A drug that
increases activity in the brain’s "garbage disposal" system has been
shown to reduce levels of toxic proteins associated with Alzheimer's disease
and other neurodegenerative disorders and improve cognitive functions in mice.
The first of
its kind research was conductedby neuroscientists at Columbia University Medical Center (CUMC) and
published in the journal Nature Medicine.
Karen E.Duff, PhD, professor of pathology and cell biology (in psychiatry and in
the Taub Institute for Research on Alzheimer'sDisease and the Aging Brain) at CUMC and at the New York State Psychiatric
Institute explained the findings:
"We
have shown for the first time that it's possible to use a drug to activate this
disposal system in neurons and effectively slow down disease.”
"This
has the potential to open up new avenues of treatment for Alzheimer's and many
other neurodegenerative diseases."
Brain cells need to continuously clear out old, worn, or damaged proteins in order to stay healthy. A small molecular cylinder called proteasome does the clearing out job. It acts as a garbage disposal and grinds up the old proteins so they can be recycled into new ones.
In the brains of patients with neurodegenerative diseases, the proteasomes become damaged and they cannot do their job of clearing up. As a result, worn out proteins accumulate in the brain’s neurons. [ওজন কমাতে প্রতিদিন আপনার কতটুকু কার্বোহাইড্রেট খাওয়া উচিৎ?]
In Alzheimer’s disease, destruction and death of nerve cells causes the memory failure, personality changes and problems in carrying out daily activities.
The brains of people with AD have an abundance of two abnormal structures: 1) Amyloid plaques – consisting largely insoluble deposits of an apparently toxic protein peptide, or fragment, called beta-amyloid, and 2) Neurofibrillary tangles – abnormal collections of twisted protein threads whose main component is a protein called tau.
Scientists used a mousemodel of neurodegeneration and found that tau protein sticks to the proteasome and slows down the process of protein disposal.
When rolipram was administered in mice, it activated the proteasome and restored protein disposal to normal levels. The drug also improved the memory of diseased mice to levels seen in healthy mice. [Read more Bloodtest for Alzheimer’s? New antibody test could accurately detect Alzheimer’sbefore symptoms appear]
Past studies have shown rolipram’s effectiveness in improving memory in mice, but the mechanism wasn’t clear to scientists.
The new research pinpointed the mechanism, which showed that rolipram inhibits PDE-4 enzyme, thereby produces a a physical change in the proteasome that increases its activity.
The study’s first author, Natura Myeku, PhD, an associate research scientist in pathology and cell biology at CUMC tried to shed light on the mechanism:
"We still don't know exactly where the activation is happening, but what's new is that we can modify the proteasome to increase its activity. There could be many other ways to do this."
Researchers believe, drugs that work by targeting proteasomes should work for any disease caused by the accumulation of abnormal proteins, including Alzheimer's, Huntington's, Parkinson's and frontotemperoraldementia.
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