Dr. Ignazio Cali received his Ph.D. in Experimental Physiopathology and Neuroscience from the University of Campania “Luigi Vanvitelli” in 2015. During his doctoral studies in the laboratory of Dr. Pierluigi Gambetti, he worked on the characterization of the molecular features and histopathological phenotypes of human prion diseases with idiopathic, genetic, and acquired etiology. In addition, Dr. Cali carried out similar characterizations in transgenic mouse models inoculated with brain extracts from various prion diseases. These studies shed light on the wide spectrum of molecular signatures and pathological phenotypes of these heterogeneous disorders.
During his postdoctoral research activity, Dr. Cali investigated the disease phenotype in young patients (<55 years) with an acquired human prion disease and comorbid amyloid β (Aβ) pathology resembling Alzheimer’s disease. From this study, he found that Aβ invariably accumulates in the wall of blood vessels, even in the absence of Aβ plaque pathology. While this finding suggests a human-to-human transmission of Aβ (and prions), it points to Aβ infections and spreading to the brain throughout the bloodstream. Dr. Cali has also characterized the histotypes of prion disease developed as secondary neurodegenerative processes in the autopsied brain of football players with chronic traumatic encephalopathy.
In 2019 Dr. Cali received a Pathway to Independence Award from the National Institute of Aging, and in 2021, he joined the faculty at Case Western Reserve University in the Department of Pathology as an Instructor and in September 2022 as a tenure track Assistant Professor.
Since 2021, Dr. Cali has served as Associate Director of the National Prion Disease Pathology Surveillance Center (NPDPSC), where he is actively engaged in identifying atypical or novel disease phenotypes.
We are interested in determining the disease phenotypes and molecular features of co-existing protein aggregates in comorbid neurodegenerative disorders, including prion disease, Alzheimer’s disease (AD), and chronic traumatic encephalopathy. A major goal of these studies is to determine whether distinct prion strains modulate Aβ and tau neurodegeneration in cases with prion disease and AD. We are also examining the molecular properties of tau (including seeding properties) in individuals with prion disease and a history of traumatic brain injury. We employ sensitive diagnostic assays for the detection of minute amounts of pathogenic proteins (RT-QuIC) in addition to animal and cell models to understand the role of each pathogenic protein in multiproteinopathies.
The Cali lab investigates the disease phenotypes and molecular features of co-existing protein aggregates in comorbid neurodegenerative disorders, including prion disease, Alzheimer’s disease, and chronic traumatic encephalopathy. Investigating whether distinct human prion diseases are associated with different Aβ and tau histotypes/molecular properties. These studies will likely answer the question of whether prion strains modulate Aβ and tau neurodegeneration. We are also examining the molecular properties of tau (including seeding properties) in individuals with prion disease and a history of traumatic brain injury. Dr. Cali's laboratory employs sensitive diagnostic assays for the detection of minute amounts of pathogenic proteins (RT-QuIC) in addition to animal and cell models to determine the role of each pathogenic protein in multiproteinopathies. The primary goal of Dr. Cali's research is to gain critical information about whether pathogenic proteins adopt different molecular features and propagation patterns (bioassay) when they co-occur, an indication for interaction (“cross-talk”) between different types of protein aggregates. Recently, Dr. Cali's lab was awarded a CJD Foundation grant to study prion seeding activity in the brains of patients with Alzheimer’s disease.
K99/R00 NIH grant AG068359;