The development of drugs for Alzheimer's disease is a cemetery for clinical trials, with over 0 failures over the past 20 years. The handful of approved treatments provide only a modest and temporary relief to symptoms such as memory loss; no stopping the progression of the disease.
In this gloomy context come the provocative results of two clinical trials highly publicized, presented today at the International Conference of the Alzheimer Association in Washington, DC Both trials tested antibodies that latch onto amyloid β, a protein that forms sticky masses in the brain of people with Alzheimer's disease. It was reported that treatment slowed cognitive decline; another found that the antibody reduces amyloid levels, many scientists have argued is the heart of the Alzheimer's brain.
The results, presented at the meeting by the biotech companies Biogen and Eli Lilly, provide some of the first "clear" evidence that the targeting of the β-amyloid protein is a promising approach for treatment Alzheimer's disease, said Dennis Selkoe, a neuroscientist at Harvard University and a leading proponent of the hypothesis called amyloid. But small and cognitive benefits that a trial showed no reduction of amyloid in the brains of people have left plenty of room for skepticism.
antibody, solanezumab Eli Lilly had failed to show a benefit over placebo in a previous trial in people with mild to moderate Alzheimer's and Lilly's own study in 2012. today, however, the company said the drug appeared to slow cognitive decline in a standard measure of about 34% in a subset of patients with mild Alzheimer's disease, which Lilly allowed to continue taking the drug after the trial has ended, 2012. A control group in the original trial which was then launched on the drug later showed similar improvements
However, the study did not Lilly actually measure the decline of amyloid Selkoe rating :. "It could go down, but we don 't know that." Participants in the Lilly trial also failed to show significant benefits in two other trials, cognitive important result that "guarantees caution to draw firm conclusions from these analyzes," the company acknowledged in a statement. hoping to see clearer benefits, the company is currently running, IIIa much phase, which will end in October 2016, only in people with mild Alzheimer's disease.
antibody adumanucab Biogen, also a record mix. He had put the effervescence in the Alzheimer community when the company announced positive results of an early study. After administering several different doses of the drug in 166 patients who had been diagnosed with early stage Alzheimer's disease, the company said that 27 people who had received the maximum dose of 10 mg per kg showed significant cognitive benefits compared to controls and reduced levels of protein.
But this dose caused brain swelling and microscopic hemorrhages in some cases, so the company decided to try a smaller dose, 6 mg. Today, the company said deflate the results of a monitoring test: Over 54 weeks the 6 mg dose showed no significant effects on cognition, although it has reduced levels of amyloid in the brain. The stock market, for one, found the results hard, first sending the stock price Biogen low after the data were released. Despite the setback, this year the company will launch a Phase III trial of 18 months with 2,700 participants in the US, said company representative Jeff Sevigny.
Much rides on the success of these monitoring tests, said neurologist Rakez Kayed from the University of Texas Medical Branch in Galveston, Texas. "If they do not arrive later and we get another black eye, it will be difficult."
Selkoe argued that new data suggests Biogen although other approaches to reducing amyloid, such as drugs that block the production and transport of molecules that contribute to amyloid accumulation and as vaccines that prime the immune system to break down the plaques should be "vigorously" pursued.
But Kayed warns that mouthwatering results should not obscure other approaches for the treatment of Alzheimer's disease. Although many researchers now agree that the amyloid β is an important trigger for Alzheimer's disease, most also think that secondary processes, such as the accumulation of another protein called tau, drive the disease in its later stages. "If we're all going in the β-amyloid and ignore other therapeutic approaches, it will be devastating," he said.
0 Komentar