Updated 6 July 2006

Alzheimer Research Forum's 10th Anniversary Symposium: Mapping the Next Decade of Alzheimer Research

An ancillary event at the International Conference on Alzheimer's Disease 2006

Date and Time: Wednesday, July 19, 1:30-3:30 p.m.
Location: Centro de Convenciones, Madrid, Spain

Discussion leaders: Konrad Beyreuther and Dennis Selkoe

Presenters include: Bart de Strooper, David Holtzman, Takeshi Iwatsubo, Frank LaFerla, David Morgan, Li-Huei Tsai, Christine Van Broeckhoven, and Bruce Yankner

Ten years ago, the Alzheimer Research Forum was formally launched in Osaka, Japan, at the ICADRD. To mark this milestone, you are invited to attend our symposium on "Mapping the Next Decade of Alzheimer Research." The symposium asks participants to consider key advances in Alzheimer disease research from the past decade and look forward in a bold attempt to craft a research agenda for the next 10 years. Our speakers will form teams and prepare short presentations in which they will attempt to synthesize major findings in several overlapping subject areas relevant to AD. The teams will work on their presentations in advance, and can choose to post drafts on Alzforum and invite suggestions from the community. In Madrid the discussion leaders will lead a group brainstorming session aimed at drafting a research roadmap for the next decade. We want to challenge the field to integrate findings and draw significant consensus toward building inclusive hypotheses that explain more fully the pathogenesis of this complex disease.

This symposium offers a chance to think about the big picture, in a lively, collegial atmosphere. We will provide lunch to preregistered attendees.

Registration is free, but advance registration is required to ensure adequate seating and refreshments.

Registration Deadline: June 1
Contact: Nico Stanculescu

Comments and Discussion

AD Research Past and Future: View Slides by Takaomi Saido
Slide 1, Slide 2, Slide 3

Comment by Nikolaos Robakis— Submitted 4 May 2006

The paper by Doglio et al. has important implications for both the biological functions of the presenilin (PS) complex and the mechanisms by which PS FAD mutations promote neurodegeneration and other structural abnormalities in AD. The paper verifies previous results that presenilins regulate the PI3K/Akt cell survival pathway through a mechanism that is independent of the γ-secretase activity (Baki et al., 2004). This report is also consistent with recent evidence that FAD mutations may promote cell death and AD-related tau hyperphosphorylation through a mechanism that involves loss of presenilin function in the PI3K/Akt/GSK-3 and other cell signaling pathways (Baki et al., 2004; Kang et al., 2005). This last concept is in contrast to the widely held view that FAD mutations cause a gain of presenilin γ-secretase function, thus increasing production of neurotoxic species like Aβ1-42 (see, however, Alzforum debate on Gain or Loss of Function—Time to Shake up Assumptions on γ-Secretase in Alzheimer disease?). The data on aph-1/aPKC/PAR-1 indicate a new pathway that may also contribute to tau phosphorylation. Clearly, new exciting data emerging in the last 2 years from several laboratories promote novel concepts not only for the biological functions of PS1 but also for the mechanisms by which presenilin FAD mutations induce the specific neuropathology associated with AD.