There is research on Alzheimer’s disease is entering a fresh phase as treatments that have taken decades to develop begin to reach patients. But according to John Hardy, a pioneer in Alzheimer’s disease research, making these advances available to people will depend on more than just scientific progress.
Writing in WIRED Health in April, Hardy, chair of the Molecular Biology of Neurological Diseases at University College London, said that in addition to more effective drugs, better diagnosis and political will are still needed to improve the treatment of Alzheimer’s disease. “We have to improve,” he said.
Hardy played a key role in identifying the central role of amyloid – a form of protein found in the brain and body – in Alzheimer’s disease in the 1990s. He and his colleagues helped establish the idea that amyloid deposits form plaques around brain cells. These plaques are thought to interfere with normal brain function, increasing brain activity and triggering inflammatory responses.
He said at the time that he was “naively optimistic” about how quickly this discovery would lead to an effective treatment. “But now we’re finally getting somewhere,” he said.
His discoveries led to the development of antibodies to prevent the formation of amyloid deposits. But these early approaches didn’t “suck amyloid out of the brains of people who already had the disease,” he said. “It was a mistake [the scientific community] made.”
“Now we know what drugs do,” Hardy said. In recent years, researchers have developed drugs such as Donanemab and Lecanemab that can remove amyloid deposits that have already formed in the brain.
A clinical trial of Lecanemab, results of which were published in 2022, showed for the first time that the drug can slow cognitive decline in people with Alzheimer’s disease.
“The problem: it didn’t stop the disease, it actually slowed it down,” Hardy said.
Generally, Alzheimer’s disease progresses over about eight to nine years, Hardy explained. Lekanemab is expected to slow this process, extending the time frame to approximately 11 or 12 years. “It makes a difference over time,” he said. “But we clearly need to improve.”
The amyloid theory is often debated, and some researchers argue that too much focus on it slows progress. Most now agree that amyloid plays a role, although how crucial it is remains disputed.
According to Hardy, progress in the treatment of Alzheimer’s disease will require both scientific and political commitment.
Improving diagnosis is a key priority, especially through the use of genetics and biomarkers, which can be used “to examine the blood chemistry of people who develop the disease.”
“We can use biomarkers [for Alzheimer’s] in the same way that we use cholesterol measurements as a biomarker for heart disease,” he said.
Treatment currently uses drugs such as Lecanemab, although in the UK only private patients have access to them. In the US, Lecanemab has been approved by the FDA and is available on Medicare.
Trials of another anti-amyloid drug, Gantenerumab, initially did not show good results, but more recent studies show that higher and longer doses can help delay symptoms. According to Hardy, it currently “looks very promising for the next type of treatment for Alzheimer’s disease.”
But improving diagnosis will require investment in dementia services in the UK and elsewhere.
Alzheimer’s disease is the most common form of dementia, but outside specialist centers, patients are often diagnosed with dementia more broadly, rather than Alzheimer’s disease itself. “Only about 60 percent of people diagnosed with dementia actually have Alzheimer’s disease,” Hardy said. “You have to get better at making a true diagnosis. And that requires investment.”
“We, scientists, have a lot to do. We need to create more effective versions of these drugs, this is in progress. We need to get earlier diagnosis,” he said. “We need to make policy changes to invest in dementia services.”