Camille Goldman
PhD
Postdoctoral Research Scientist
I completed my PhD at the Icahn School of Medicine at Mount Sinai in New York (USA) in 2025, under the supervision of Dr. Joel Blanchard and Dr. Alison Goate. My thesis work focused on developing iPSC-derived models of human brain tissue to study the molecular mechanisms promoting Lewy body diseases. I particularly focused on the contribution of APOE4 and cholesterol dysregulation in astrocytes on neuronal pathology. I am currently a postdoctoral researcher in Dr. Hugo Fernandes' laboratory. My research is focused on mixed pathologies in Alzheimer's disease (AD). AD is characterized by the toxic aggregation of the proteins amyloid-b and tau. However, there is mounting evidence that the majority of AD patients also have TDP-43 and a-synuclein co-pathologies. However, do not currently understand how the different pathological processes interact to contribute to neurodegeneration and cognitive decline. I am using iPSC neurons and microglia to identify how protein aggregates isolated from "pure-pathology" and "mixed-pathology" AD donor brains uniquely alter neuroinflammatory pathways to contribute to neurodegeneration.
Recent publications
Genetically encoded and modular subcellular organelle probes reveal dysfunction in lysosomes and mitochondria driven by PRKN knockout.
Journal article
Goldman C. et al, (2025), iScience, 28
Genetically Encoded and Modular SubCellular Organelle Probes (GEM-SCOPe) reveal lysosomal and mitochondrial dysfunction driven by PRKN knockout.
Journal article
Goldman C. et al, (2025), bioRxiv
Cholesterol-mediated Lysosomal Dysfunction in APOE4 Astrocytes Promotes α-Synuclein Pathology in Human Brain Tissue.
Journal article
Mesentier-Louro LA. et al, (2025), bioRxiv
Disruption of lysosomal proteolysis in astrocytes facilitates midbrain organoid proteostasis failure in an early-onset Parkinson's disease model.
Journal article
Morrone Parfitt G. et al, (2024), Nat Commun, 15
Reconstruction of the Blood-Brain Barrier In Vitro to Model and Therapeutically Target Neurological Disease.
Journal article
Goldman C. et al, (2023), J Vis Exp

