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Biotech / Medical : NTII - Miscellaneous -- Ignore unavailable to you. Want to Upgrade?

To: John McCarthy who wrote (1188)	8/12/2005 9:00:06 AM
From: Pogeu Mahone	Respond to of 1296

Nasal spray clears Alzheimer’s brain plaques 20:00 11 August 2005 NewScientist.com news service Alison Motluk Related Articles Antibody treatment raises hope in Alzheimer's fight 16 April 2005 Alzheimer's plaques imaged in living brains 13 March 2005 Early detection of Alzheimer's with bio-barcoding 05 February 2005 Search New Scientist Contact us Web Links Brigham and Women’s Hospital, Boston Joanne McLaurin, University of Toronto Alzheimer’s disease, Medline Plus Journal of Clinical Investigation A new nasal vaccine for Alzheimer’s disease has cleared plaques from the brains of affected mice and will be tested in humans in 2006. Most previous attempts to produce a therapeutic vaccine have involved antibodies against beta amyloid, a naturally-occurring protein which is widely considered to cause the disease. In Alzheimer’s patients, beta amyloid forms plaques that seem to destroy neurons. But the antibody approach ran into problems three years ago, when a promising vaccine trial was halted after 15 of 360 volunteers developed swelling in the brain. Now Howard Weiner, at Brigham and Women’s Hospital in Boston, US, and his colleagues have tried a new strategy. Weiner was intrigued by the fact that brain inflammation in the earlier trial coincided with exceptional clearance of beta amyloid. He did some experiments and found that mice with Alzheimer’s treated to develop multiple sclerosis-like brain inflammation also cleared the beta amyloid from their brains. “Sometimes inflammation is good,” he says. His team discovered that in inducing inflammation they were activating cells in the brain known as microglia, whose job it is to ingest unwanted material. In this case, the microglia were ingesting the beta amyloid. Interestingly, in mice without beta amyloid plaques, no activation took place. Striking results The researchers now knew they wanted to switch on the microglia, but they also wanted to do it using drugs safe for humans. They decided on a combination of glatiramer acetate (Copaxone), an approved MS drug that acts as a decoy for errant immune-system attacks, and Protollin, an adjuvant that stimulates innate immunity. It was given as a nasal mist, a technique Weiner’s lab has had a long interest in. “And it worked,” says Weiner. The combination reduced amyloid beta in the mouse brains by 83% compared to controls. “The results were quite striking,” says Joanne McLaurin at the University of Toronto, Canada, who has worked extensively on Alzheimer’s vaccines. The idea that inflammation might be helpful in clearing amyloid plaques was first raised a few years ago by a different team, she notes: “The idea is very interesting.” As always, the question is whether what works in an animal model will work in humans. “Anytime you move from mouse to man there are risks,” says Weiner. Journal reference: Journal of Clinical Investigation (DOI:10.1172/JCI23241)