Overview

Dr. Delic graduated from the University of South Florida in 2015 with a Ph.D. in cell and molecular biology.
His doctoral work was aimed at identifying strategies to prevent age and neurodegenerative disease
associated mitochondrial dysfunction. He completed his postdoctoral training at the University of Alabama
at Birmingham (UAB), in the Neurology department, Center for Neurodegeneration, and Experimental
Therapeutics (CNET), now home to a Udall Center of Excellence in Parkinson disease. His research focus
while at UAB was to determine the effectiveness of LRRK2 targeted therapeutics in preclinical rat models
of PD. At the end of 2018 Dr. Delic joined the New Jersey VA Health Care System, as an associate director
of the Lab of Molecular Biology (LMB), to study the relationship between TBI and PD both of which are
overrepresented in the U.S. Veteran population. He formally joined Rutgers NJMS, department of
Pharmacology, Physiology and Neuroscience in March 2021.

Education

PHD, 2015, University of South Florida, Cell and Molecular Biology
M.S., 2009, University of South Florida: Morsani College of Medicine, Molecular Medicine

Curriculum Vitae

View CV

Relevant Publications

Delic V, Karp J, Klein J, Stalnaker JK, Murray KE, Ratliff WA, Myers EM, Beck KD, Citron BA. Pyridostigmine bromide, chlorpyrifos, and DEET combined Gulf War exposure insult depresses mitochondrial function in neuroblastoma cells. J Biochem Mol Toxicol. 2021 Sept. 1. In press.

Delic V, Ratliff WA, Citron BA. Sleep Deprivation, a Link Between Post-Traumatic Stress Disorder and Alzheimers Disease. J Alzheimers Dis. February 16, 2021. PMID: 33459652

Ratliff WA, Saykally JN, Keeley KL, Driscoll DC, Murray KE, Okuka M, Mervis RF, Delic V, Citron BA. Sidestream Smoke Affects Dendritic Complexity and Astrocytes After Model Mild Closed Head Traumatic Brain Injury. Cell Mol Neurobiol. 2021 Jan 8. PMID: 33417143

Ratliff WA, Delic V, Pick CG, Citron BA. Dendritic arbor complexity and spine density changes after repetitive mild traumatic brain injury and neuroprotective treatments. Brain Res. 2020 Nov 1. PMID: 32292111

Ratliff WA, Qubty D, Delic V, Pick CG, Citron B. Repetitive Mild Traumatic Brain Injury and Transcription Factor Modulation. J Neurotrauma. 2020 Sep 1. PubMed PMID: 3229211

Delic V, Beck KD, Pang KCH, Citron BA. Biological links between traumatic brain injury and Parkinson's disease. Acta Neuropathol Commun. 2020 Apr 7;8(1):45. Review. PMID: 32264976

Delic V, Noble K, Zivkovic S, Phan TA, Reynes C, Zhang Y, Phillips O, Claybaker C, Ta Y, Dinh VB, Cruz J, Prolla TA, Bradshaw PC. The effects of AICAR and rapamycin on mitochondrial function in immortalized mitochondrial DNA mutator murine embryonic fibroblasts. Biol Open. 2018 Nov 16;7(11). PMID: 30177551

Delic V, Chandra S, Abdelmotilib H, Maltbie T, Wang S, Kem D, Scott HJ, Underwood RN, Liu Z, Volpicelli- Daley LA, West AB. Sensitivity and specificity of phospho-Ser129 ??-synuclein monoclonal antibodies. J Comp Neurol. 2018 Aug 15;526(12):1978-1990. PMID: 29888794

Delic V, Kurien C, Cruz J, Zivkovic S, Barretta J, Thomson A, Hennessey D, Joseph J, Ehrhart J, Willing AE, Bradshaw P, Garbuzova-Davis S. Discrete mitochondrial aberrations in the spinal cord of sporadic ALS patients. J Neurosci Res. 2018 Aug;96(8):1353-1366. PMID: 29732581

10. Harms AS, Delic V, Thome AD, Bryant N, Liu Z, Chandra S, Jurkuvenaite A, West AB. ??-Synuclein fibrils recruit peripheral immune cells in the rat brain prior to neurodegeneration. Acta Neuropathol Commun. 2017 Nov 21;5(1):85. PMID: 29162163

Areas Of Interest

TTraumatic Brain Injury (TBI)

Drug discovery

Metabolism

Neuro regeneration

Neurodgegeneration

Neuroprotection

Parkinson disease

Course List

CBNP5032Q		Behav, Cogni, & Clinical NS
NEURN5040		Neurobiology of Disease

Exercise and pharmacological LRRK2 inhibition for preventing PD

Much of what we know about idiopathic Parkinson disease (PD) molecular biology, comes from our
study of rare familial forms of PD. Gain of function mutations in Leucine Rich Repeat Kinase 2 (LRRK2) that
increase its kinase activity have been shown to cause familial PD that is indistinguishable in its pathology
and disease progression from that of idiopathic PD. This similarity suggests that abnormal LRRK2 activity
in the absence of mutations may also cause or accelerate existing PD. Abnormal LRRK2 activity in the
absence of a gain of function mutations could be caused by untimely cell specific expression, miss-
localization, post translational modification, or by an increase in abundance of inappropriate substrates.
LRRK2 is a nexus point between various cell processes that can affect protein aggregation, metabolic
dysfunction, and intercellular signaling and therefore of great therapeutic interest. We are currently funded
to determine 1) if TBI can cause and/or accelerate existing PD pathology 2) if LRRK2 activity, localization,
and abundance are affected by TBI in a cell specific manner and 3) does inhibition of LRRK2 slow down
progression of PD-like pathology in cell culture and animal models of PD and TBI.