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Disruption of mechanical signaling in the brain may cause Alzheimer's disease
Last reviewed: 03.07.2025
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New research from the University of Liverpool represents a significant step forward in our understanding of Alzheimer's disease, revealing how a breakdown in mechanical signalling in the brain can lead to the development of the condition, which accounts for 60-80% of dementia cases worldwide.
A team of researchers led by Professor Ben Goult from the University of Liverpool have studied the role of two proteins found in the brain and suggest that the stability of their interaction is crucial for the formation and retention of memory. Disruption of this mechanical signalling chain may lead to the development of the disease. This is the first time such a link has been established, opening up new possibilities for therapeutic interventions.
A paper recently published in the journal Open Biology suggests that amyloid precursor protein (APP), known for its role in the formation of amyloid plaques that are a hallmark of Alzheimer's disease (AD), directly interacts with talin, a synaptic scaffold protein.
Talin-APP interactions are proposed for the first time to be key to the mechanical integrity of synapses in the brain. Disruptions in APP processing observed in Alzheimer's disease disrupt mechanical signaling, leading to synaptic degradation and memory loss, contributing to disease progression. The study also showed that removing talin from cells in culture significantly altered APP processing.
Professor Ben Goult, University of Liverpool, said: "Alzheimer's disease is a devastating neurodegenerative disorder characterised by memory loss and cognitive impairment. It is a global public health problem but little is known about the mechanisms that lead to the disease. However, our paper provides a new piece of the puzzle and makes a significant advance in research.
"Our work shows that APP plays a fundamental role in the mechanical connection of synapses in the brain and that its processing is part of the mechanical signaling that maintains synaptic integrity. However, misprocessing of APP due to altered mechanical signals disrupts this chain, leading to synaptic degradation and possibly explaining memory loss.
"Most excitingly, our work highlights the intriguing possibility of using existing anti-cancer drugs that stabilize focal adhesions to restore the mechanical integrity of synapses. This is still a theoretical proposal, but we are already conducting studies to test whether this could be a new approach to slowing the progression of Alzheimer's disease.
"Further research is needed to test the hypotheses arising from these new data. Nevertheless, this is a significant moment in our better understanding of the disease, which may bring us closer to earlier diagnosis and treatment."