Despite considerable efforts to find a cure, Alzheimer’s disease (AD) at present cannot be treated adequately, as there is no therapy available to significantly slow down disease progression, halt the disease or prevent it.
During the past years, researchers from the German-based biotech company Probiodrug have generated a compelling body of evidence that a particular variant of the notorious A beta peptide, which clumps together in the brain of AD patients to the typical plaques, is the major culprit. This variant is formed through a hitherto unknown reaction of a brain enzyme called glutaminyl cyclase (QC) and carries a pyroglutamic residue at its N-terminus. This renders it much more neurotoxic than the unmodified A-beta and also significantly reduces its solubility so that it starts aggregating.
Today, this hypothesis is not an outsider opinion any more. On Monday, November 22, well-known Alzheimer researchers from Germany (Christian Haass, Stephan v. Hörsten, Marcus Fändrich, Thomas Bayer, Steffen Roßner, and Stephan Schilling), the U.S. (Cynthia Lemere, Lennart Mucke, Steve Jacobsen), Austria (Reinhold Schmidt), and Japan (Takaomi Saido) will meet at Probiodrug´s Halle (Saale) headquarter to provide the latest findings in the light of this hypothesis and to discuss novel therapeutic strategies. One of the approaches pursued by Probiodrug is inhibiting the formation of the toxic A-beta variant by small molecule inhibitors of the QC enzyme.
The public symposium entitled “Neurodegenerative Disorders During Aging – Contemporary Research and New Therapies” will take place on Weinberg Campus in Halle (Saale) on Monday, November 22, 2010, from 10am to 3pm. The detailed program can be found on Probiodrug‘s website.