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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Mervyn
Last Name:Monteiro
Title:Professor
Advanced Degrees:Ph.D.
Affiliation:University of Maryland, Baltimore
Department:Department of Anatomy and Neurobiology, BioMET
Street Address 1:Room N352
Street Address 2:725 West Lombard Street
City:Baltimore
State/Province:MD
Zip/Postal Code:21201
Country/Territory:U.S.A.
Phone:410-706-8132
Fax:410-706-8184
Email Address: 
Disclosure:
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View all comments by Mervyn Monteiro
Clinical Interests:
Prion Diseases, Neurodevelopmental Disorders (Down syndrome, etc.), Polyglutamine Disorders (Huntington's, etc.), Alzheimer Disease, Tauopathies, Aging Process, Parkinson Disease
Research Focus:
Apoptosis/Cell cycle, Signal transduction, Genetics, A-beta PP/A-beta, Molecular and Cell biology, Neurobiology, Oxidative Stress, Protein structure/chemistry, Tau/Cytoskeleton
Work Sector(s):
University
Researcher Bio
EDUCATION:
BSc with 1st Class Honors in Microbiology, June 1979; Queen Elizabeth College, University of London, England, U.K.
Ph.D. in Microbiology and Molecular Biology, January 1983; Nat. Ins. for Medical Res. (MRC) Mill Hill, London, Dept of Microbiology; Thesis title: Characterization of the replication terminus of the Bacillus subtilis chromosome.
Post-doctoral, January 1983 - December 1986; Nat. Ins. for Medical Res. Mill Hill London, Department of Developmental Biochemistry; Advisor: Dr. Robert Cox: Research Projects: Actin and tubulin genes of Physarum.
Post-doctoral, December 1986 - August 1989; The Johns Hopkins University, School of Medicine, Advisor: Dr. Don Cleveland; Research Project: Expression of neurofilament genes in fibroblasts and transgenic mice.
Assistant Professor Sept 1989 - June 1996.
Associate Professor July 1996 - June 2002.
Professor July 2002 -present. University of Maryland, UMBI and School of Medicine

AWARDS AND HONORS Helen R. White Prize 1979 (Queen Elizabeth College- most promising student in Microbiology); MRC postgraduate scholarship 1979 - 1983; MRC Staff (Post-doctoral fellow) 1983 - 1986. Awarded Traveling Grants from The Royal Society and the Wellcome Trust 1986; American Heart Association post-doctoral fellowship award 1987 - 1989; Certificate of Merit. Young Investigators' Day 1989 -The Johns Hopkins University.
SERVICE 1992 Site Visit Reviewer Program Project grant on ALS (NINDS); 1992 Ad Hoc Reviewer for Neurology (B-1) Study Section of National Institutes of Health; 1992 Ad Hoc Reviewer for Neurological Sciences (NLS1) Study Section of National Institutes of Health; 1995 Ad Hoc Reviewer for Neurological Sciences (ZRG1-NLS1) Study Section of NIH; 1996 Ad Hoc grant reviewer for NSF; 1996 Ad Hoc reviewer for NIH Fogarty International center grant; 1997 Ad Hoc reviewer Program Project Grant, NIA. 2001- present MDCN1 NIH Regular member; 1998, & 2000-Correspondent for The Alzheimer's Research Forum Web site (ASCB meetings and World AD congress). 2001- Alzheimer’s Association Ad Hoc reviewer.
Top Papers
1. Monteiro, M.J., Hicks, C., Gu, L. and Janicki, S. (1994). Determinants for intracellular sorting of cytoplasmic and nuclear intermediate filaments. J. Cell Biol. 127:1327-1343.

2. Monteiro, M.J. and Mical, T. (1996) Resolution of kinase activities during the HeLa cell cycle: Identification of kinases with cyclic activities. Experiment Cell Research 223:443-451.

3. Starr, R., Attema, B., DeVries, G. and Monteiro, M.J. (1996) Neurofilament phosphorylation is modulated by myelination. J. Neuroscience Research 44:328-337.

4. Xiao, J., Perry, G., Troncoso, J. and Monteiro, M.J. (1996) a Calcium-calmodulin-dependent kinase II is associated with paired helical filaments of Alzheimer's disease. J. Neuropath & Exp. Neurol. 55:954-963.

5. S. Janicki and Monteiro, M.J. (1997) Increased Apoptosis arising from Increased Expression of the Alzheimer’s Disease-associated Presenilin-2 Mutation (N141I). J. Cell Biol. 139:485-495.

6. T. Mical and Monteiro, M.J. (1998) The role of sequences unique to nuclear intermediate filaments in the targeting and assembly of human lamin B: Evidence for lack of interaction of lamin B with its putative receptor. J. Cell Science 111:3471-3485.

7. Stabler, S.M. Ostrowski, L.L. Janicki, S.M. and Monteiro, M.J. (1999) A myristoylated calcium binding protein that preferentially interacts with the Alzheimer’s Disease Presenilin 2 protein. J. Cell Biol. 145:1277-1292.

8. Janicki S.M. and Monteiro, M.J. (1999) Presenilin overexpression arrests cells in the G1 phase of the cell cycle. Arrest potentiated by the Alzheimer’s Disease PS2(N141I) mutant. Am. J. Pathol. 155:135-144.

9. Mah, A., Perry, G., Smith M.A., and Monteiro, M.J. (2000) Identification of ubiquilin, a novel presenilin interactor that increases presenilin protein accumulation. J. Cell Biology. 151: 847-862.

10. Janicki, S.M., Stabler, S.M. and Monteiro, M.J. (2000) Familial Alzheimer’s Disease Presenilin-1 mutants potentiate cell cycle arrest. Neurobiology of Aging 21:829-836.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
The exact mechanism that leads to neurodegeneration (cell loss).
What are the top three papers (not yours) you have read recently?
Bence et al. Science 292:1552-1555 (2001) Impairment of the Ubiquitin-Proteasome System by Protein Aggregation.

Vassar et al. Science 286: 735-741. (1999) B-secretase cleavage of Alzheimer's Amyloid precursor protein by the transmembrane aspartic protease BACE.

Warrick et al. Nature genetics 23:425-428 (1999) Supression of polyglutamine-mediated neurodegeneration in Drosophila by the molecular chaperone HSP70.
If resources were not limited, what research projects would you pursue?
A systematic approach of studying genes involved in neurodegeneration in animals (mouse, C.elegans and Drosophila) and cell cultures by inactivating or misexpressing the culprit proteins and their associated proteins.
What is your leading hypothesis?
Cell in AD die by apoptosis due to cell stress.
&
Protein misfolding causes dysfunction of the Ubiquitin-proteasome system in neurodegenerative diseases.
What piece of missing evidence would help prove it?
Culture and animals models demonstrating the exact mechanism for how cells first succumb to the death signals.
What is your fallback position?
Don't know as yet. Will wait till the cookie crumbles!

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