The next breakthrough for Alzheimer’s disease will require more than just science

Alzheimer’s research is Entering a new phase, where treatments that took decades to develop begin to reach patients. But getting these advances to people will depend on more than just scientific progress alone, according to leading Alzheimer’s researcher John Hardy.

Speaking at WIRED Health in April, Hardy, head of the Department of Molecular Biology of Neurological Diseases at University College London, said that alongside more effective drugs, there is still a need for better diagnostics and political will to improve Alzheimer’s treatment. He added: “We have to improve.

Hardy was instrumental 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 disrupt normal brain function, increase activity and trigger inflammatory responses.

At the time, he said he was “naively optimistic” about how quickly this discovery would lead to an effective treatment. “But now, finally, we are getting somewhere,” he said.

His findings led to the development of antibodies designed to prevent the formation of amyloid deposits. But these early methods didn’t “suck amyloid out of the brains of people who already had the disease,” he said. “This was the mistake [the scientific community] to make.”

“We now know what the drugs are supposed to do,” Hardy said. In recent years, researchers have developed drugs such as Donanemab and Lecanemab that can remove amyloid deposits that have already formed from the brain.

A clinical trial of Lecanemab, the results of which were published in 2022, showed for the first time that the drug could slow cognitive decline in people with Alzheimer’s disease.

“The problem: It didn’t stop the disease, it slowed it down,” Hardy said.

In general, Alzheimer’s disease develops over about eight or nine years, Hardy explained. Lecanemab is expected to slow this process, increasing the time frame to about 11 or 12 years. “It makes a difference in time,” he added. “But obviously we have to get better.”

The amyloid theory is often debated, with some researchers arguing that too much focus on it has slowed progress. Now, most people agree that amyloid plays a role, although how important it is is still a matter of debate.

For Hardy, making progress toward a cure for Alzheimer’s disease will require scientific and political commitment.

Improving diagnosis is a key priority, especially through the use of genetics and biomarkers, which can be used “to look at the blood chemistry of those who develop the disease.”

“We can use biomarkers [for Alzheimer’s] In the same way we use cholesterol measurements as a biomarker for heart disease.

Drugs such as Lecanemab are now used for treatment, although in the UK they are only accessible to private patients. In the United States, Lecanemab is approved by the Food and Drug Administration (FDA) and is available in Medicare.

Trials of another anti-amyloid drug, Gantenerumab, initially failed to show strong results, but more recent studies show that higher and longer doses can help delay symptoms. “He now seems very optimistic for the next type of treatment for Alzheimer’s,” Hardy says.

However, 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 centres, patients are often diagnosed with dementia more broadly than specifically with Alzheimer’s disease. “Only about 60 percent of people diagnosed with dementia actually have Alzheimer’s disease,” Hardy said. “You have to get better at making true diagnoses. That requires investment.”

“We scientists have things to do,” he said. “We have to make more effective versions of these drugs, and that is a work in progress. We have to get an earlier diagnosis.” “We must have policy change to invest in dementia services.”