Past Webinar
M1 Receptors Play a Central Role in AD Pathology and Cognition
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Introduction
Our thanks to Neuron for providing free access to this paper for the purposes of this live discussion.
Caccamo A, Oddo S, Billings LM, Green KN, Martinez-Coria H, Fisher A, LaFerla FM. M1 receptors play a central role in modulating AD-like pathology in transgenic mice. Neuron. 2006 Mar 2;49(5):671-82. Read paper
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Frank LaFerla led this Webinar on 5 July 2006. Readers are invited to submit additional comments by using our Comments form at the bottom of the page.
Background
Background Text
ARF News Story: Cholinergic Transmission and Aβ: Boosting M1 Receptors Treats Model
An impressive data set that appeared yesterday in Neuron shows that a specific M1 muscarinic receptor agonist can reverse both cognitive deficits as well as the amyloid and tau pathology in the APP/PS1/tau triple transgenic mice mouse model of AD. The publication, from Frank LaFerla and colleagues from the University of California at Irvine and Abraham Fisher at the Israel Institute for Biological Research in Ness Ziona, advances a story that garnered significant attention when the investigators presented their preliminary results on the small molecule AF267B at the 2004 Society for Neurosciences meeting in San Diego.
The compound was licensed at that time to TorreyPines Therapeutics, Inc. (formerly Neurogenetics, Inc.) in San Diego, who made their own news this week by announcing that they have initiated a second Phase I trial of the compound in humans. The trial, which is expected to yield results as soon as next June, might give an early indication of whether the compound is capable of affecting Aβ or tau metabolism or cognitive function in humans ... Read more
References
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Further Reading
Papers
- Wodicka L, Dong H, Mittmann M, Ho MH, Lockhart DJ. Genome-wide expression monitoring in Saccharomyces cerevisiae. Nat Biotechnol. 1997 Dec;15(13):1359-67. PubMed.
Panelists
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Frank LaFerla, Ph.D.
University of California, Irvine
Current Scientific Advisory Board Member
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