There’s news in the world of Alzheimer’s research.
In a phase three trial, drug companies Biogen and Eisai reported this week that Lecanemab, an experimental monoclonal antibody, reduced cognitive decline caused by the disease by 27% after 18 months.
Researchers have been scrambling to find a treatment for Alzheimer’s for decades. Where do these new results put us in the global race to cure this devastating degenerative disease?
What do we know?
Around 2,000 people with early-onset Alzheimer’s took part in the trial, which started in March 2019. Half of the participants were given two injections per week of Lecanemab, while the others received a placebo.
At the start and end of the trial, researchers measured the severity of the participants’ dementia symptoms. After 18 months, the treatment group scored 0.45 points below the group that was given the placebo — a 27% reduction.
"If the data holds up to scrutiny, this is indeed fantastic news," said Tara Spires-Jones, a professor of neurodegeneration at the University of Edinburgh’s UK Dementia Research Institute. "While this is not a ‘cure’ in that it doesn’t bring people back to normal, slowing cognitive decline and preserving the ability to perform normal daily activities would still be a huge win because people could live well for longer with Alzheimer’s disease."
A disease without a cure
Alzheimer’s is a devastating and so far uncurable disease that impacts more than 50 million people globally, according to data from the BrightFocus Foundation, which funds scientific research on Alzheimer’s.
"When you tell a patient that they have Alzheimer’s, they ask you, ‘What can you do? Do you have a treatment?’ But there is no drug. Of course, there are many things we can do to help ... but still, we don’t have much more than that to propose to our patients," Nicolas Villain, a physician at the Pitié-Salpêtrière Hospital in Paris and associate professor of neurology at Sorbonne University, told DW.
So far, there are still no treatments that can stop or reverse the progression of the disease. And though the results of this trial seem encouraging, they are preliminary and haven’t been peer-reviewed.
Researchers caution against overselling the results before more research is conducted.
"The stated benefits are fairly small and will need to be balanced against the risks of side effects including inflammation and bleeding in the brain," said Charles Marshall, a senior lecturer and honorary consultant neurologist at Wolfson Institute of Population Health at Queen Mary University of London. He was not involved in the research.
Amyloid proteins and Alzheimer’s
Part of the enthusiasm this new drug has sparked in Alzheimer’s research communities is its potential validation of the theory that the disease is tightly connected to a protein called amyloid-beta.
Like all drugs that end in "mab", which stands for monoclonal antibody, Lecanemab is an antibody and specifically targets the amyloid-beta protein.
Antibodies can attach to specific foreign substances, like viruses, and play an essential role in how our immune system responds to pathogens.
Humans naturally produce the amyloid-beta protein — it is encoded in a gene in our chromosome 21, one of the 23 pairs of chromosomes in the human body.
When too many of these proteins accumulate in the brain, they can form plaques, which many researchers believe could be the cause of the damage inflicted by Alzheimer’s. Lecanemab is said to work by clearing these plaques.
However, some researchers aren’t fully convinced of a connection between the amyloid-beta protein and Alzheimer’s.
"There is a lot of evidence for the amyloid hypothesis, but there are some that think that amyloid is the cause of everything in Alzheimer’s, while others like me think amyloid is important but there are other factors," said Villain.
In September 2016, Biogen started a phase three clinical trial for a drug called Aducanumab, which also targets amyloid-beta proteins.
The trial was stopped in March 2019. According to a Biogen press release, it was canceled because researchers believed the studies would not have met their main goals.
The reasons why the trial was halted are still unclear. But months later, the company received accelerated approval of Aducanumab by the Food and Drug Administration (FDA) in the US. The European Medicines Agency (EMA) rejected the drug.
A November 2020 article by Mayo Clinic researcher David Knopman and collaborators published in Alzheimer’s and Dementia said that the evidence was not good enough to justify the application for approval.
"Compared to Aducanumab, which was approved by the FDA on proof of principle without any clinical benefits being shown, this appears to show clinical benefits," said Peter Passmore, a professor of aging and geriatric medicine at Queen’s University Belfast, in response to the results of the Lecanemab trial.
Edited by: Clare Roth