Accumulations (plaques) of the protein beta-amyloid are one of the hallmarks of Alzheimer’s disease. Now, research recently published in the Journal of Neuroscience suggests that low-dose aspirin may reduce plaque formation.
Previous clinical studies suggested that aspirin might reduce the risk of developing Alzheimer’s disease. The new study shows that low-dose aspirin stimulates lysosomes – sphere-shaped organelles that remove cellular debris. In mice genetically engineered to show changes that resemble Alzheimer’s disease, a month’s treatment with oral aspirin reduced the number of betaamyloid plaques.
More specifically, aspirin increased the activity of a protein called peroxisomeactivated receptor alpha (PPAR alpha). This increases the expression of the gene that encodes another protein (transcription factor EB) which, in turn, switches on genes that produce lysosomes. This mechanism suggests that aspirin might also treat lysosomal storage diseases, a group of rare but usually serious inherited metabolic disorders.
“The results of our study identify a possible new role for one of the most widely used, common, over-the-counter medications in the world,” says lead author Kalipada Pahan, professor of neurological sciences, biochemistry and pharmacology, at Rush Medical College, Chicago.
“Understanding how plaques are cleared is important to [develop] effective drugs that stop the progression of Alzheimer’s disease.”