Alzheimer's disease: a black streak
Trials of drugs for Alzheimer's disease have not yielded results
Then, on August 24, Eli Lilly admitted that its version – solanezumab – also failed to achieve its goal.
Both drugs targeted beta-amyloid, a protein that forms plaques in the brain that lead to memory impairment and dementia. Having been defeated, the researchers still do not abandon the amyloid hypothesis (see here about the insulin theory), but pin their hopes on new methods of clinical trials and plan to test the drugs on patients with early forms of Alzheimer's disease.
Many observers, however, note that investors are frightened by the loss of hundreds of millions of dollars spent on useless trials, and will no longer support the development of drugs for Alzheimer's disease and other types of dementia.
Beta-amyloid plaques are thought to damage neurons by destroying their connections with neighbors. But there is only indirect evidence of this: at autopsy, the number of plaques corresponds to the severity of the disease. In addition, mutations have been identified in the gene responsible for beta-amyloid, which increase the risk of developing the disease or, on the contrary, protect against it. Nevertheless, despite all the money invested in drugs directed against these plaques, there was no result, and there is no result. "First of all, we must finally confirm or refute the amyloid hypothesis," emphasizes Paul Eisen from the University of California at San Diego (USA).
The first test results of solanezumab were not very encouraging. The drug was supposed to block beta-amyloid before the protein forms plaques. In patients with mild and moderate forms of the disease, he could neither slow down the deterioration of memory and other cognitive functions, nor prevent the loss of the ability to perform simple tasks like eating and personal hygiene. But other studies have shown that the drug still slowed the progress of cognitive impairment in the case of mild forms of the disease. Specific figures will be released only in the fall.
Well, bapineuzumab was designed to awaken the immune system and encourage it to deal with plaques. However, two trials involving approximately 2,400 patients did not show any benefits of the drug compared to placebo. Perhaps the fact is that bapineuzumab is toxic and it is administered in very small doses.
Researchers are inclined to believe that the problem is not so much in targeting beta-amyloid as in the timing of treatment. "We start therapy too late," says, for example, Ronald Petersen from the Mayo Clinic (USA). According to him, like fatty plaques in the coronary arteries, beta-amyloid clots accumulate throughout life. And just like statins designed to lower cholesterol, amyloid blockers should be taken in middle age in order to prevent problems in retirement.
But no one knows when exactly. You can't grab every thirty-year-old on the street and take him to a polyclinic for long-term experiments.
However, next year three studies will begin at once, which will test whether antiamyloid drugs can prevent early symptoms of Alzheimer's disease and cognitive impairment in patients with an appropriate genetic predisposition or high levels of beta-amyloid.
During one of them, the drug krenezumab, developed by Genentech, will be tested. The Colombian family will act as test subjects, which has a rare mutation that significantly increases the risk of Alzheimer's disease at an advanced age. The project with a budget of $100 million is aimed at family members who have not yet shown any symptoms, and will last five years. Scientists will also try to identify biomarkers that allow evaluating the effectiveness of this and other drugs based on brain scans or analysis of cerebrospinal fluid.
Two other projects are still looking for money. Let's hope that the failures of this summer will not scare away sponsors.
Prepared based on Nature News: Alzheimer's drugs take a new tack.
Portal "Eternal youth" http://vechnayamolodost.ru06.09.2012