A study in mice found levels of amyloid-beta proteins, which accumulate to create the plaques, fell 90% after scientists blocked an enzyme that forms them. Researchers believe this enzyme could be a new therapeutic target to fight Alzheimer's disease.
Lead author Sung Ok Yoon, an associate professor at Ohio State University in the US, said: 'These mice are models for the most aggressive form of Alzheimer's disease and produce the highest amount of amyloid-beta peptides. This 90% reduction is the biggest drop in amyloid-beta levels that has been reported so far by treating animal models with drugs or genetic manipulations.'
In the study, researchers disabled an enzyme in mice called jnk3, which creates the precursors to plaques. Humans have the same enzyme. These mice had been bred to possess the same mutations found among people with early onset Alzheimer's disease. After six months, amyloid-beta levels had dropped by 90%, which was maintained as a 70% reduction over 12 months.
Researchers found that removing jnk3 also improved cognitive performance. Mice with jnk3 removed had 80% of normal cognitive function, whereas mice with jnk3 intact had just 40% of normal function.
Researchers believe jnk3 strengthens a stress-response cycle in the brain that leads to raised levels of amyloid-beta and therefore increases the number of plaques.
Researchers saw that, when mice begin to develop Alzheimer's plaques, the average time asleep during the day fell from 40 to 30 minutes per hour.
Senior author Dr David Holtzman, head of the Department of Neurology at Washington University in the US, said: 'If sleep abnormalities begin this early in the course of human Alzheimer's disease, that could provide an easily detectable sign of pathology.'
He added: 'As we start to treat Alzheimer's patients before the onset of dementia, the presence or absence of sleep problems may be an indicator of whether the treatments are succeeding.'