Alzheimer’s : can aspirin reduce “toxic” plaque?
A new study published in the Journal of Neuroscience suggests that regular intake of low-dose aspirin may prevent the formation of amyloid plaques in the brain. These plaques are mainly responsible for Alzheimer’s disease.
PATIENT COMES FIRST, HUMAN COMES FIRST
READ THE ARTICLE
If the results of the new research are reproduced in humans, they could lead to the use of aspirin as a treatment for Alzheimer’s disease.
Alzheimer’s disease is a form of dementia that affects 1 in 65 elderly people in the United States. The disease is characterized by the accumulation of a toxic, “sticky”, protein fragment in the brain, called beta-amyloid.
These protein aggregates, in the form of “clusters,” disrupt communication between brain cells, trigger the onset of an inflammatory response, and activate immune brain cells, eventually causing degeneration and neuronal death.
Although the exact cause of the disease remains unknown, β-amyloid accumulation is considered the most important.
As a consequence of the above, it could theoretically appear that the possible and in some way activation or enhancement of the brain mechanisms responsible for the clearance of cellular waste, would slow down the progression of the disease.
So far, there are studies linking lysosomal dysfunction in the removal of “cellular waste” with the accumulation of β-amyloid in the brain. There are also studies linking aspirin intake to a lower risk of Alzheimer’s disease.
Recently, new research, led by Dr. Kalipada Pahan, professor of neurological sciences, biochemistry, and pharmacology at the Rush Medical College in Chicago, “reveals” the relationship between the above two elements, aspirin and lysosomes, in the reduction of amyloid plaque in the brain of mice.
Low-dose aspirin reduces amyloid plaque.
“Understanding how to clear amyloid plaques is important for developing effective drugs that stop the progression of Alzheimer’s disease,” says Dr. Pahan.
Explaining, he mentions that a protein called TFEB (Transcription Factor EB), contributes significantly to the regulation of brain waste clearance mechanisms.
TFEB is a transcription factor known as the “major regulator of lysosomal biogenesis.”
Dr. Pahan and his team quantified β-amyloid in the brains of genetically modified mice with Alzheimer’s-like symptoms and then administered aspirin.
Upon completion of the experiment, it was found that aspirin intake increased TFEB, which in turn stimulated lysosome production and activity. Importantly, low-dose oral aspirin reduced amyloid plaque in both male and female mice.
These findings may be beneficial not only for people with Alzheimer’s disease, but also for treating other lysosomal storage disorders, a group of 50 rare conditions with symptoms ranging from mild to severe brain disease.
“The results of our study probably identify a new role for aspirin, one of the most widely used common drugs in the world, that of its involvement in the treatment of Alzheimer’s disease and other dementia-related diseases,” says Dr. Pahan.