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Thomas van Groen, PhD

Thomas van Groen, PhD
 
Associate Professor
Department of Cell, Developmental and Integrative Biology
THT 912
Phone: (205) 934-5940
Email: vangroen@uab.edu

After obtaining my Ph.D. in Neurobiology at the Universiteit van Amsterdam, Amsterdam, The Netherlands in 1985, I have published more than 70 peer reviewed full-length papers. My postdoctoral trainings were in neuroanatomy and in behavioral analysis. My research focuses on three projects, 1) on the role of ABeta; production and clearance in Alzheimer’s disease and 2) the role of hypertension, blood vessels and inflammation in this process, and 3) the general aging process. My first research line is primarily focused on the use of therapeutic agents (e.g., amyloid beta42 binding peptides that reduce oligomers which may be promising in the alleviation or delay of age-related neural and cognitive changes in AD. A second research interest is the role of vascular pathology in Alzheimer’s disease, especially the relation between white matter infarcts and AD pathology. While clinical data strongly suggest that small infarcts contribute significantly to cognitive decline, the causal relationship is still not clearly defined. Our studies have shown that small ischemic infarcts both increase Aß deposition and decrease cognition. Furthermore, we have found that white matter infarcts (compared to grey matter infarcts) have a significantly worse outcome. Currently, we are focusing on the role of oligomers in the development of Alzheimer’s disease pathology and cognitive deficits. Finally, we are studying the relation between increased Aβ pathology, inflammation and synaptic pathology.

My expertise is in Alzheimer’s disease-related and aging-related neurodegeneration and neuropathology in the brain. Furthermore, I have extensive rodent behavioral expertise, and I have been the Technical Director of the UAB Behavioral Assessment Core for the last 10 years. Finally, my lab is well positioned to do animal cognitive assessments, including neurological deficit analysis, spatial and non-spatial learning and memory tests, and the analysis of circadian activity, including eating, drinking and sleeping patterns.

Research/Clinical Interest

Treatment of Alzheimer's disease with small abeta-oligomer binding peptides

My research focuses on three projects, 1) on the role of Abeta production and clearance in Alzheimer’s disease and 2) the role of inflammation in this process, and 3) the general aging process. My first research line is primarily focused on the use of therapeutic agents (e.g., amyloid β binding peptides and/or dietary intervention) that may be promising in the alleviation or delay of age-related neural and cognitive changes. A second research interest is the role of vascular pathology in Alzheimer’s disease, especially the relation between white matter infarcts and AD pathology. While clinical data strongly suggest that small infarcts contribute significantly to cognitive decline, the causal relationship is still not clearly defined. Our studies have shown that small ischemic infarcts both increase Aß deposition and decrease cognition. Furthermore, we have found that white matter infarcts (compared to grey matter infarcts) have a significantly worse outcome. Currently, we are focusing on the role of oligomers in the development of Alzheimer’s disease pathology and cognitive deficits.

Selected Publications

  1. α(2A) adrenergic receptor promotes amyloidogenesis through disrupting APP-SorLA interaction. Chen Y, Peng Y, Che P, Gannon M, Liu Y, Li L, Bu G, van Groen T, Jiao K, Wang Q. Proc Natl Acad Sci U S A. 2014 Dec 2;111(48):17296-301 [PMID 25404298]
  2. Focal cerebral ischemia in rats alters APP processing and expression of Abeta peptide degrading enzymes in the thalamus. Oral treatment with the d-enantiomeric peptide D3 improves the pathology and behavior of Alzheimer's Disease transgenic mice. Aileen Funke S, van Groen T, Kadish I, Bartnik D, Nagel-Steger L, Brener O, Sehl T, Batra-Safferling R, Moriscot C, Schoehn G, Horn AH, Müller-Schiffmann A, Korth C, Sticht H, Willbold D. ACS Chem Neurosci. 2010 Sep 15;1(9):639-48 [PMID 22778851]
  3. Functional roles of amyloid-beta protein precursor and amyloid-beta peptides: evidence from experimental studies. Hiltunen M, van Groen T, Jolkkonen J. J Alzheimers Dis. 2009;18(2):401-12 [PMID 19584429]
  4. Neurodevelopmental impairment following neonatal hyperoxia in the mouse. Ramani M, van Groen T, Kadish I, Bulger A, Ambalavanan N. Neurobiol Dis. 2013 Feb;50:69-75 23064437 A Novel 1,4-Dihydropyridine Derivative Improves Spatial Learning and Memory and Modifies Brain Protein Expression in Wild Type and Transgenic APPSweDI Mice. Jansone B, Kadish I, van Groen T, Beitnere U, Moore DR, Plotniece A, Pajuste K, Klusa V. PLoS One. 2015 Jun 4;10(6):e0127686 [PMID 26042808]
  5. Treatment with Aβ42 binding D-amino acid peptides reduce amyloid deposition and inflammation in APP/PS1 double transgenic mice. van Groen T, Kadish I, Funke A, Bartnik D, Willbold D. Adv Protein Chem Struct Biol. 2012;88:133-52. [PMID 22814708]
  6. Reviewing reasons for the decreased CSF Abeta42 concentration in Alzheimer disease. Spies PE, Verbeek MM, van Groen T, Claassen JA. Front Biosci. 2012 Jun 1;17:2024-34 [PMID 22652762]
  7. Transgenic AD model mice, effects of potential anti-AD treatments on inflammation, and pathology. van Groen T, Miettinen P, Kadish I. J Alzheimers Dis. 2011;24(2):301-13. [PMID 21239852]
  8. Axonal tract tracing for delineating interacting brain regions: implications for Alzheimer's disease-associated memory. van Groen T, Miettinen P, Kadish I. Future Neurol. 2014 Jan 1;9(1):89-98. [PMID 24678267]
  9. Age-related brain pathology in Octodon degu: blood vessel, white matter and Alzheimer-like pathology. van Groen T, Kadish I, Popović N, Popović M, Caballero-Bleda M, Baño-Otálora B, Vivanco P, Rol MÁ, Madrid JA. Neurobiol Aging. 2011 Sep;32(9):1651-61 [PMID 19910078]
  10. Lesion-induced hippocampal plasticity in transgenic Alzheimer's disease mouse models: influences of age, genotype, and estrogen. Kadish I, van Groen T. J Alzheimers Dis. 2009;18(2):429-45 [PMID 19584452]
  11. Treatment with D3 removes amyloid deposits, reduces inflammation, and improves cognition in aged AβPP/PS1 double transgenic mice. van Groen T, Kadish I, Funke SA, Bartnik D, Willbold D. J Alzheimers Dis. 2013;34(3):609-20 [PMID 23271316]