A new study has found that stress can trigger Alzheimer's disease by encouraging the accumulation of key proteins in the brain.
The newly discovered pathway leading to neurodegeneration in Alzheimer's disease (AD) may unlock the door to new approaches for treating the disease.
The findings focus on the tau protein, whose abnormal aggregation (clumping) has long been known to drive the nerve damage in AD. New research shows that the tau protein directs the formation of stress granules, which are molecular complexes that allow nerve cells to adapt to stresses, such as injury.
The tau-stress granule complex is usually short lived, but in the setting of chronic stress, tau persistently forms into a cluster, leading to the degeneration of nerve cells seen in AD.
Boston University School of Medicine (BUSM) researcher Benjamin Wolozin explained, "Scientists have known for a long time that during disease, tau protein gets modified, changes its location in nerve cells and then aggregates."
According to Wolozin, with this finding, comes hope. His team found that reducing the amount of one of the key stress granule proteins, TIA1, prevented tau aggregation and nerve cell degeneration.
Wolozin and his team are now planning to test their research findings in animal models of Alzheimer's disease.
The study is published in the journal Cell Reports.
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