It is never easy to lose someone you care about, and it may be even harder when you are forced to lose that person slowly. For many who have experienced Alzheimer’s first hand, those who have been a witness to the mental decline of another, saying goodbye is easier said than done as the process of losing is never clear cut. The truth is that when it comes to these types of degenerative brain disorders, there are more questions than answers; but as recent research has proven, we may be getting some clarification soon.
While writing for the journal Nature, British scientists believe that they are a step closer to understanding neurodegenerative diseases like Alzheimer’s, Parkinson’s and Creutzfeld-Jacob Disease (CJD). Through their research with mice with prion disease (the mouse equivalent of CJD), this group of scientists have found a way to effectively stop the cell death that would otherwise have occurred in and caused irreparable damage to the brain.
Whether human of mouse, when the brain experiences the type of degradation wrought by neurodegenerative disease proteins within the brain fold improperly in on itself. As they continue to “mis-fold,” these proteins begin to accumulate and form plaque in the brain—a major component of Alzheimer’s and Parkinson’s. Addressing this unusual behavior, the scientists were able to get a clearer view of how the cells in the brain are turned off and die. Professor Giovanna Mallucci, of the toxicology unit at the University of Leicester, who led the research explains, “What’s exciting is the emergence of a common mechanism of brain cell death, across a range of different neurodegenerative disorders, activated by the different mis-folded proteins in each disease.”
As proteins morph into these incompatible forms, the brain’s natural reaction is to act in self-defense—in this case, the brain would begin to switch off the production of new proteins. Once the problem is solved, it will switch back on again. However, in mice with prion disease this defense mechanism is cancelled leaving the disease to progress and the brain ill equipped to take on the increasing threat. Searching for a remedy to this problem, scientists decided to inject a protein into the brains of the mice that would turn off or block the “off” switch, thus restarting the mechanism that would stop the production of these proteins.
And just as soon as this method was employed, the damaged brain cells were protected and protein levels were reinstated. What is more, the brain cells were able to signal back and forth to one another—as if the damage never occurred. In the end it was noted that the mice from the experiments not only lived, but they lived longer. “While neurodegenerative diseases can have many different triggers, this study suggests that they may act through a common mechanism to damage nerve cells,” explained Eric Karran, the director of research at the charity group Alzheimer’s Research UK. “The findings present the appealing concept that one treatment could have benefits for a range of different diseases.”
While the research is still ongoing, the results are huge. As the work continues, it is clear that we are seeing steps in a positive direction. According to molecular neurobiologist Professor Roger Morris, of the King’s College in London, “There are good reasons for believing this response, identified with prion disease, applies also to Alzheimer’s and other neurodegenerative diseases.” With an estimated 18 million people across the globe diagnosed with Alzheimer’s, and approximately one in 100 people over 60 years affected with Parkinson’s, the time for progress could not be any more important.
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