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Biotech / Medical : Elan Corporation, plc (ELN) -- Ignore unavailable to you. Want to Upgrade?

To: Icebrg who wrote (3555)	11/14/2002 7:31:10 AM
From: Icebrg	Read Replies (1) \| Respond to of 10345

SFN 2002 - Day 2 - Monday 4 November 2002 Report: Can Alzheimer's be stopped outside the brain? Investigators: Blas Frangione, Cynthia Lemere and Tom Wisniewski 4 November 2002 by Apoorva Mandavilli Learning from the failure of the Alzheimer's vaccine trial earlier this year, researchers are now devising safer variations of the immunization approach as a means to treat the disease. The key, they say, is to develop drugs that stay clear of the blood-brain barrier. Alzheimer's disease is characterized by plaques containing the amyloid-beta (A-beta) peptide. The predominant hypothesis in the field holds that plaques are the cause, rather than the byproduct, of the disease. Researchers have therefore focused on decreasing amyloid-beta production, and clearing the amyloid deposits by immunization. A vaccine trial begun by Elan pharmaceuticals and Wyeth-Ayerst was stopped abruptly early this year when some patients developed severe brain inflammation. The companies are now investigating what caused the inflammation, said Peter Seubert, a member of the Elan team, but no answers are forthcoming. To gain insight into the offending mechanisms, neurologist Cynthia Lemere is investigating Alzheimer's in Caribbean vervet monkeys. The monkeys live to about 20 years in captivity and, in the last years of their life, develop amyloid plaques similar to those seen in humans, said Lemere, assistant professor of neurology at Harvard University. When the researchers injected the monkeys with the A-beta, the monkeys generated antibody titers, Lemere reported. Although antibodies were seen in both plasma and the cerebrospinal fluid, CSF levels were "more than an order less than plasma" levels, she said. The primate model may help researchers understand immune responses induced by the vaccine, she added. Inflammation may have resulted either from A-beta toxicity, or because of autoimmunity. The 42-amino-acid peptide used by Elan crosses the blood-brain barrier, and may seed the formation of more fibrils, according to New York University researchers Blas Frangione and Tom Wisniewski. The researchers have developed a vaccine from the first 30 amino acids of the peptide, which they say is just as effective as, but safer than, the Elan vaccine. In general, they say, researchers may want to use "non-toxic A-beta derivatives" and compounds that do not cross the blood-brain barrier. For example, researchers have previously suggested adding compounds that bind to A-beta in the plasma, outside the central nervous system. Binding shifts the equilibrium between soluble amyloid in the plasma and plaque-associated amyloid in the brain, turning the plasma into a "sink" for amyloid, they suggested. Lemere and her colleagues have developed at least two such agents that appear to draw amyloid from the brain to the plasma. The compounds, Gelsolin and GM1, reduce A-beta without entering the brain. Although many of the teams have made progress, there is still no conclusive evidence that immunizing against the amyloid-beta peptide has any benefit in those with advanced forms of the disease. Those working in animal models vaccinate at an early stage, long before the disease is likely to be discovered in humans. Unless scientists develop tools to detect the disease in its early stages, says Mayo Clinic researcher Todd Golde, any treatment may be powerless to restore cognitive deficits. The best researchers may be able to do, he said, is prevent the disease from progressing further. news.bmn.com