In order to prevent spam,
this email address cannot be copied.
Researcher Profile - Paul Coleman Get Newsletter
Alzheimer Research Forum - Networking for a Cure Alzheimer Research Forum - Networking for a CureAlzheimer Research Forum - Networking for a Cure
  
What's New HomeContact UsHow to CiteGet NewsletterBecome a MemberLogin          
Papers of the Week
Current Papers
ARF Recommends
Milestone Papers
Search All Papers
Search Comments
News
Research News
Drug News
Conference News
Research
AD Hypotheses
  AlzSWAN
  Current Hypotheses
  Hypothesis Factory
Forums
  Live Discussions
  Virtual Conferences
  Interviews
Enabling Technologies
  Workshops
  Research Tools
Compendia
  AlzGene
  AlzRisk
  Antibodies
  Biomarkers
  Mutations
  Protocols
  Research Models
  Video Gallery
Resources
  Bulletin Boards
  Conference Calendar
  Grants
  Jobs
Early-Onset Familial AD
Overview
Diagnosis/Genetics
Research
News
Profiles
Clinics
Drug Development
Companies
Tutorial
Drugs in Clinical Trials
Disease Management
About Alzheimer's
  FAQs
Diagnosis
  Clinical Guidelines
  Tests
  Brain Banks
Treatment
  Drugs and Therapies
Caregiving
  Patient Care
  Support Directory
  AD Experiences
Community
Member Directory
Researcher Profiles
Institutes and Labs
About the Site
Mission
ARF Team
ARF Awards
Advisory Board
Sponsors
Partnerships
Fan Mail
Support Us
Return to Top
Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Paul
Last Name:Coleman
Title:Professor
Advanced Degrees:Ph.D.
Affiliation:University of Rochester Medical Center
Department:Center on Aging and Developmental Biology
Street Address 1:601 Elmwood Ave.
City:Rochester
State/Province:NY
Zip/Postal Code:14642
Country/Territory:U.S.A.
Fax:(585) 273-1132
Email Address: 
Disclosure:
(view policy) 
 
View all comments by Paul Coleman
Clinical Interests:
Alzheimer Disease, Aging Process
Research Focus:
DNA microarrays, Diagnosis, Microscopy, Animal Models, Neuropathology, Proteomics, Tau/Cytoskeleton, Apoptosis/Cell cycle, Neurobiology, Bioinformatics/Statistics, Molecular and Cell biology
Work Sector(s):
University
Web Sites:
Professional: http://www.urmc.rochester.edu/Aab/aging/index.htm
Researcher Bio
Ph.D. Univ. Rochester, 1953
1 Lt., US Army Medical Research Lab 53-56
Res.Asst Prof,.Tufts Univ.56-59
Associate M.I.T. Computer Center 57-59
Fellow, Johns Hopkins Medical 59-62
Assoc. Prof. Physiol., U. Maryland 62-67
Professor, Univ. of Rochester 67 - present
Director, Alzheimer Disease Center 90-present
Editor-in-Chief, Neurobiology of Aging 88- present
Top Papers
Buell & Coleman (1979) Dendritic growth in aged human brain and failure of growth in senile dementia. Science, 206: 854-856.

Eberwine, Yeh, Miyashiro, Cao, Nair, Finnell, Zettle and Coleman (1991) Analysis of gene expression in single neurons. P.N.A.S., 89: 3010-3014.

Callahan & Coleman (1995) Neurons bearing neurofibrillary tangles are responsible for selected synaptic deficits in Alzheimer's disease. Neurobiol. Aging, 16: 311-314.

Chow, Cox, Callahan, Weimer, Guo and Coleman (1998) Expression profiles of multiple genes in single neurons of Alzheimer's disease. P.N.A.S. 95: 9620-9625.

Morsch, Simon & Coleman (1999) Neurons may live for decades with neurofibrillary tangles. J. Neuropath & Exptl. Neurol., 58: 188-197.

Callahan, Vaules & Coleman (1999) Quantitative decrease in synaptophysin message and increase in cathepsin D message expression in Alzheimer's disease neurons. J. Neuropath & Exptl. Neurol., 58: 275-287.

Callahan, Vaules & Coleman (2002) Progressive reduction of synaptophysin message in single neurons in Alzheimer's disease. J. Neuropath & Exptl. Neurol. In Press.

Yao & Coleman (2002) Deficits in expression of genes related to synaptic vesicle trafficking in frontal cortex of Alzheimer's disease. Neurobiol. of Disease. In Press

.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Description of the entire molecular cascade of AD from first cause(s) to cell death - and the functional neurobiological consequences of the progression of this cascade.
What is your leading hypothesis?
Not really a hypothesis, but more related to experimental approach: that information derived from single brain cells is more valuable than information derived from homogenates that contain many cell types as well as cells in different stages of disease.
What is your fallback position?
To work with homogenates.

Print this page
Email this page
Alzforum News
Papers of the Week
Text size
Share & Bookmark
Desperately

Antibodies
Cell Lines
Collaborators
Papers
Research Participants
Copyright © 1996-2013 Alzheimer Research Forum Terms of Use How to Cite Privacy Policy Disclaimer Disclosure Copyright
wma logoadadad