E. Stutzmann
This study shows that excess ER-Ca2+ release via RyR contributes to mitochondrial dysfunction in AD neurons, leading to cellular pathology and that pharmacological inhibition of RyR-Ca2+ release can reverse these effects.
1 citation - PhysiologyMolecular MetabolismPeer-reviewed
NCLX controls hepatic mitochondrial Ca2+ extrusion and couples hormone-mediated mitochondrial Ca2+ oscillations with gluconeogenesis
Mahmoud Taha, Essam A. Assali, Tsipi Ben Kasus Nissim…·Israel Sekler
This study identifies NCLX as the primary mitochondrial Ca2+ extruder in hepatocytes, linking hormone-mediated mitochondrial Ca2+ oscillations to gluconeogenesis.
11 citations - NeuroscienceProceedings of the National Academy of SciencesPeer-reviewed
Protein mishandling and impaired lysosomal proteolysis generated through calcium dysregulation in Alzheimer's disease
Sarah Mustaly-Kalimi, Wacey Gallegos, Robert A. Marr…·Grace E. Stutzmann
This study identifies calcium dysregulation via RyR as a driver of lysosomal dysfunction and protein aggregation in Alzheimer's disease, showing that dantrolene can restore proteolytic activity in AD models.
- NeuroscienceeLifePeer-reviewed
Mitochondria decode firing frequency and coincidences of postsynaptic APs and EPSPs
Ohad Stoler, Alexandra Stavsky, Yana Khrapunsky…·Ilya A. Fleidervish
The paper shows that neuronal mitochondria respond to firing frequency and EPSP-spike timing by modulating Ca2+ and NAD(P)H levels, affecting metabolic rate and synaptic efficacy.