MADRID, July 21 (UPI) -- The dreaded illness Alzheimer's disease -- the sickness that gradually robs people of their minds and bodies -- remains incurable -- but, doctors hope, not unbeatable.
At this week's 10th International Conference on Alzheimer's Disease and Related Disorders in Madrid, doctors warned that unless they discover ways to slow down or halt the disease, the health services of the world will be bankrupted.
The Chicago-based Arthritis Association estimated that 4.5 million people in the United States and 15 million worldwide have Alzheimer's disease. By 2050, 16 million people will be fighting the disease.
"I can tell you that when we started about 20 years ago we had little hope that we could find drugs that could impact this disease," said Howard Fillit, executive director of the Institute for the Study of Aging in New York.
But today there are already several drugs marketed that slow the disease, and Fillit told United Press International, "There is an absolute explosion in the number of drugs in development. We are going to change the world in the next five to 10 years."
Fillit moderated a news briefing at which researchers described some of those drugs, most of which are still at the fringes of discovery. Many others were also scrutinized by the 5,000-plus clinicians and allied healthcare professionals drawn to Madrid for the weeklong meeting.
In one new treatment, researchers at Eli Lilly, Indianapolis, Ind., developed an antibody that targets an abnormal beta-amyloid particle in the brain. Amyloid is one of the substances that, when out of control, interrupts brain messaging and builds damaging structures in the brain.
Eric Siemers, a Lilly researcher, said the amyloid-beta antibody was tested in 19 Alzheimer's patients. They were given a single dose of the drug and observed that the amount of amyloid protein in the blood rose markedly. Siemers suggested that means that the antibody is binding with the unwanted amyloid product and bringing it into the blood stream and out of the brain.
However, cognitive functioning tests did not indicate that the drug was making any impact on the disease. Nevertheless, Siemers said studies will continue in larger groups of patients.
Another attack on amyloid-associated aberrant behavior in Alzheimer's disease was launched by Ashley Bush, a consultant to Prana Biotechnology of Parkville, Australia.
He looked at the abnormal handling of essential brain metals -- copper, zinc and iron -- and how that leads to formation of beta-amyloid oligomers, or abnormal assemblies -- in the brain.
He and colleagues developed PBT2, an analog of the antiquated antibiotic clioquinol. When mice with Alzheimer's-like disease were treated with PBT2, half of the plaques in the animal brains disappeared.
Bush said that on the basis of the study, a phase 2 trial in humans with PBT2 has been initiated.
Other researchers hunting for the reason that tramiprosate (Alzhemed) -- now in phase 3 clinical studies in the United States and Europe -- appears to improve outcomes in Alzheimer's disease found that the drug prevents cells in the brain from dying.
Scientists studying the brain cells of rats observed that in the presence of amyloid beta, 58 percent of neurons underwent programmed cell death known as apoptosis. But when the cells were protected with tramiprosate, the cellular death toll was lowered by 40 percent.
"We saw a strong additional neuroprotective effect. This, with further verification, will take this drug forward and into a potentially rich new area of efficacy studies," said Daniel DeLorme, vice president for research at Neurochem Inc. in Laval, Quebec, Canada.
Paul Aisen, professor of neurology at Georgetown University Medical Center, Washington, added, "The molecular cause of Alzheimer's disease is the amyloid peptide. The amyloid peptide accumulates in the Alzheimer's brain and is damaging to neurons and synapses and neuronal function in general. We've known for some time that treatment with tramiprosate reduces the accumulation of amyloid in the brain. With this study, our information has been extended to show that it is also protective against amyloid-mediated neuronal damage. That's what's new here."
Alain Robillard, associate clinical professor in neurology at Maisonneuve-Rosemont Hospital, University of Montreal-affiliate hospital, told UPI, "The mode of action that we have in evidence here indicates and supports what we supposed in the phase 2 trial. It appears possible that the mechanism of action of this drug will prevent fewer plaques from forming, ergo, less disease."
Doctors in Switzerland are moving forward with a new cholinesterase inhibitor, now known as ZT-1, being developed by Debiopharm of Lausanne, even though early tests didn't show significant results.
Emmanuel Tamches, the project director for Debiopharm, told UPI he believes further double-blind testing will show that the drug is at least as effective as donepezil (Aricept) and may have fewer side effects, including less chance of heart-rhythm disturbances.
Still other possible drugs include Gaithersburg, Md.-based Panacea Pharmaceuticals' PAN-811, an agent that in laboratory experiments protected primary neurons from amyloid toxicity.
And Neuro Pharma of Madrid went to the oceans to find inhibitors of glycogen synthase kinase-3-beta. That compound is necessary for halting a cascade of molecular events that feeds the Alzheimer's process. Palinurin and tricantin, substances extracted from a marine sponge, appear to inhibit glycogen synthase kinase-3-beta in laboratory testing.
"We are very encouraged to see a diversity of approaches to treating Alzheimer's showing some level of success," Fillit said. "We must pursue every available avenue. The urgency has never been higher."