Researchers at the University of California, Riverside have proposed that amyloid beta disrupts tau protein function inside neurons, potentially triggering Alzheimer's disease. The findings challenge the focus on external plaques as the primary cause.
The study, published in PNAS Nexus, suggests amyloid beta competes with tau for binding sites on microtubules, which serve as transport routes within nerve cells. When amyloid beta accumulates, it can displace tau and impair this network.
Ryan Julian, the lead author and chemistry professor at UC Riverside, stated that both proteins are required for an Alzheimer's diagnosis but many labs examine only one. Experiments showed the proteins bind with similar strength.
The theory links the process to aging and reduced autophagy, which normally clears excess proteins. It may also explain why some treatments targeting plaques have not succeeded.
If confirmed, the model could shift drug development toward protecting microtubules or clearing amyloid beta inside cells before damage occurs.
