The True Cause of Alzheimer’s Disease May Not Be Amyloid Plaques

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The True Cause of Alzheimer’s Disease May Not Be Amyloid Plaques, Challenging Decades-Old Theories

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Breakthrough Discovery: The True Cause of Alzheimer’s Disease May Not Be Amyloid Plaques, Challenging Decades-Old Theories

In the brains of Alzheimer’s patients, abnormal levels of β-amyloid proteins cluster together to form plaques (brown regions), which accumulate between neurons and disrupt cellular function. Meanwhile, abnormally aggregated tau proteins accumulate inside neurons, forming tangles (blue regions) that impair synaptic communication between nerve cells.

New research from Emory University in the United States suggests that proteins accumulating around amyloid deposits, rather than the deposits themselves, may play a key role in the progression of Alzheimer’s disease. The research team has found compelling evidence that Alzheimer’s may be driven by a different mechanism, offering new directions for treatment.

In a paper published in Cell Reports Medicine, Todd E. Golde, Director of the Goizueta Institute at Emory University’s Neurodegenerative Disease Center, and Yona Levites, Associate Professor at Emory University School of Medicine, explained how β-amyloid deposits, long known to accumulate in the brains of Alzheimer’s patients, may act as a scaffold for other proteins. Since many of these proteins have known signaling functions, their presence around β-amyloid deposits (known as plaques) could be the actual culprit in causing brain cell damage, rather than the amyloid itself.

In Alzheimer’s patients, amyloid proteins build up and form sticky plaques that disrupt brain function and lead to cognitive decline. The biggest mystery has been how exactly this happens. According to the most widely accepted hypothesis, the accumulation of β-amyloid disrupts communication between cells and activates immune cells, eventually destroying brain cells.

In this study, Golde, Levites, and their colleagues proposed a new hypothesis, highlighting a different role for β-amyloid—a simple protein formed in all brains but typically dissolved through natural processes.

Using cutting-edge analytical techniques, they identified and measured the levels of over 8,000 proteins in the brains of Alzheimer’s patients and in similar proteins in mice. They focused on the proteins with the fastest increasing levels and discovered over 20 proteins that co-accumulate with β-amyloid in both human and mouse brains. As their research continues, they anticipate finding more.

Golde stated, “Once we identified these new proteins, we wanted to know if they were merely markers of Alzheimer’s or if they could actually alter the fatal pathology of the disease. To answer this, we focused on two proteins: midkine and pleiotrophin. Our research showed that they accelerate amyloid aggregation in test tubes and mice. In other words, these additional proteins may play a significant role in the process that leads to brain damage, rather than the amyloid itself. This suggests that they could be the basis for new therapies for this devastating brain disease that has been so difficult to treat over the years.”

While the basic principles of Alzheimer’s have been understood for over a century, progress in finding a cure has been slow, often characterized by cycles of initially promising treatments failing in trials and ongoing debates over competing theories on how best to explain the disease’s impact on the brain. As researchers noted, the initial linear amyloid cascade concept is now seen as overly simplistic. Studies have revealed extremely complex changes occurring in individual brains over decades as Alzheimer’s pathology develops.

Notably, in addition to β-amyloid, the accumulation of multiple amyloid proteins is associated with over 30 human diseases affecting tissues and organs throughout the body. Since this new study proposes a different process in Alzheimer’s development, it may offer new approaches for discovering therapeutic targets for other diseases.

The True Cause of Alzheimer’s Disease May Not Be Amyloid Plaques, Challenging Decades-Old Theories

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