Phenylbutyrate may improve report in Alzheimer's disease
The study developed by researchers at CIMA opens new perspectives for the treatment of other dementias.
A drug used in a hereditary metabolic disorder subject improves the report of animal models of Alzheimer's disease. The study developed by researchers at research center Applied Medicine (CIMA) of the University of Navarra has been published in the journal Neuropsychopharmacology.
The work shows that this drug (sodium phenylbutyrate), indicated until now in patients with urea cycle disorders, facilitates the synthesis of proteins responsible for neuronal connection, thereby increasing the learning capacity of mice. "These findings provide a new perspective for the treatment of Alzheimer's disease and related dementias. In addition to reversing the cognitive deficit, the levels of some histopathological markers characteristic of Alzheimer's disease are diminished in the brains of these animals. Phenylbutyrate adds a new alternative to the drugs already available, which are focused on slowing down the development of this devastating disease," explains Dr. Ana García-Osta, researcher at area Neurosciences and lead author of work, in which Ana Ricobaraza, Mar Cuadrado, Alberto Pérez Mediavilla, Diana Frechilla and Joaquín del Río have participated. They are researchers from the laboratory of Neuropharmacology and Behavior at CIMA.
The study was performed in genetically modified mice that represent a model of Alzheimer's disease and develop cognitive impairment with age. Through a learning test and report the researchers found that aged mice treated with phenylbutyrate showed a report similar to healthy mice.
Currently, the team at research is focusing its line of work on discovering the mechanism of action of this drug. "As it is already available clinically and well tolerated, if confirmed to be therapeutically effective in humans it could be applied in Alzheimer's disease in a deadline shorter time than other drugs under study."
Alzheimer's disease is an age-associated neurodegenerative disorder characterized by progressive deterioration of cognitive and intellectual functions due to a loss of connections between neurons. "For report to take hold, a number of cellular and molecular mechanisms need to be activated. The interruption of these processes affects the ability to learn and the storage of new memories," says Dr. Ana García-Osta.