A few weeks ago, a team of Japanese neurologists claimed to have identified the initial trigger of Alzheimer’s disease. It concerns a kind of molecular “seed”: Peak 1 beta-amyloid. According to scientists, this historic breakthrough could pave the way for better screenings and, above all, the development of a viable treatment to eradicate the disease before its onset.
The answer to a crucial question in the fight against the disease
For quite some time, science has known a precise mechanism at work in people with Alzheimer’s disease. The brain of these patients sees beta-amyloids accumulate progressively in the form of plaques (often called “senile” plaques), which lead to neuronal suffocation and thus memory loss. However, one question remained unanswered: why do these proteins cluster so suddenly? The National Center of Neurology and Psychiatry in Tokyo (Japan) says it has found the answer, as demonstrated by a study published in Brain Communications on July 20, 2026.
The neurologists highlighted the role of a little-known molecule: Peak 1 beta-amyloid. In the brain, this protein acts as a kind of “seed” or magnet, whose mere presence is enough to trigger the cascade leading to the accumulation of beta-amyloids. The scientists tested their theory by injecting the protein into healthy mice. After four months, the animals had developed plaques and displayed cognitive decline. The researchers then confirmed the presence of this Peak 1 beta-amyloid in human patients who had died from Alzheimer’s disease.
“These studies contribute to a better understanding of the molecular mechanisms behind the accumulation of senile plaques in Alzheimer’s disease. These works should enable the development of new treatments and preventive measures against dementia, in order to try to slow down this accumulation,” reads an official press release detailing the Japanese study.
A drug for the general public within a decade
For researchers, there is cause for optimism since this protein appears in the body roughly two decades before the first visible symptoms. It should be noted that current drugs aim to destroy already formed plaques, which yields rather limited results. Scientists indicated that future treatments will directly target the Peak 1 beta-amyloid protein to prevent it from acting. The goal is therefore simply to intervene upstream to avert the disease’s appearance.
The aim of the neurologists is to develop within one to two years non-invasive screening methods to detect the protein. This could involve blood-based biomarkers or imaging tests. However, the Japanese team is also thinking long-term. Indeed, they have already begun a project to select therapeutic compounds for initiating clinical trials, with a view to developing a viable treatment for the general public within about ten years.
Finally, it is worth reminding that Alzheimer’s disease is the leading cause of dementia among the elderly. In France, this condition affects around 1.4 million people, with nearly 225,000 new cases each year. Worldwide, Alzheimer’s disease affects about 38 million people—representing 60 to 70% of dementia cases—with around 10 million new cases each year.
