Alzheimer’s disease is usually described as a degenerative neurological condition, one that is commonly associated with memory loss and confusion.
There’s a growing pile of research indicating that dementia might just be the traumatic culmination of numerous factors outside of the central nervous system, which could provide better targets for early diagnosis and even prevention.
Now an international team from Canada and China has identified a series of breakdowns throughout the body that appear to induce the nerve damage responsible for Alzheimer’s symptoms.
“Alzheimer’s disease is clearly a disease of the brain, but we need to pay attention to the whole body to understand where it comes from, and how to stop it,” says researcher Weihong Song from the University of British Columbia.
Alzheimer’s disease develops as neurons in key areas of the outer parts of the brain die. This loss of function is linked with a build-up of a protein called beta-amyloid and the deformation of another protein called tau.
A great deal of progress has been made in recent years on the structures of these chemicals and ways we might be able to treat amyloid plaques and tangled tau.
Nonetheless, researchers still aren’t fully clear on how the whole process starts in the first place. Hints have been found in common genes and behaviours such as poor sleep, but connecting the dots still proves elusive.
In this latest study, researchers wondered if the accumulations of beta-amyloid found in the neurons of those with Alzheimer’s could come from somewhere outside the brain altogether.
Beta-amyloid proteins are produced when a precursor protein found in the membranes of many different tissues is clipped in two, so technically can be produced anywhere in the body.
More importantly, they can cross the near-impenetrable wall of cells separating blood vessels from the brain’s precious grey matter.
“The blood-brain barrier weakens as we age,” says Song.
“That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”
To test if beta amyloid proteins produced elsewhere in the body can not only cross the barrier but establish the pathology responsible for Alzheimer’s, the researchers carried out a procedure called parabiosis on pairs of mice.
One member of each couple was genetically modified to carry a mutated human gene for producing high levels of beta amyloid.
