Paul E. Gottschall, Ph.D.

Phone: 686-8655
Fax: 686-5510


B.S. – Wright State University, 1978
M.S. – Wright State University, 1980
Ph.D. –  Michigan State University, 1986
Postdoc – Tulane University School of Medicine, 1989

Research Interests

Synaptic plasticity is a neuronal mechanism essential for memory formation and recall, and altered plasticity and synaptotoxicity occur in various types of dementia including Alzheimer’s disease (AD).  In the brain, lecticans, which are chondroitin sulfate-bearing proteoglycans, are deposited with other extracellular matrix molecules in extracellular regions adjacent to synaptic active zones.  The presence of lecticans, particularly an abundant lectican termed brevican, are thought to stabilize synapses that have undergone plasticity during the formation and consolidation of memories.  Data from the laboratory has supported the concept that lecticans modulate additional synaptic plasticity and that markedly increased brevican deposition that occurs with age and in AD contribute to the decline in plasticity that occurs, pre-clinically, in disease progression.  The main objective of the research program is to determine how lecticans, and the proteases that cleave them, modulate synaptic plasticity in age-related diseases of the nervous system such as AD.  In AD brain, pathological senile plaques consist of various aggregated forms of the peptide Aβ, and certain soluble, oligomeric isoforms of Aβ that exist surrounding plaques are toxic to synapses.  Substantial evidence from the lab supports the hypothesis that excess brevican deposited at these sites combine with oligomeric Aβ and may play a role in blocking synaptic plasticity and other synaptic functions.  The role that lecticans may have in the loss of synapses is not known and is one of the aims of the laboratory.  Since all currently approved drugs for AD merely suppress symptoms, and not the progression of the disease, lecticans that interact with the synapse provide a novel target for testing pharmacological compounds that affect matrix synthesis, deposition and signaling which would improve synaptic plasticity and potentially delay or inhibit the progression of AD.  Numerous drugs, termed ROCK inhibitors, are available that can inhibit the intracellular signaling of brevican, and these drugs may have the potential to change the alteration in plasticity induced by brevican and brevican association with Aβ.

Recent Research Support

Completed Research
117-10062  UAMS Internal Medical Research Endowment (MRE) Award  (PI)  (01/01/16 – 12/31/16)
“Synapse-associated brevican in human AD tissue”

117-1006099 UAMS Translational Research Award  (PI)  (10/01/14 – 09/30/15)
“Targeting lecticans to enhance synaptic plasticity in Alzheimer’s Disease”

41536  UAMS Tobacco Funds Equipment Grant  (PI)  (07/01/13 – 06/30/13)
“Odyssey Imaging System Li-Cor Odyssey CLx”

R01AG022101  NIH/NIA  (PI)  (07/01/06 – 06/30/11)
“Proteoglycans, synaptic plasticity in aging and disease”

Chapter Award Society for Neuroscience, Washington, D.C. 2010
“Community outreach for neuroscience”


Yamada-Goto N, Ochi Y, Katsuura G, Yamashita Y, Ebihara K, Noguchi M, Fujikura J, Taura D, Sone M, Hosoda K, Gottschall PE, Nakao K. Neuronal cells derived from human induced pluripotent stem cells as a functional tool of melanocortin system. Neuropeptides. pii: S0143-4179(16)30201-3, 2017. PMID 28434791

Howell MD, Bailey LA, Cozart MA, Gannon BM, Gottschall PE.  Intrahippocampal administration of chondroitinase increases plaque-adjacent synaptic marker and diminishes amyloid burden in aged APPswe/PS1dE9 mice. Acta Neuropathologica Comm. 3: 54, 2015. PMID 26337292

Gottschall PE, Howell MD.  ADAMTS expression and function in central nervous system injury and disorders.  Matrix Biology. doi: 10.1016/j.matbio.2015.01.014, 44-46: 70-76, 2015. PMID  25622912

Phelan KD, Shwe UT, Abramowitz J, Wu H, Rhee SW, Howell MD, Gottschall PE, Freichel M, Flockerzi V, Birnbaumer L, Zheng F.  TRPC5 and TRPC1/4 channels contribute to seizure and excitotoxicity by distinct cellular mechanisms.  Mol Pharmacol. 83: 429-438, 2013. PMID 23188715

Howell MD, Torres-Colladdo AX, Iruela-Arispe L, Gottschall PE.  Selective decline of synaptic protein levels in the frontal cortex of female mice deficient in the metalloproteinase ADAMTS1.  PLoS ONE. 7(10): e47226, 2012. PMID 23071766

Howell MD, Gottschall PE.  Altered synaptic marker abundance in the hippocampal stratum oriens of Ts65Dn mice is associated with exuberant expression of versican.  ASN Neuro. 4(1): e00073, 2012. PMID 22225533

Howell MD, Gottschall PE.  Lectican proteoglycans, their cleaving metalloproteinases, and plasticity in the central nervous system extracellular microenvironment.  Neuroscience. 217:6-18, 2012. PMID 22626649

Gottschall PE, Barone FC.  Important role for caveolin-1in focal cerebral ischemia-induced blood-brain barrier injury. J Neurochem. 120: 4-6, 2012.  (“Editorial Highlight”) PMID 22017357

View Dr. Gottschall’s Publication List