A simple blood test can detect signs of brain damage in people at risk for Alzheimer’s disease, even before symptoms such as confusion and memory loss arise, argue scientists in a study published today.
The tests, researchers say, manages to identify in the blood a protein from the skeleton of the neurons (brain cells) called light chain neurofilament, and can also be used to detect signs of brain damage associated with other neurodegenerative diseases, such as multiple sclerosis.
When there is injury or death of neurons, what happens in Alzheimer’s disease, the most common form of dementia that has no cure, this protein ‘flows’ into the cerebrospinal fluid – which ‘bathes’ the brain and spinal cord – and from it enters the bloodstream.
The detection of high levels of the protein in the cerebrospinal fluid has been pointed out as a sign that some neurons have suffered injuries. However, obtaining a sample of cerebrospinal fluid requires its collection of the spinal cord with a needle, a method to which people are reluctant.
A team of scientists at the University of Washington and the German Center for Neurodegenerative Diseases have started a population study that included families with rare genetic mutations that cause Alzheimer’s disease (at 30, 40 and 50 years).
According to a statement from the University of Washington School of Medicine, which is investigating the ‘roots’ of the disease, there is a 50 per cent probability that a parent with one of those mutations will transmit the genetic error to a child, and then , have symptoms of dementia near the age when the father or mother had them.
The scientists evaluated 409 people, of whom 247 were carriers of a genetic mutation inherited from the parents and the remainder without gene alterations. Of all the people who accompanied them, half of whom more than once, had blood samples, brain imaging, and cognitive tests.
People who had a genetic error revealed higher blood-brain protein concentrations – light chain neurofilament – and these concentrations increased over time.
In contrast, people with a ‘normal’ gene had low, stable levels of the same protein. This difference was identified 16 years before the expected onset of cognitive symptoms associated with Alzheimer’s disease, according to the University of Washington statement.
In addition, researchers looked at images of people’s brains and found that protein concentrations increased at the same rate that a part of the brain involved in memory shrunk and thinned.
To understand whether blood-thinning neurofilament levels could be used as markers of cognitive degradation, scientists collected data from 39 people with genetic mutations that cause Alzheimer’s disease.
Through cognitive and brain imaging tests, they found that people whose blood samples had previously shown a rapid rise in protein concentrations were more likely to show signs of brain atrophy and decreased cognitive abilities (memory, reasoning …).
For one of the coordinators of the study, Mathias Jucker of the German Center for Neurodegenerative Diseases, it will be important to confirm if the results obtained will be the same when Alzheimer’s disease manifests itself later (which occurs in the elderly and the form more frequent) and determine the period of time from which changes in the protein should be evaluated to have a good clinical diagnosis.