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Symposim 2006

"Molecular Basis of Neurological Disease"

Dr. Colin L. Masters & Dr. Konrad Beyreuther

4th SYMPOSIUM
OCTOBER 23-24, 2006

Download Full Brochure (PDF)
Registration deadline: October 17th

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AWARDEES & KEYNOTE SPEAKERS

Colin L Masters, B Med Sci (Hons), MBBS, MD, FRCPath, FRCPA, FAA

Konrad Beyreuther, PhD, Prof. Dr. rer. nat. Dr. med. h.c.

Colin Masters’ and Konrad Beyreuther’s achievements have provided a path to the current development of therapeutic strategies for Alzheimer’s and other neurodegenerative diseases, affecting the quality of life of millions of people worldwide. They have pioneered studies of the biochemistry of the changes found in the brains of persons dying from Alzheimer’s and Creutzfeldt-Jakob diseases.

From their discoveries of the sequence of the Aβ amyloid protein in the brain plaques of Alzheimer’s disease, which facilitated cloning the gene for the amyloid precursor protein and revealed for the first time the proteolytic origin of the Aβ protein from neurons, they have gone on to elucidate the pathways leading to the accumulation and toxicity of Aβ in the aging human brain. These pathways have been of great importance in the development of a variety of drug targets, some directed at the secretases that facilitate the release of amyloid Aβ protein from nerve cells or directed at lipids of the lipid bilayer (especially cholesterol) that control secretase activity, and others directed at the toxicity and aggregation of the Aβ protein itself. Thus, from a state twenty years ago when virtually nothing was understood  about the molecular basis of Alzheimer’s disease, the studies of Masters and Beyreuther are widely acknowledged as having had a major influence on the direction of a now worldwide research effort.

The next five years are exceptionally promising with the real prospect of developing new drugs aimed at the Aβ amyloidogenic pathway (γ and β-secretase inhibitors; statins; metal protein attenuating compounds or MPACs) and applying pre-clinical diagnosis using Aβ as the target (PET scans, blood and CSF assays). Their work has also opened up new insights into other major neurodegenerative diseases (such as Creutzfeldt-Jakob and Parkinson’s diseases) in which aggregated proteins accumulate, providing clues to therapeutic interventions for multiple disease states.

Session Topics

  • Channelopathies
  • Neurodegeneration
  • Neurobiology of Stress & Gonadal Hormone Action
  • Neuro-oncology
  • Neurovirology & Neuroimmunology

Call for Posters

In addition to invited speakers, poster presentations will be chosen from submitted abstracts. Abstracts are invited on all aspects of the Molecular Basis of Neurological Disease and must be submitted by the October 9th deadline. Submitted abstracts will be reviewed by the Scientific Program Committee.  Notification of acceptance will be sent to you by email.

Abstract Format

  • Abstracts should be submitted in Adobe PortableDocument Format (.pdf).
  • The abstract should fit within a rectangle 6"x9”.
  • The abstract length is not to exceed ONE page.
  • The text should be left justified and single-spaced with character size set to 12 point, and a Times New Roman font selected.
  • The title should be typed in CAPITAL and BOLD.
  • The authors' names should appear on a new line immediately beneath the title, with the presenting author's name underlined.
  • The authors' affiliations should be placed on a separate line immediately beneath the authors' names.
  • The abstract should introduce the purpose of the study, summarize the methods, present the results and discuss major conclusions.