Background pattern of a brain with neural connections
Joel Blanchard

Joel Blanchard

Co-PI (Core Leadership)

Icahn School of Medicine at Mount Sinai

Joel Blanchard is an Assistant Professor of neuroscience at the Icahn School of Medicine at Mt. Sinai, a member of the Loeb Alzheimer’s center and the Black Family Stem Cell Institute. His research combines engineering, stem cell biology, and neuroscience to create new technology and approaches for investigating and therapeutically targeting the human brain. Joel completed his post-doctoral training at MIT in the laboratory of Dr. Li-Huei Tsai where he developed in vitro models of the blood-brain barrier and myelination and applied these models to discover key mechanisms underlying vascular and white matter pathologies in Alzheimer’s disease. Joel received doctoral training at the Scripps Research Institute in California working with Dr. Kristin Baldwin and Dr. Richard Lerner. His work has led to numerous publications, patents, and awards including the ISSCR merit award, Glenn Foundation Post-doctoral Fellowship, and a CIRM pre-doctoral fellowship.

Teams

Vangheluwe

Themes

Circuitry and Brain-Body Interactions

Tags

Behavioral Behavior/Behavioral studies Mouse model Optogenetics Activity Assay

Recent ASAP Preprints & Published Papers

Cholesterol-mediated Lysosomal Dysfunction in APOE4 Astrocytes Promotes α-Synuclein Pathology in Human Brain Tissue

The pathological hallmark of neurodegenerative disease is the aberrant post-translational modification and aggregation of proteins leading to the formation of insoluble protein inclusions. Genetic factors like *APOE4* are known to increase the prevalence and severity of tau, amyloid, and α-Synuclein inclusions. However, the human brain is largely inaccessible during this process, limiting…

Loss of the lysosomal lipid flippase ATP10B leads to progressive dopaminergic neurodegeneration and Parkinsonian motor deficits

ATP10B, a transmembrane lipid flippase located in late endosomes and lysosomes, facilitates the export of glucosylceramide and phosphatidylcholine by coupling this process to ATP hydrolysis. Recently, loss-of-function mutations in the ATP10B gene have been identified in Parkinson's disease patients, pointing to ATP10B as a candidate genetic risk factor. Previous studies…

Team Vangheluwe

Peter Vangheluwe

Peter Vangheluwe

Lead PI (Core Leadership)
Veerle Baekelandt

Veerle Baekelandt

Co-PI (Core Leadership)
Joel Blanchard

Joel Blanchard

Co-PI (Core Leadership)
Joseph Lyons

Joseph Lyons

Co-PI (Core Leadership)
Ellen Sidransky

Ellen Sidransky

Co-PI (Core Leadership)
Veronique Daniels

Veronique Daniels

Project Manager

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