Researchers have developed a method to create a new blood marker capable of detecting whether or not a person has Alzheimer’s disease


Researchers from Lund University, together with the Roche pharmaceutical company, have developed a method to create a new blood marker capable of detecting whether or not a person has Alzheimer’s disease.

If the method is approved for clinical use, the researchers hope eventually to see it used as a diagnostic tool in primary healthcare.

This autumn, they will start a trial in primary healthcare to test the technique.

Currently, a major support in the diagnostics of Alzheimer’s disease is the identification of abnormal accumulation of the substance beta-amyloid, which can be detected either in a spinal fluid sample or through brain imaging using a PET scanner.

“These are expensive methods that are only available in specialist healthcare.

In research, we have therefore long been searching for simpler diagnostic tools,” says Sebastian Palmqvist, associate professor at the unit for clinical memory research at Lund University, physician at Skåne University Hospital and lead author of the study.

In this study, which is a collaboration between several medical centres, the researchers investigated whether a simple blood test could identify people in whom beta-amyloid has started to accumulate in the brain, i.e. people with underlying Alzheimer’s disease.

Using a simple and precise method that the researchers think is suitable for clinical diagnostics and screening in primary healthcare, the researchers were able to identify beta-amyloid in the blood with a high degree of accuracy.

“Previous studies on methods using blood tests did not show particularly good results; it was only possible to see small differences between Alzheimer’s patients and healthy elderly people.

Only a year or so ago, researchers found methods using blood sample analysis that showed greater accuracy in detecting the presence of Alzheimer’s disease.

The difficulty so far is that they currently require advanced technology and are not available for use in today’s clinical procedures,” says Sebastian Palmqvist.

The results are published in JAMA Neurology and based on studies of blood analyses collected from 842 people in Sweden (The Swedish BioFINDER study) and 237 people in Germany.

The participants in the study are Alzheimer’s patients with dementia, healthy elderly people and people with mild cognitive impairment.

The method studied by the researchers was developed by Roche and is a fully automated technique which measures beta-amyloid in the blood, with high accuracy in identifying the protein accumulation.

“We have collaborated with Roche for a long time and it is only now that we are starting to approach a level of accuracy that is usable in routine clinical care around the world,” says Oskar Hansson, professor of neurology and head of the unit for clinical memory research at Lund University.

The researchers believe that this new blood sample analysis could be an important complement for screening individuals for inclusion in clinical drug trials against Alzheimer’s disease or to improve the diagnostics in primary care which will allow more people to get the currently available symptomatic treatment against Alzheimer’s disease.

“The next step to confirm this simple method to reveal beta-amyloid through blood sample analysis is to test it in a larger population where the presence of underlying Alzheimer’s is lower.

We also need to test the technique in clinical settings, which we will do fairly soon in a major primary care study in Sweden.

We hope that this will validate our results,” concludes Sebastian Palmqvist.

A long-term study supports earlier suggestions that testing the blood for levels of a certain protein could be a noninvasive way to track the progress of Alzheimer’s disease.

The protein is called neurofilament light. It spills out of damaged and dying nerve cells, into the cerebrospinal fluid and then travels from there into the bloodstream.

Previous studies have already demonstrated that blood levels of neurofilament light are higher in people with diseases, such as Alzheimer’s, that destroy nerve cells and tissue in the brain. However, few of these have been long-term investigations.

The new study, which features in JAMA Neurology, suggests that measuring blood levels of neurofilament light could indicate whether drugs for treating Alzheimer’s disease are working. As yet, there is no noninvasive way of doing this.

The findings follow those of another investigation that showed that measuring neurofilament light in the blood could identify Alzheimer’s disease 10 years or more before the emergence of symptoms such as decline in thinking and memory.

However, the earlier study was limited to identifying people with a rare, inherited, early-onset form of Alzheimer’s disease that usually strikes before the age of 65.

The more recent research applies to sporadic Alzheimer’s disease, a far more common, late-onset type that most often strikes after the age of 65.

“Taken together,” says lead study author Dr. Niklas Mattsson, a physician at Skåne University Hospital who also does research at Lund University, both in Sweden, “these studies indicate that [neurofilament light] in the blood can be used to measure damage to brain cells in various forms of Alzheimer’s disease.”

Alzheimer’s disease and brain changes

About 60–80% of people with dementia have Alzheimer’s disease.

The disease is complex and not easy to diagnose.

The most common early symptom of Alzheimer’s disease is short-term memory loss, and this, together with other symptoms of cognitive and physical deterioration that result from loss of brain cells, gradually worsens over time.

Eventually, the disease can stop people from being able to live independently, as they lose the ability to relate to others and their environment.

According to figures from the Alzheimer’s Association, there are 5.8 million people living with Alzheimer’s disease in the United States, and this number is likely to rise to just under 14 million by 2050.

There is currently no cure for Alzheimer’s disease.

There are some treatments that can alleviate some of the symptoms for a little time, but none, as yet, can stop the disease from progressing.

The changes in the brain that accompany Alzheimer’s disease begin a long time before the early symptoms start to appear.

These changes include the toxic buildup of tau and beta-amyloid proteins that damage nerve cells’ ability to communicate and function and eventually cause their death.

More information: Performance of Fully Automated Plasma Assays as Screening Tests for Alzheimer Disease–Related β-Amyloid Status. JAMA Neurol. Published online June 24, 2019. DOI: 10.1001/jamaneurol.2019.1632

Journal information: Archives of Neurology
Provided by Lund Universit


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