Gregory W. Konat, PhD, MS, LM

Professor Emeritus

Organization:

West Virginia University School of Medicine

Department:

Biochemistry and Molecular Medicine

Classification:

Unknown

Professor Emeritus

Organization:

West Virginia University School of Medicine

Department:

Department of Neuroscience

Classification:

Faculty

Professor Emeritus

Organization:

West Virginia University School of Medicine

Department:

Rockefeller Neuroscience Institute (SOM)

Classification:

Faculty

• PhD, University of Southern Denmark

Selected recent publications:

Konat, G.W. (2025) Neuroplasticity elicited by peripheral immune challenge with a viral mimetic. Brain Res. 1846:149239.

Petrisko T.J., Konat G. (2021) Peripheral viral challenge increases c-fos level in cerebral neurons. Met. Brain Dis. 36:1995-2002.

Petrisko, T. J., Srinivas, S., Bloemer, J., Pinky, P.D., Du, Y., Setti, S., Suppiramaniam, V., Konat, G.W*., Reed, M.N.* (2020) Neuronal CXCL10/CXCR3 axis mediates the induction of cerebral hyperexcitability by peripheral viral challenge. Front. Neurosci. 14:220:1-11. *co-senior authors

Petrisko, T., Konat, G. (2019) Peripheral viral challenge exacerbates experimental autoimmune encephalomyelitis. Met. Brain Dis. 34:675–679.

Petrisko, T., Konat, G. (2017) Peripheral viral challenge triggers hippocampal production of inflammatory proteins. Met. Brain Dis. 32:1249-1254.

Hunsberger, H.C., Konat, G.W.* and Reed, M.N.* (2017) Peripheral viral challenge elevates extracellular glutamate in the hippocampus leading to seizure hypersusceptibility. J. Neurochem. 141:341-346. *co-senior authors

Hunsberger, H.C., Wang, D., Petrisko, T.J., Alhowail, A., Setti, S.E., Suppiramaniam, V., Konat, G.* and Reed, M.N.* (2016) Peripherally restricted viral challenge elevates extracellular glutamate and enhances synaptic transmission in the hippocampus. J. Neurochem. 138:307-316. *co-senior authors

Konat, G. (2016) Cerebral response to peripheral challenge with a viral mimetic. Neurochem. Res. 41:144-155.

Michalovicz, L.T., Lally, B. and Konat, G.W. (2015) Peripheral challenge with a viral mimic upregulates expression of the complement genes in the hippocampus. J. Neuroimmunol. 285:137-142.

Michalovicz, L.T. and Konat, G.W. (2014) Peripherally restricted acute phase response to a viral mimic alters hippocampal gene expression. Met. Brain Dis. 29:75-86.

Kirschman, L.T., Fil, D., Borysiewicz, E. and Konat, G.W. (2011) Peripheral immune challenge with dsRNA enhances kainic acid-induced status epilepticus. Met. Brain Dis. 26:91-93.

Konat, G.W., Lally, B.E., Toth, A.A. and Salm, A.K. (2011). Peripheral immune challenge with viral mimic during early postnatal period robustly enhances anxiety-like behavior in young adult rats. Met. Brain Dis. 26:237-40.

Fil, D., Borysiewicz, E. and Konat, G.W. (2011) A broad upregulation of cerebral chemokine genes by peripherally-generated inflammatory mediators. Met. Brain Dis. 26:49-59.

Konat, G.W., Borysiewicz, E. Fil, D. and James, I. (2009) Peripheral challenge with double stranded RNA elicits global upregulation of cytokine gene expression in the brain. J. Neurosci. Res. 87:1381-1388.

Publication links:

https://www.ncbi.nlm.nih.gov/myncbi/1HC_6YMuFaj5z/bibliography/public/?page=1 

https://www.researchgate.net 

Neurobiology and Anatomy; Center for Basic and Translational Stroke Research

The existence of active communication pathways between the peripheral immune system and the central nervous system (CNS) has been well established. This communication plays an important role in both health and disease. The primary mechanisms involve the generation of blood-borne inflammatory factors that gain access to the CNS whereby they alter the activity of neuronal circuits. A stellar example of the immune-to-brain communication is the induction of a slew of behavioural changes collectively referred to as “sickness behavior” in response to peripheral inflammation elicited by infections, injuries, or other immune stimuli. Sickness behavior represents a protective mechanism that promotes the recovery/survival of the affected individuals and prevents the spread of infection within the population. However, peripheral inflammation has also been shown to exacerbate ongoing neuropathologies, e.g., dementia in Alzheimer disease (AD), relapses in multiple sclerosis (MS), seizures in susceptible individuals, as well as worsen the outcome of stroke. My research interests are primarily focused on molecular and cellular mechanisms by which peripherally generated inflammatory factors alter CNS function.

My previous major research endeavours entailed the regulation of toll like receptors (TLRs) in glial cells, oxidative chromatin degradation, structural and functional characterization of myelin-associated glycoprotein (MAG) gene as well as molecular aspects of myelin membrane formation.