Back to Main

Faculty Detail    
Name THOMAS VAN GROEN
 
Campus Address THT 912 Zip 0006
Phone 205-934-5940
E-mail vangroen@uab.edu
Other websites Behavioral core
     

Education
Undergraduate  Utrecht University    1975  BS 
Graduate  University of Amsterdam    1985  PhD 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Associate Professor
Secondary  Neurobiology  Neurobiology Associate Professor
Center  Neurology   Alzheimer's Disease Center Associate Professor
Center  Center for Biophysical Sciences/Engineering  Center for Biophysical Sciences/Engineering Associate Professor
Center  General Clinical Research Center  Comprehensive Neuroscience Center Associate Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Associate Professor
Center  Medicine  Ctr Cardiovasc Bio Associate Professor
Center  Neurology   Ctr Neurodegeneration & Exp Ther (CNET) Associate Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Neuroscience 
Pathobiology and Molecular Medicine 

Biographical Sketch 
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 7 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.

Society Memberships
Organization Name Position Held Org Link
EBBS  member  http://www.ebbs-science.org/cms/ 
IBANGS  member  www.ibangs.org/ 
Society for Neuroscience  member  http://www.sfn.org/ 

Research/Clinical Interest
Title
Treatment of Alzheimer's disease with small abeta-oligomer binding peptides
Description
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 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 
Publication PUBMEDID
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 
23271316 
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 
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.
 
22814708 
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 
22778851 
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
 
22652762 
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.

 
21239852 
Transgenic AD model mice, effects of potential anti-AD treatments on inflammation, and pathology.
van Groen T, Miettinen P, Kadish I.

 
2123985 
Characterization of Atp1a3 mutant mice as a model of rapid-onset dystonia with parkinsonism.

DeAndrade MP, Yokoi F, van Groen T, Lingrel JB, Li Y.

Behav Brain Res. 2011 Jan 20;216(2):659-65
 
20850480 
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
 
19910078 
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
 
19584452 
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
 
19584429 

Keywords
Alzheimer's disease, pathology, amyloid beta, peptides, cognition, behavioral assessment