Plaque May Not Be The Culprit
A new theory of Alzheimer’s disease takes a look at the role of brain plaques in a different light.
Plaque has long been considered the gooey substance that coat and kill brain cells, taking with it the ability for a person to retain their memory, personality, cognitive thinking and humanity.
But emerging research is reconsidering whether plaque may actually offer a protective coating to fight off attacks by free-floating bits of toxic protein, amyloid beta. If so, the drugs currently under development such as bapineuzumab, represents research heading in the wrong direction.
Bapineuzumab, a monoclonal antibody predicted to be a blockbuster drug to treat about 26 million with Alzheimer's worldwide and is currently under development by Pfizer, Johnson & Johnson, and Elan.
New research out of Mount Sinai’s Alzheimer’s Disease Research Center found mice that form amyloid beta called oligomers, but never plaque, developed the same thinking problems as mice with plaque and oligomers.
When genes were added to create more plaque, the mice got no worse, reports Reuters.
Published in the Annals of Neurology, the findings “suggests that plaques were not necessary and the addition of plaque did not make the oligomer-induced memory problems any worse,” according to Dr. Sam Gandy of Mount Sinai School of Medicine.
That may explain why the current lines of drugs that treat symptoms have not been effective.
Research Continues Anyway
In releasing results in 2008 about the phase II trial of bapineuzumab, Wyeth and Elan disclosed that the drug failed to improve the cognitive functioning in 234 Alzheimer’s patients after 18 months of treatment, reports BNET.
Still, the drug companies heralded the drug’s efficacy in patients missing the gene variant ApoE4, which increases the risk of Alzheimer’s.
Columnist David Hamilton writes for BNET, “Without doubt, there’s a huge need for effective Alzheimer’s treatments. But companies like Wyeth and Elan do themselves — and patients — no favors by torturing their data and hyping all-but-meaningless results this way. (Of course, analysts and gullible investors do themselves no favors by believing these ginned-up results, either.) No one should be surprised if, two years from now, bapineuzumab ends up as dead as Myriad Genetics’ recently failed Alzheimer’s drug, Flurizan.”
In the meantime, research continues on bapineuzumab and Pfizer plans to release results of its phase 3 trial in 2012 and 2014. #