A team of scientists from the Boston University School of Medicine recently discovered that stress could trigger Alzheimer's disease. In the study published in the journal Cell Reports, stress is reportedly encouraging the accumulation of major proteins in the brain, leading to Neurodegeneration.
The Study
Based on the latest findings, scientists concentrated on the tau protein, a type of protein that is abundant in neurons of the central nervous system. Unfortunately, its abnormal clustering in the brain, which is triggered by the formation of stress granules, has been found a culprit to nerve damage and degeneration that is distinctive of Alzheimer's disease, Daily Mail notes.
What Are Tau Proteins?
Tau proteins are key proteins responsible for stabilizing microtubules. According to News Medical, these proteins are commonly found in nerve cells as well as in oligodendrocytes and astrocytes. But when Tau proteins become defective and fail to adequately stabilize microtubules, neurodegenerative diseases like Alzheimer's disease can develop.
Tau Proteins And Stress Granules
In a recent study, scientists revels the tau proteins leads the formation of stress granules, the molecular complexes that allow nerve cells to acclimatize to stresses like injury. Even though tau-stress granule complex is usually short lived, tau persistently forms into a cluster in chronic stress, leading to the degeneration of nerve cells seen in Alzheimer's disease.
"Scientists have known for a long time that during disease, tau protein gets modified, changes its location in nerve cells and then aggregates," Boston University School of Medicine researcher and pharmacology and neurology professor Dr. Benjamin Wolozin explained, as per Medical Xpress.
In healthy nerve cell, tau proteins exist in a part of the nerve cell called the axon. It is a long and slender part of the cell that carries electrical impulses away from the neuron's body.
By moving the tau proteins from the axon to the nerve cell body, it helps the nerve cells respond to stressful conditions, stimulating the formation of stress granules. Unexpectedly, the relationship of tau with stress granules triggered the clustering of tau.
Even though it may not cause a problem in most short-term stresses, it can pose a risk of Alzheimer's disease in chronic stresses, leading to excessive, persistent accumulation of stress granules containing aggregated tau. Because of this, the abnormal accumulations can ultimately damage nerve cells, causing degeneration.
Development For New Treatments
The latest findings give Wolozin and his team a glimmer of hope for the potential development of new Alzheimer's disease treatment. According to Wolozin, the reduction in quantity of one of the major stress granule proteins, TIA1, prevented tau aggregation and nerve cell degeneration.
"While still in its early stages, this work points to entirely new approaches to treating Alzheimer's disease," Wolozin admitted, adding his team planned to test their research findings in animal models of Alzheimer's disease.
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