Alzheimer’s protein attacks different brain regions, studies suggest combination therapy is needed

Scientists have found that two proteins associated with Alzheimer’s disease target different brain regions, suggesting that current single-target treatments may not be sufficient to effectively combat the disease. The study, published in molecular psychiatry, reveals how tau and beta-amyloid jointly disrupt the brain circuits that control memory and emotions.

Using a new mouse model that mimics the mark of Alzheimer’s disease, researchers from neuroscience researchers at the University of Barcelona found that the accumulation of tau protein in the hippocampus in the hippocampus can lead to memory problems, while beta-amyloid causes Emotionally distressing symptoms, anxiety and fear.

“Although both proteins accumulate in the brains of Alzheimer’s patients, most animal models used to study the disease usually focus on only one of these factors,” explained Maria Dolores Capilla, the lead author of the study. “In our study, we generated a transgenic mouse model that exhibits TAU and beta-amyloid accumulation, allowing us to analyze their individual and joint effects.”

The discovery challenges current treatments, often targeting only one of these toxic proteins. “Existing therapies have not yet obtained obvious clinical benefits. Our study shows that a treatment that addresses multiple disease mechanisms, such as phosphorylated tau and beta-amyloid, can be more effective,” UAB Biochemistry and Molecular Biology Carles Saura of the department said.

The team found that when both proteins are present, they work together to aggravate brain inflammation and cellular dysfunction, creating a more severe impact than using either protein alone. This synergy helps explain why previous treatments targeting only one protein may have shown limited success in clinical trials.

The study also showed that female mice showed more severe symptoms in specific brain regions, reflecting clinical observations that women often experience faster cognitive decline in Alzheimer’s disease. This gender-specific vulnerability is still bad and needs further investigation.

In addition to determining how these proteins affect different brain circuits, the study also found changes in multiple genes related to inflammation and synaptic function-connection between brain cells. These genetic changes occur in areas of the brain that are critical for memory and emotional processing, providing new potential goals for therapeutic interventions.

This study represents a significant shift in understanding how Alzheimer’s disease develops and progresses. Although further studies are needed to confirm these findings in humans, the results suggest that future treatments may require targeting multiple disease mechanisms simultaneously to be effective.

This comprehensive approach to understanding Alzheimer’s disease can help explain why current treatments show limited success and point to new directions in developing more effective therapies that simultaneously address multiple aspects of the disease.