Scientists believe that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain, according to numerous media reports.
The Guardian newspaper has particularly picked up on this exciting study emanating from Cambridge University.
Researchers believe that gene patterns which are located in specific areas of the brain may help to explain why the disease tends to emanate in certain regions before later spreading.
Such patterns were located in the areas of healthy brains which were primed to produce certain proteins.
Scientists involved in the study believe that the natural defences on which the body relies become less able to prevent protein build-up as cells age, and this becomes apparent first in the areas most genetically primed for protein overgrowth.
While this is very much an embryonic theory, it is hoped in the future that it may be possible to target particularly vulnerable areas of the brain for Alzheimer’s treatment; thus making such efforts more efficient and effective.
The study was carried out by researchers from Cambridge University and received no specific funding.
It was published in the peer-reviewed journal, Science Advances, which requires a subscription in order to access.
This was an experimental study comparing data from healthy human brains against data about which regions of the brain are affected in early-stage Alzheimer’s disease.
Researchers used data relating to 500 samples of tissue from the post-mortems of six healthy human brains, all from people aged 24 to 57, none of whom had Alzheimer’s disease.
They analysed 19,700 genes to see which affected protein expression in the brain.
Researchers found that neurones were less likely to express genes protecting against protein build-up, and more likely to express genes promoting protein growth, compared with other brain cells.
When comparing brain maps, those regions of the brain in which tissues were more susceptible to protein expression correlated well with the brain regions that first show signs of Alzheimer’s disease.
The researchers commented on their results in the study.
“Our results identify a quantitative correlation between the histopathological staging of AD [Alzheimer’s disease] and the specific expression patterns of the genes corresponding to the proteins that coaggregate in plaques and tangles.”
Findings related to immune response suggest inflammation should also be considered important, indicating that, “the vulnerability of specific tissues in AD may result from the sum of a number of factors, including genetic control of protein exprssion, natural defences against protein overgrowth, and the response of the immune system.”
This research offers an intriguing insight into one possible factor contributing to Alzheimer’s, but does not demonstrate any way of recognising who will develop the condition.
Additionally, scientists have no knowledge regarding a suitable manipulation of gene expression.
It is not even known whether protein plaques and tangles actually cause Alzheimer’s disease.
So any cure or effective treatment for the debilitating condition remains a long way off.
What can be said is that the latest research sheds light on the complex conditions which contribute to Alzheimer’s vulnerability.