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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Zsuzsanna
Last Name:Nagy
Title:Dr
Advanced Degrees:MD, DPhil
Affiliation:University of Birmingham
Department:Neuroscience Division
Street Address 1:Medical School
City:Bimringham
State/Province:West Midlands
Zip/Postal Code:B15 2TT
Country/Territory:United Kingdom
Phone:0121-4158135
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 6 March 2006]
View all comments by Zsuzsanna Nagy
Clinical Interests:
Aging Process, Alzheimer Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Parkinson Disease
Research Focus:
Molecular and Cell biology, Apoptosis/Cell cycle, Diagnosis, Chemistry/Pharmacology, Clinical trials, Drug screening
Work Sector(s):
University
Web Sites:
Professional: http://www.neuroscience.bham.ac.uk/
Researcher Bio
My research career started as a second year medical student when I decided to take up a Student Research Assistant position in the Departments of Human Anatomy and Pharmacology (University of Medicine and Pharmacy Tirgu Mures, Romania) in 1985. Parallel to my university education I carried out four years research (1985-1989) on the teratogenic effects of a hypno-sedative drug (Glutetimid) in rats, mice and in cell culture.
In 1991 I was awarded a one-year scholarship by the Transylvanian Academic Exchange Trust (Oxford, UK) that enabled me to come, as an academic visitor, to Oxford. I spent that year in the Human Anatomy department investigating the teratogenic effects of Retinoic acid. These studies concentrated mainly on the development of peripheral nerves in rat embryos. The expanding horizons also brought about the seemingly considerable career change. After five years of research into nervous system development in 1992 I started working on neurodegeneration. The Oxford Project to Investigate Memory and Ageing (OPTIMA) offered the perfect environment for the study of Alzheimer's disease and other age-related neurodegenerative disorders. OPTIMA also provided support for me to complete a DPhil thesis and welcomed me back as a post-doc in 1995. The work on neurodegeneration led me, in 1996, to the discovery that neurones in the hippocampus in Alzheimer’s disease express markers of cell division cycle re-entry. Much of my work since 1997 has been directed towards understanding the significance of cell cycle-related cellular events in the pathogenesis of Alzheimer’s disease and other forms of neurodegeneration. I have also been working in the last two years on possible diagnostic implications of aberrant cell cycle control in Alzheimer’s disease. Concurrently I extended my studies of the central nervous system to search for the molecular basis of the cell cycle aberrations seen in Alzheimer’s disease neurones as well as to cell culture systems and animal models.
I moved to the University of Birmingham Medical School in 2004.
Top Papers
1. A D Smith, K A Jobst, C Johnston, C Joachim, Z Nagy. Apolipoprotein-E genotyping in diagnosis of Alzheimer’s disease. The Lancet. 1996, 348, 483-484.
2. Zs Nagy, M M Esiri, A D Smith. Expression of cell division markers in the hippocampus in Alzheimer’s disease and other neurodegenerative conditions. Acta Neuropathol 1997, 93, 294-300.
3. Zs Nagy, M M Esiri, A-M Cato, A D Smith. Cell cycle markers in the hippocampus in Alzheimer’s disease. Acta Neuropathol 1997, 94, 6-15.
4. Zs Nagy, M M Esiri. Apoptosis-related protein expression in the hippocampus in Alzheimer’s disease. Neurobiol Aging 1997, 18 (6), 565-571.
5. Zs Nagy, M M Esiri, A D Smith. The cell division cycle and the pathophysiology of Alzheimer’s disease. Neuroscience 1998, 87, 4, 731-739
6. Zs Nagy, M M Esiri. Neuronal cyclin expression in the hippocampus in temporal lobe epilepsy. Experimental Neurol - Neurodegeneration 1998, 150, 240-247.
7. Zs Nagy, M Z Smith, M M Esiri, L Barnetson and A D Smith. Hyperhomocysteinaemia in Alzheimer’s disease and expression of cell cycle markers in brain. JNNP 2000, 69, 565-566.
8. Zs Nagy, M Combrinck, M Budge, R McShane. Cell cycle kinesis in lymphocytes in the diagnosis of Alzheimer’s disease. Neurosci Letters. 2002, 317, 2, 81-84.
9. EJ Milwain, Zs. Nagy. Depressive symptoms increase the likelihood of cognitive impairment in elderly people with sub-clinical Alzheimer pathology. Dementia and Geriatric Cognitive Disorders. 2005, 19, 1, 46-50.
10. Zs. Nagy. The last neuronal division: a unifying hypothesis for the pathogenesis of Alzheimer’s disease. J Cell Mol Med. 2005, 9,3, 531-541.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Causes and pathogenesis
What are the top three papers (not yours) you have read recently?
1. Delobel P, Lavenir I, Ghetti B, Holzer M, Goedert M. Cell-Cycle Markers in a Transgenic Mouse Model of Human Tauopathy: Increased Levels of Cyclin-Dependent Kinase Inhibitors p21Cip1 and p27Kip1. Am J Pathol. 2006 Mar;168(3):878-87.

2. Webber KM, Casadesus G, Zhu X, Obrenovich ME, Atwood CS, Perry G, Bowen RL, Smith MA. The cell cycle and hormonal fluxes in Alzheimer disease: a novel therapeutic target. Curr Pharm Des. 2006;12(6):691-7.Related Articles, Links

3. Yang Y, Varvel NH, Lamb BT, Herrup K. J Neurosci. Ectopic cell cycle events link human Alzheimer's disease and amyloid precursor protein transgenic mouse models. 2006 Jan 18;26(3):775-84.Related Articles, Links
If resources were not limited, what research projects would you pursue?
Cell cycle research in animal models of neurodegeneration
What is your leading hypothesis?
Cell cycle deregulation in neurones as the pathogenic mechanism leading to Alzheimer's disease.
What piece of missing evidence would help prove it?
A good animal model
What is your fallback position?
The cell cycle activation may be non-specific phenomenon in neurones (stress response?) in the aged brain and it might be associated with neurodegeneration in general not an AD-specific pathway.

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