Tag: A-beta peptide

Innovation Radar: Approved Drug Counters Effects of Alzheimer’s in Mice

An FDA-approved drug called bexarotene counters many of the effects of Alzheimer’s disease in mouse models, researchers report. The build-up of protein fragments called amyloid-beta is a key feature of the disease; everyone’s brain produces amyloid-beta, but in healthy individuals, enzymes break the fragments down, with help from a protein called ApoE. Paige Cramer and colleagues knew that bexarotene activates a protein that helps switch on the ApoEgene, and they hypothesized that the drug might therefore enhance the clearance of amyloid-beta in the brain. They gave the drug to mice engineered to have an Alzheimer’s-like condition and observed that levels of the protein fragments in the mice’s brains dropped substantially within just a few days. The mice also showed improvements in their cognitive, social and olfactory performance. Bexarotene, also known as Targretin, is currently used to treat a form of skin cancer and has a favorable safety profile, the authors note. The drug activates the nuclear receptor protein known as RXR, which binds one of two other nuclear receptors, PPAR and LXR. These receptor pairs then activate the transcription of the ApoE gene.

The research is published online by the journal Science at this week’s Science Express website.

Company News: Probiodrug to Host Alzheimer Symposium

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.