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New Treatment for Alzheimer’s and Huntington’s Diseases
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New Treatment for Alzheimer’s and Huntington’s Diseases
Relies on Addressing the Beta-Amyloid Pathway.

Comments by J. C. Spencer

Ridding the brain of toxic amyloid plaques is viewed as a key target in slowing the course of Alzheimer's disease.  The amyloid pathway is THE MAIN HALLMARK OF ALZHEIMER'S DISEASE.  Here are two articles that deal with Alzheimer’s, Huntington’s, and the beta-amyloid pathway.  WHATEVER WORKS is what families with Alzheimer’s or Huntington’s members want to see.  Research has concluded what the problem is.  Throwing billions of dollars at the problem may not be the solution, but scientists are trying.  Part of the problem is that every drug, regardless of the hope it may help, adds more toxins to the body. 

Meanwhile, I suggest we look further at cutting healthcare costs by switching out regular sugar with a glyconutrient called trehalose.  The first article below is about GSK paying $28.5 million up front for a vaccine deal that may help address the beta-amyloid challenge.  The second article is an abstract from a published paper showing that the sugar trehalose may hold the answer for Alzheimer’s and Huntington’s disease by addressing the beta-amyloid challenge.

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October 24, 2008
GSK Pays Affiris $28M Up Front in Alzheimer's Vaccine Deal

(BioWorld Today Via Acquire Media NewsEdge) GlaxoSmithKline Biologicals SA, of Rixensart, Belgium, and Affiris GmbH entered a collaboration agreement granting GSK exclusive rights to Affiris's Alzheimer's disease vaccine programs targeting the beta-amyloid pathway.

Under the terms, Vienna, Austria-based Affiris will receive an up-front payment of 22.5 million (US$28.5 million) and could be eligible for future milestone payments and royalties. The total potential value of the agreement could reach 430 million in the event of full commercial success of the candidate vaccines.

As part of the deal, GSK is acquiring exclusive rights to develop and commercialize two Alzheimer's disease vaccine candidates that are based on Affiris' Affitope technology and are in Phase I development. Affiris also is granting GSK an exclusive option to develop and commercialize alternative Alzheimer's disease vaccine candidates, which are in preclinical development. The agreement is subject to government approval, GSK said.

Ridding the brain of toxic amyloid plaques is viewed as a key target in slowing the course of Alzheimer's disease. As GSK spokeswoman Sarah Alspach put it, the amyloid pathway is "the main hallmark of Alzheimer's disease," and thus an attractive target for new therapeutic approaches.
Nitasha Manchanda, an analyst with Decision Resources, offered a more tempered view, saying it's "still not really clear if this is the best target." But it's also "too early to rule this out as a significant approach," she told BioWorld Today.

Although amyloid remains a highly touted drug target for Alzheimer's disease, it has shown lackluster results in some recent studies, including a Phase III trial of Salt Lake City-based Myriad Genetics Inc.'s Flurizan; a Phase II study of bapineuzumab (AAb-001) from partners Dublin, Ireland-based Elan Corp. plc, and Madison, N.J.-based Wyeth; and a Phase III study of Alzhemed from Canadian firm Neurochem Inc. (See BioWorld Today, Aug. 28, 2007, July 31, 2008, and Aug. 21, 2008.)

Despite those recent setbacks, pharma companies continue to show interest in a range of approaches to fighting Alzheimer's. For example, Pfizer Inc. recently paid $225 million up front to Medivation Inc. to co-develop and market Dimebon, the biotech company's experimental drug for Alzheimer's and Huntington's disease. Dimebon (dimebolin) is believed to work by improving the mitochondrial function impaired in Alzheimer's disease. (See BioWorld Today, July 31, 2008, and Sept. 4, 2008.)

In August, German drugmaker Boehringer Ingelheim GmbH and Belgium's Ablynx NV extended their Alzheimer's drug development collaboration for another year. Boehringer also signed a deal with Evotec AG, of Hamburg, Germany, to jointly identify new targets in the treatment of Alzheimer's.

Earlier this year, CoMentis Inc. entered a $760 million deal with Japan's Astellas Pharma Inc. to develop a compound for Alzheimer's. And another Japanese drugmaker, Eisai Co. Ltd., has extended a 2007 deal with TorreyPines Therapeutics Inc., to discover targets for the disease.

In a 2007 deal with Coley Pharmaceutical Group Inc., Merck & Co. paid $4 million up front for rights to Coley's VaxImmune technology for use in developing vaccines for infectious disease and Alzheimer's.

Elan and Wyeth's ACC001 is the furthest ahead among those pursuing an immune therapy for Alzheimer's disease, Manchanda said. But that program is an active vaccine, and it is unclear whether an active antibody would have a longer-lasting effect, she added.

That could be a problem if the therapy causes an adverse reaction, and treatment needs to be stopped.

In contrast, Manchanda said that passive vaccines like those being developed by Affiris would have to be reinjected in patients to keep beta-amyloid at bay. Thus, the passive vaccine might be safer than active, because if a patient shows a reaction, treatment could be stopped, she explained.

Clinical trials of Elan's and Wyeth's AN-1792, a synthetic form of the beta-amyloid peptide, were suspended in 2002 when clinical signs consistent with encephalitis were reported in four patients. Development of the companies' ACC-011 Alzheimer's vaccine was halted due to a patient developing skin lesions, identified as a suspected case of vasculitis (inflammation of blood vessels), though the study later was restarted. (See BioWorld Today, April 21, 2008.)

While various other therapeutic approaches are being pursued in Alzheimer's disease such as tau-based programs, Manchanda said she believes that amyloid may be "the best bet" for pharmaceutical companies looking for potential new Alzheimer's drugs. Tau-based programs, such as those from TauRx Therapeutics Ltd. and Allon Therapeutics Inc., are in earlier stages and it will be a while before they reach the pivotal stage, she said.

Other therapies, like Medivations' Dimebon, are being developed to improve cognition but may not address the underlying disease, Manchanda said.

Still other firms like Winston-Salem, N.C.-based Targacept Inc. and London-based AstraZeneca plc each have products in development whose functions are similar to those of approved cholinesterase inhibitors but target different brain receptors.

Alzheimer's disease affects more than 26 million people worldwide, creating a $4 billion market.

Currently available drugs - Aricept (donepezil, Pfizer), Exelon (rivastigmine, Novartis AG), Cognex (tacrine, First Horizon Pharmaceutical Corp.), Reminyl (galantamine, Shire Pharmaceuticals Group plc) and Namenda (memantine, Forest Laboratories Inc.) - boost memory and cognition but cannot slow the course of the disease.


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Trehalose differentially inhibits aggregation and neurotoxicity of beta-amyloid 40 and 42.

Liu R, Barkhordarian H, Emadi S, Park CB, Sierks MR.

Department of Chemical and Materials Engineering, Arizona State University, Box 876006, Tempe, AZ 85287-6006, USA.

A key event in Alzheimer's disease (AD) pathogenesis is the conversion of the peptide beta-amyloid (Abeta) from its soluble monomeric form into various aggregated morphologies in the brain. Preventing aggregation of Abeta is being actively pursued as a primary therapeutic strategy for treating AD.

Trehalose, a simple disaccharide, has been shown to be effective in preventing the deactivation of numerous proteins and in protecting cells against stress. Here, we show that trehalose is also effective in inhibiting aggregation of Abeta and reducing its cytotoxicity, although it shows differential effects toward Abeta40 and Abeta42. When co-incubated with Abeta40, trehalose inhibits formation of both fibrillar and oligomeric morphologies as determined by fluorescence staining and atomic force microscopy (AFM). However, when co-incubated with Abeta42, trehalose inhibits formation only of the fibrillar morphology, with significant oligomeric formation still present. When aggregated mixtures were incubated with SH-SY5Y cells, trehalose was shown to reduce the toxicity of Abeta40 mixtures, but not Abeta42.

These results provide additional evidence that aggregation of Abeta into soluble oligomeric forms is a pathological step in AD and that Abeta42 in particular is more susceptible to forming these toxic oligomers than Abeta40. These results also suggest that the use of trehalose, a highly soluble, low-priced sugar, as part of a potential therapeutic cocktail to control Abeta peptide aggregation and toxicity, warrants further study.


Last Updated ( Dec 02, 2008 at 11:22 AM )