Psoriasis drug may treat Alzheimer's
A drug approved for treatment of a skin disorder may boost brain functioning in Alzheimer's disease, scientists have found.
Berlin: A drug approved for treatment of a skin disorder may boost brain functioning in Alzheimer's disease, scientists have found.
Researchers at the Department of Psychiatry and Psychotherapy of the University Medical Center of Johannes Gutenberg University Mainz (JGU) in Germany found that a drug approved for treatment of the dermal disorder psoriasis stimulates the activity of the enzyme ADAM10 in the brain of Alzheimer's patients.
There is good evidence from basic research that this enzyme should be capable of suppressing Alzheimer's disease-related effects such as impaired cerebral function and that it thus might improve learning and memory capacity in patients, researchers said.
There is still no consensus on what triggers the most common form of the disease, late-onset Alzheimer's. However, it is generally accepted that the activity of certain enzymes called secretases plays a role here.
These enzymes cleave proteins on cell membranes, releasing the products of this cleavage process into the extracellular space.
In Alzheimer's there is increased cleavage of the amyloid precursor protein by beta-secretase, leading to the formation of amyloid-beta peptides.
These peptides aggregate, damage nerve cells, and are the main component of the so-called Alzheimer's plaques that accumulate in the brains of patients. The alpha-secretase ADAM10 is a competitor of beta-secretase.
It cleaves the amyloid precursor protein in such a way that the synthesis of amyloid beta-peptides is prevented while the growth factor APPs-alpha, which protects nerve cells, is released.
Dr Kristina Endres and Professor Falk Fahrenholz of the Mainz University Medical Center took this information as their starting point.
Working in collaboration with other researchers, the scientists demonstrated that oral administration of a psoriasis medication in a group of Alzheimer's patients results in elevated levels of APPs-alpha in their spinal fluid.
This is interpreted as a stimulation of the activity of the alpha-secretase ADAM10, which in turn would result in the reduced accumulation of Alzheimer's plaques, researchers said.
The results of the study have been published in the journal Neurology.