We may have entered the era of Alzheimer's treatments, as a second drug in less than a year has been shown to halt the progression of the disease. Eli Lilly has reported that its drug, donanemab, reduces the progression of Alzheimer's disease by approximately one-third. However, two volunteers, and possibly a third, died due to brain swelling.
Donanemab functions similarly to lecanemab, which made headlines around the globe when its ability to slow the disease was demonstrated. Both are antibodies similar to those produced by the body to combat viruses. However, these are designed to eliminate beta amyloid, a tenacious substance found in the brain, from the body.
Alzheimer's disease is characterized by the formation of amyloid deposits in the intercellular spaces between brain cells. Dr. Cath Mummery, clinical lead of the cognitive-disorders clinic at the UK's National Hospital for Neurology and Neurosurgery, stated that the decades-long struggle to discover effective treatments for Alzheimer's disease is shifting.
The complete details of Eli Lilly's trial have not yet been published. However, the main findings have been disclosed. Participating were 1,734 individuals in the earliest phases of Alzheimer's.
Donemab was administered on a monthly basis until the cerebral plaques disappeared. Overall, the progression of the disease was delayed by about 29%, and by 35% in a subset of patients believed to be more likely to respond.
Those who received the drug maintained a greater capacity to engage in daily activities, such as discussing current events, driving, and engaging in interests. However, swelling of the brain was a common adverse effect, affecting up to one-third of patients.
Despite being detected on brain imaging, it was largely asymptomatic or mild. However, 1.6% developed hazardous brain swelling, which was directly responsible for two deaths and contributed to the death of a third volunteer.
Dr. Mark Mintun, vice president of neuroscience research and development for Eli Lilly, mentioned that in the coming months, the company will initiate the procedure to have its drug approved for use in hospitals.
Dr. Liz Coulthard from the University of Bristol stated that there were "significant side-effects" and a lack of long-term data, but that the drug could "help people with Alzheimer's live well for a longer period of time." After decades of suffering and failure, the fact that two drugs slow the disease by targeting amyloid in the brain has persuaded scientists that they are on the right track.
Prof. John Hardy of the UK Dementia Research Institute, whose work 30 years ago led to the concept of targeting amyloid, stated that this should dispel any lingering doubts regarding this approach. Alzheimer's Research UK's Dr. Susan Kolhaas stated, "We're on the cusp of a first generation of Alzheimer's disease treatments, something that many deemed impossible only a decade ago."
However, these medications only appear to be effective in the earliest phases of the disease, before the brain is irreparably damaged. Even if they are approved in the United Kingdom, a revolution in disease diagnosis would be required to make a difference.
1-2% of individuals undergo brain scans or spinal-fluid analysis to determine whether they have Alzheimer's disease or another form of dementia for which the medications are ineffective. NHS would have to determine if they could be afforded. Lecanemab costs over £21,000 per individual per year.
