Giulio Maria Pasinetti is the Program Director of the Center on Molecular Integrative Neuroresilience[1] and is the Saunders Family Chair in Neurology at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York City.

Pasinetti investigates the biological processes that occur when, during aging, subjects with normal cognitive function convert into the very earliest stages of Alzheimer's disease (AD) and then to frank dementia.

[12] By conducting genome wide association studies to clarify the molecular mechanisms in subjects with T2D who might be predisposed to the onset of Alzheimer's disease,[13] Pasinetti found that a subpopulation of individuals with T2D have a genetic predisposition to AD based on the evidence of shared common T2D/AD single nucleotide polymorphisms in gene pathways involved in chromatin modification enzymes, among others.

These studies provide new information about the potentially detrimental role of commonly prescribed drugs that can be used as a reference for physicians to consider, particularly when treating chronic degenerative disorders such as AD.

[27][28][29] Following these findings, as Chief of the Friedman Brain Institute Center of Excellence for Novel Approaches to Neurodiagnostics and Neurotherapeutics, Pasinetti developed drug discovery programs for Alzheimer's disease.

[32] In a study released on February 2, 2018, scientists from the Icahn School of Medicine at Mount Sinai, led by Dr. Giulio Maria Pasinetti, described an extensive analysis of two novel grape-derived phytochemicals, or natural essential nutrients, dihydrocaffeic acid (DHCA) and malvidin-3’-O-glucoside (Mal-gluc), which might be developed as therapeutic agents for the treatment of depression.

It was demonstrated that treatment with both DHCA and Mal-gluc is effective in attenuating depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of cells from the bone marrow of stress-susceptible mice.

Pasinetti's lab is now working on tracing "downstream" molecular pathways in preclinical rodent models of mTBI, to eventually tie them back to TBI or PTSD symptoms and allow for identification of potential new drug targets to be further developed in the clinical setting.