A study of mice shows how proteasomes, a cell’s waste disposal system, may break down during Alzheimer’s disease, creating a cycle in which increased levels of damaged proteins become toxic, clog proteasomes, and kill neurons. The study, published today (Monday 21 December 2015), in Nature Medicine and supported by the National Institutes of Health, suggests that enhancing proteasome activity with drugs during the early stages of Alzheimer’s disease may prevent dementia and reduce damage to the brain.
Rolipram was initially developed as an antidepressant but is not used clinically due to its side effects.
James Pickett, Head of Research at Alzheimer’s Society said: “No treatments are currently available that slow the progress of Alzheimer’s – a disease which is caused by the proteins, amyloid and tau, which clump together and cause damage in the brain.
“This study in mice appears to show that the drug, rolipram – which was first developed to treat depression – can restart the waste disposal system in brain cells and flush out the toxic clumps. This prevented memory problems in the mice studied, but only in those that showed signs of the early stages of Alzheimer’s disease.
“This discovery suggests a new way in which people with dementia could be helped, but it is still very early stages and there are many hurdles to overcome before we know if it’s effective in people. Repurposing existing drugs is a promising approach to treat dementia and Alzheimer’s Society is funding several on-going trials testing a range of drugs used for other conditions, from diabetes to arthritis.”