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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Thomas
Last Name:van Groen
Title:Dr.
Advanced Degrees:PhD
Affiliation:University of Alabama at Birmingham
Department:Cell Biology
Street Address 1:1900 University Boulevard
Street Address 2:THT 912
City:Birmingham
State/Province:AL
Zip/Postal Code:35294-0006
Country/Territory:U.S.A.
Phone:205 934 5940
Fax:205 934 7029
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 12 July 2006]
View all comments by Thomas van Groen
Clinical Interests:
Aging Process, Stroke and Trauma, Alzheimer Disease, Parkinson Disease, Prion Diseases, Neurodevelopmental Disorders (Down syndrome, etc.), Tauopathies
Research Focus:
Microscopy, Brain imaging, Molecular and Cell biology, Oxidative Stress, A-beta PP/A-beta, Neuropathology, Neurobiology, Neuroimmunology, Animal Models, Tau/Cytoskeleton
Work Sector(s):
University
Researcher Bio
NAME: Thomas van Groen

BORN: 28-04-1953

Dutch citizen

HOME Address: Birmingham, AL


WORK Address:University of Alabama at Birmingham,
1900 University Blvd, THT 912, Birmingham AL, 35294-0006, USA
205 934 5940
205 934 7029

EDUCATION: HBS-B 1965-1971
Rijksuniversiteit Utrecht 1971-1975
Kandidaatsexamen 26-05-1975
Universiteit van Amsterdam
Doctoraalexamen 26-11-1980 (cum laude)
Promotie 20-11-1985


PROFESSIONAL TRAINING:

1975-1977 Physiology of the olfactory system in rabbits and study of their olfactory related behaviour. MS thesis project.
University of Amsterdam; Dr. G Verberne

1975-1978 Instructor, in course of Animal Physiology.
University of Amsterdam

1978 Pharmacology of the CNS of the cockroach.
University of Amsterdam; Dr. T. Piek

1979 History of biology.
University of Amsterdam; Dr. D. Hillenius

1980 Physiology of the olfactory and accessory olfactory bulb in rabbits.
University of Amsterdam; Dr. F.H. Lopes da Silva

1981-1985 Physiology and anatomy of the entorhinal-hippocampal system.
University of Amsterdam/ Vrije Universiteit;
Drs. F.H. Lopes da Silva/ A.H.M. Lohman


1986-1987 Anatomy and physiology of the cingulate and subicular cortices.
University of Alabama at Birmingham; Dr. J.M. Wyss

1988-1989 Anatomy and physiology of the hippocampal system, and Study of rat
behaviour following lesions in the hippocampal system.
University of Edinburgh; Drs. R.G.M. Morris/D. Willshaw

1989-1997 Anatomy, physiology and aging of the limbic system.
University of Alabama at Birmingham; Dr. J.M. Wyss

1997-2005 Anatomy of the limbic system, study of rat and mouse behavior related to the limbic system, and transgenic animal models for Alzheimer's disease.
University of Kuopio.

2000 Appointed Docent in Neurobiology by University of Kuopio.


EMPLOYMENT: Instructor 01-04-1975 to 10-09-1978 by UvA
(University of Amsterdam)

Researcher 01-10-1981 to 31-03-1985 by FUNGO
(Fundamental Medical Research Organization of ZWO)

Researcher 01-05-1985 to 31-10-1985 by UvA
(University of Amsterdam)

Research associate 01-01-1986 to 31-12-1987 by UAB
(University of Alabama at Birmingham)

Research fellow 01-01-1988 to 31-04-1989 by MRC
(University of Edinburgh, Scotland)

Research associate 01-04-1989 to 31-09-1990 by UAB
(University of Alabama at Birmingham)

Research instructor 01-10-1990 to 31-09-1993 by UAB
(University of Alabama at Birmingham)

Assistant professor 01-10-1993 to 31-03-1997 by UAB
(University of Alabama at Birmingham)

Senior Researcher 01-04-1997 to 31-01-05 by UK
(University of Kuopio)

Research associate professor 01-02-05 to present by UAB
(University of Alabama at Birmingham)

Associate Director of Behavioral Core 01-06-05 to present by UAB
(University of Alabama at Birmingham)Professional Societies
Finnish Neuroscience Association
Dutch Society for the Advancement of Medical Research
Society for Neuroscience
International Brain Research Organization (IBRO)
European Brain and Behaviour Society (EBBS)
International Behavioural And Neural Genetics Society (IBANGS)
Top Papers
Liu Liu L, Ikonen S, Heikkinen T, Heikkilä, M, Van Groen T. and Tanila H. Effects of fimbria-fornix lesion and amyloid pathology on spatial learning and memory in transgenic APP+PS1 mice. Behav Brain Res 134:433-445, 2002.

Liu L, Ikonen S, Tapiola T, Tanila H, van Groen T. Fimbria-fornix lesion does not affect APP levels and amyloid deposition in the hippocampus of APP+PS1 double transgenic mice. Exp Neurol 177:565-574, 2002.

Kadish I. and Van Groen Th. Differences in lesion-induced hippocampal plasticity between mice and rats. Neuroscience 100:499-509, 2003.

Van Groen Th, Kadish I. and Wyss JM. Old rats remember old tricks: Memories of the water maze persist for at least twelve months. Behav Brain Res. 136:247-255, 2002.

Van Groen Th, Miettinen P, and Kadish, I. The entorhinal cortex of the mouse: Organization of the
projection to the hippocampal formation. Hippocampus 13:133-149, 2003.

Van Groen Th, Liu L, Ikonen S. and Kadish I. Diffuse amyloid deposition, but not plaque number, is reduced in APP/ PS1 double transgenic mice by pathway lesions. Neuroscience 2003.

van Groen T, Puurunen K, Maki HM, Sivenius J, Jolkkonen J. Transformation of diffuse
beta-amyloid precursor protein and beta-amyloid deposits to plaques in the thalamus after transient occlusion of the middle cerebral artery in rats. Stroke 36:1551-1556, 2005
Huuskonen J, Suuronen T, Miettinen R, van Groen T, Salminen A. A refined in vitro model to study inflammatory responses in organotypic membrane culture of postnatal rat hippocampal slices. J Neuroinflammation 2:25, 2005
van Groen Th, Kiliaan A, Kadish I. Deposition of mouse amyloid β in humanAPP/ PS1 double and single AD model transgenic mice. Neurobiol. Dis, accepted, 2006
What is the greatest void to date in our knowledge of Alzheimer's Disease?
What really causes the disease, if there even is one cause. Likely there are more.
If resources were not limited, what research projects would you pursue?
Combine transgenic models (AD and non-AD)and compare transgenic AD models, finding out why certain brain areas are more susceptible to Abeta deposition.
What is your leading hypothesis?
AD is caused by misregulation of APP and tau processing, causing axonal/synaptic changes. Leading to synaptic dysfunction and memory loss.
What piece of missing evidence would help prove it?
Finding the relation between APP/ABeta deposition and/or tau dysregulation and synaptic/axonal changes.
What is your fallback position?
Tau is the only culprit.

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