Breakthrough Alzheimer’s Drug Slows Disease Progression in Early Stages: Donanemab Shows Promise in New Trial

Experimental Drug Shows Promise in Slowing Alzheimer’s Disease Progression

An experimental drug called donanemab has demonstrated the ability to slow the progression of Alzheimer’s disease in individuals who start taking it during the early stages of the disease. Although the drug does not improve symptoms, it has shown significant benefits in terms of disease progression. In a study of 1,736 participants, 47% of those who took donanemab at the earliest stages of Alzheimer’s had no disease progression on certain measures after one year, compared to 29% who took a placebo.

The results of the study, presented by donanemab’s manufacturer Eli Lilly at the Alzheimer’s Association International Conference (AAIC) in Amsterdam, are being hailed as “very encouraging” by neurologist Reisa Sperling from Harvard Medical School. The findings are particularly notable because they closely resemble those of a similar drug called lecanemab, leading researchers to believe they are on the right track.

Donanemab is a monoclonal antibody that targets amyloid, a protein that damages neurons in individuals with dementia. However, like other drugs in its category, donanemab can potentially cause a serious condition called amyloid-related imaging abnormalities (ARIA), which can lead to brain bleeding and seizures. In Eli Lilly’s trial, approximately one-quarter of the participants developed ARIA, and three individuals died as a result of the condition. It was found that ARIA was most common among those carrying the APOE4 genetic variation, which increases the risk of Alzheimer’s.

Furthermore, the drug appears to be less effective in individuals with high levels of tau, another brain protein associated with Alzheimer’s. Those with low or moderate levels of tau who took donanemab experienced a 35% slower decline over 76 weeks compared to those who took a placebo. However, for individuals with high tau levels, the decline remained the same regardless of whether they took donanemab or a placebo. It is worth noting that the role of tau in Alzheimer’s is still not fully understood.

Interestingly, cognitive decline significantly slowed in individuals with minor cognitive impairment who started taking donanemab, with some experiencing up to a 60% reduction. The drug also cleared approximately 90% of amyloid from the brain. Once minimal amyloid levels were reached, these individuals were switched to a placebo. Even after the switch, those who had initially received donanemab continued to decline at a slower rate compared to those who had only received a placebo.

These findings highlight the importance of early detection and treatment of Alzheimer’s. Clinical trials are currently investigating whether drugs like lecanemab and donanemab can prevent the disease in individuals who have not yet developed symptoms. Bart De Strooper, an Alzheimer’s researcher at University College London, emphasizes the significance of preventing amyloid accumulation based on the trial results.

However, experts raise concerns about the practical implementation of drugs like donanemab. It is unclear how physicians should proceed once amyloid is no longer present in the brain, and screening for ARIA and identifying suitable candidates for treatment may prove challenging. Eli Lilly has submitted for FDA approval and expects to receive a response by the end of the year. The company has not disclosed the potential cost of donanemab if approved, but similar drugs have been priced at over $26,000 per year.