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

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  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 Aβ 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. 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 peptides Description My research focuses on three projects, 1) on the role of Aβ 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 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  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  tochondrial calcium uptake capacity as a therapeutic target in the R6/2 mouse model of Huntington's disease. Perry GM, Tallaksen-Greene S, Kumar A, Heng MY, Kneynsberg A, van Groen T, Detloff PJ, Albin RL, Lesort M. Hum Mol Genet. 2010 Sep 1;19(17):3354-71   20558522  Characterization of a novel transgenic rat carrying human tau with mutation P301L. Korhonen P, van Groen T, Thornell A, Kyrylenko S, Soininen ML, Ojala J, Peltomaa E, Tanila H, Salminen A, Mandelkow EM, Soininen H. Neurobiol Aging. 2011 Dec;32(12):2314-5   20097445  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  Knockout of plasminogen activator inhibitor 1 gene reduces amyloid beta peptide burden in a mouse model of Alzheimer's disease. Liu RM, van Groen T, Katre A, Cao D, Kadisha I, Ballinger C, Wang L, Carroll SL, Li L. Neurobiol Aging. 2011 Jun;32(6):1079-89   19604604  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  Focal cerebral ischemia in rats alters APP processing and expression of Abeta peptide degrading enzymes in the thalamus. Hiltunen M, Mäkinen P, Peräniemi S, Sivenius J, van Groen T, Soininen H, Jolkkonen J. Neurobiol Dis. 2009 Jul;35(1):103-13   19426802

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

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