New Theories on How Alzheimer’s Emerges and Spreads in the Brain

A team of chemists at the University of California, Riverside, has proposed a unifying theory that may explain how Alzheimer’s disease emerges in the brain. According to the research published on April 5, 2026, the disease may develop as two key proteins compete inside brain cells.

Alzheimer’s disease, the most common form of dementia, has long been linked to the accumulation of two specific proteins: amyloid-beta and tau. While these proteins have been studied extensively, the relationship between them and their roles in the origins of the disease have remained subjects of scientific contention.

The Role of Amyloid-Beta and Tau

Amyloid-beta peptides are sticky fragments of a larger protein. In the brains of individuals with Alzheimer’s, these fragments clump together to form plaques. Evidence suggests that these plaques can emerge approximately 20 years before any clinical symptoms of the disease appear.

Tau proteins serve a different primary function, normally stabilizing microtubules, which act as the internal scaffold of brain cells. However, in the progression of Alzheimer’s disease, tau detaches from these microtubules. This process leads to the formation of tau tangles—knots of misfolded proteins that clog the interior of diseased neurons.

Some research indicates that these tau tangles may serve as a more accurate indicator of a patient’s cognitive status than the presence of amyloid-beta plaques.

A Theory of Protein Competition

The new study from the University of California, Riverside, suggests that the emergence of the disease is driven by a competition between these two proteins to bind to microtubules. This proposed mechanism ties the two hallmarks of Alzheimer’s together, potentially resolving conflicting ideas regarding which protein is more significant or which forms first.

For years, neuroscientists have debated whether these proteins cause the disease or are simply symptoms of it. Many research laboratories have focused their efforts on the role of one protein while ignoring the other, creating a fragmented understanding of the disease’s progression.

In addition to having dementia, [an] Alzheimer’s diagnosis requires both [amyloid-beta] and tau buildup in the brain

Ryan Julian, chemistry professor at the University of California, Riverside

By viewing the interaction as a competition for the same cellular structures, the researchers aim to provide a more comprehensive framework for understanding how the disease takes hold in the brain.