Berislav Zlokovic, M.D., Ph.D.

Director, Zilkha Neurogenetic Institute
Professor and Chair, Department of Physiology & Biophysics
Director, Center for Neurodegeneration & Regeneration
Zilkha Neurogenetic Institute
Keck School of Medicine of USC

Over the course of 20 years, Dr. Zlokovic has demonstrated that damage to the blood-brain barrier and microcirculation has a key role in the development of a neurodegenerative process in diseases such as Alzheimer’s disease and related neurodegenerative disorders. Collectively, he proposed that vascular-mediated neurodegeneration may underlie cognitive decline. These discoveries are of exceptional importance to understanding pathogenesis of neurodegenerative disorders and dementias, including Alzheimer’s disease. Besides academic interests, Zlokovic is co-founder with Mr. Selim K. Zilkha of three biotechnology companies with a mission to develop new therapies for the aging and damaged brain, including: ZZ (Zilkha-Zlokovic) Alztech, which focuses on development of new therapeutics and diagnostics for Alzheimer’s disease and manufacturing of a recombinant lipoprotein receptor for Alzheimer’s disease treatment; ZZ (Zilkha-Zlokovic), Biotech, which focuses on manufacturing recombinant secon-generation analog of activated protein C for stroke; Socratech L.L.C., which focuses on vascular genes and drug screening in Alzheimer’s disease.

Funded Research

Project Description Researchers Funding
PICALM Gene Therapy and Drug Screening for Abeta Clearance

PICALM is a highly validated genetic risk factor for Alzheimer’s disease (AD). Here, we report that PICALM reductions in AD and murine brain endothelium correlate with amyloid–beta (Abeta) pathology and cognitive impairment. Moreover, PICALM deficiency diminishes Abeta clearance across the murine blood–brain barrier (BBB) and accelerates Abeta pathology that is reversible by endothelial PICALM re–expression.

2015
$375,170
The Role of PICALM Mutations in Alzheimer’s Disease

Alzheimer’s disease (AD), the most common form of dementia in the elderly, is now the most expensive disease in the United States. The search for biological understanding of AD has expanded toward new risk factors, particularly genes. With the breakthrough of human genetics and high-throughput sequencing, PICALM, the gene encoding phosphatidylinositol binding clathrin assembly protein, has been identified as a new risk gene for AD.

2015
$100,000
The role of PICALM in vascular clearance of amyloid-B and neuronal injury

PICALM, the gene encoding phosphatidylinositol binding clathrin assembly (PICALM) protein, plays a key role in endocytosis, a process which regulates the function of cell receptors and synaptic transmission. Several GWAS studies of AD have replicated the association of PICALM with AD and shown relationships with neurodegenerative processes underlying disease. Additionally, low levels of PICALM in brain and cerebral microvessels have been recently shown in late onset AD. The role of PICALM in AD pathogenesis remains, however, elusive.

2014
$250,000
The role of PICALM in vascular clearance of amyloid-β

PICALM, the gene encoding phosphatidylinositol binding clathrin assembly (picalm) protein, plays a key role in endocytosis, a process which regulates the function of cell receptors and synaptic transmission. PICALM is one of the most highly validated Alzheimer’s disease (AD) risk factors. Its role in AD, however, is unknown. A recent genome-wide screen for modifiers of amyloid-b peptide (Aβ) toxicity in yeast has identified the key role of the yeast homologue of PICALM.

2012
$100,000