Cancer Drug Shows Promise in Reducing Early Brain Hyperconnectivity in Alzheimer’s Disease

By Dr. Natalie Singh, MPH – Health Editor, archynewsy.com

March 9, 2026

Neuroscientists at King’s College London have identified a key mechanism driving the earliest stages of Alzheimer’s disease – an unexpected increase in neural connectivity. This groundbreaking discovery, published in Translational Psychiatry, also suggests a potential new therapeutic avenue: repurposing a cancer medication to counteract this hyperconnectivity and potentially slow disease progression.

Understanding the Early Stages of Alzheimer’s Disease

For years, Alzheimer’s disease has been primarily understood as a condition characterized by the loss of synapses – the connections between neurons. However, this new research challenges that conventional wisdom. Scientists have observed that, in the very initial phases of the disease, the number of connections between brain cells actually increases. This phenomenon correlates with mild cognitive impairment (MCI), often considered a precursor to full-blown Alzheimer’s disease [1].

The research, conducted using brain cells in a laboratory setting, demonstrated that even low levels of amyloid-beta, a protein fragment associated with the formation of plaques in the brains of Alzheimer’s patients, can induce this hyperconnectivity. This pattern closely mirrors the changes observed in the brains of individuals experiencing MCI [3].

“The results of this new study contribute to a new way of thinking about Alzheimer’s disease,” explains Kaiyu Wu, the study’s first author from the Institute of Psychiatry, Psychology & Neuroscience at King’s College London. “Instead of starting with synapse loss, the disease may begin with too many poorly organized connections, combined with subtle but targeted changes in protein production.” Over time, this unstable state could make brain circuits more vulnerable, eventually leading to the synaptic failure and cognitive decline seen in later stages of the disease.

Amyloid-Beta and Hyperconnectivity: A Self-Reinforcing Loop

The study shows that low doses of amyloid-beta protein over a period of five days can cause hyperconnectivity between brain cells. Researchers also identified changes in the levels of 49 proteins, including its own precursor, that work together to increase connectivity in the early stages of the disease [4].

“This suggests the system may act as a self-reinforcing loop in which amyloid-beta promotes conditions that lead to even more amyloid-beta,” explained Kaiyu Wu.

Repurposing a Cancer Drug for Alzheimer’s Treatment

Previous work from the same research group at King’s, led by Professor Karl Peter Giese, identified a drug target that might be able to alter protein production associated with synapse increases. This target, MAP kinase interacting kinase (MNK), is also the target of the clinically licensed drug eFT508, currently used in cancer clinical trials [2]. The drug has not been used to investigate or treat Alzheimer’s disease before.

The team found that eFT508 prevented the increase in connectivity caused by amyloid-beta exposure. They also found that the drug was able to restore 70% of the altered protein production after amyloid-beta exposure.

Professor Giese, senior author on the paper and Professor of Neurobiology of Mental Health at IoPPN, King’s College London, said: “Our research suggests a promising drug treatment for memory loss in mild cognitive impairment and early Alzheimer’s disease. Next, our findings need to be validated first in suitable animal models, before clinical trials can commence.”

Looking Ahead

Michelle Dyson, Chief Executive Officer at Alzheimer’s Society, stated that this study builds our knowledge of brain cell changes in early-stage Alzheimer’s disease and suggests that with intervention, we may be able to counteract some of these changes as Alzheimer’s disease develops [3]. She emphasized the importance of drug repurposing as a promising avenue for research in the fight against dementia, which affects around one million people in the UK.

This research represents a significant shift in our understanding of Alzheimer’s disease and opens up new possibilities for therapeutic intervention. While further research and clinical trials are necessary, the findings offer hope for developing effective treatments to slow or prevent the progression of this devastating disease.