Early detection of Alzheimer’s disease through blood biomarker

Persons with a genetic predisposition for Alzheimer’s disease show changed blood mirrors that have been damaged neuronal contacts of damaged neuronal contacts 11 years before the expected start of dementia symptoms. This is clear in the levels of the protein “beta-synuclein”. An international team, including researchers from DZNE, ULM University Hospital and University Medicine Halle report these findings in the magazine “Alzheimer and dementia“. The biomarker studied here may help to detect neurodegeneration at an early stage and therefore to indicate a sufficient time to start treatment.

New drugs for the treatment of Alzheimer’s disease, the most common form of dementia, are currently available. These “amyloid antibodies” cause the removal of minor deposits from the brain and can delay the disease progression. However, treatment in the initial phase of the disease is a condition. “Early diagnosis is therefore becoming increasingly important. But at the moment Alzheimer’s is usually diagnosed quite late. That is why we need progress in diagnostics. Otherwise we will not be able to use the full potential of these new medicines,” says Dr. Patrick Öckkl, a leader of the research group leader at Dzne’s ULM site and in the Neurology department at the Ulm University Hospital. “That is why we have been studying beta synuclein for some time. Blood mirrors of this protein reflect neuronal damage and can be determined relatively easily. We see a potential biomarker for the early detection of neurodegeneration. This assessment is supported by our current research results.” The potential for application probably extends beyond Alzheimer’s, according to the scientist: “This marker gives neuronal damage to it that can also arise from a stroke. Our research shows that it is particularly relevant in the context of Alzheimer’s disease.”

Fragments of the synapses

Beta-Synuclein is a protein that is mainly found at the nodes between neurons. These so-called synapses, as a result of which neurons exchange signals with each other, gradually break down in the course of Alzheimer’s disease: as a result, beta synuclein is released, the bloodstream comes in from the brain and can then be detected by blood test. “Our research shows that synaptic breakdown starts very early. It starts before cognitive impairment manifests itself,” says Öckkl. “This makes beta-synuclein a marker that reacts in a pre-symptomatic stage. In particular, this means that the blood mirrors of the protein rise.”

Family disease of Alzheimer’s

The findings are based on data from Dian, an international research network dedicated to the hereditary form of Alzheimer’s disease, caused by mutations in the genome. Because these genetic anomalies can be passed on to descendants, cases of dementia are in the families of the affected individuals. “The hereditary variant of Alzheimer’s is very rare and can manifest itself in early or middle adulthood. From a pathological point of view, however, it is very similar to the sporadic variant of Alzheimer’s, which is much more common and usually does not occur before senior age,” says Prof. Markus Halle, that also a play of the Department of the Department,, that, which is also a play of the Department of the Department,, who, who is also a play of the Department of the Department or Neurtijk,,, that, which is also a play of the Department of the Department or Neurton’s Department,, that also, of the Department or NEURTO MEDIETITY,, that, of the Department or Neurton,, who also, of the Department or Neurton’s Department,, who is also a play of the Department or Neurton. Current research. Based on current knowledge, these genomic errors almost inevitably lead to dementia. It is possible to estimate when the symptoms are likely to begin. “For a person with a mutation, it is possible to predict the years until the start of the symptoms of dementia. Experience tells us that this can be calculated on the basis of the age at which cognitive disorders took place for the first time with older family members,” Otto explains. “This estimate is available to all participants in Dian and makes it possible to place disease progression in a period of time.”

Blood marker correlates with symptomatology

In the current study, blood of more than 100 adults with such gene mutations were investigated for beta synuclein. These persons were between their mid -thirty and mid -40s. All participants in the study were assessed on cognitive performance: about a third signs of dementia, while the remaining test subjects had no symptoms. In some cases, the researchers could also characterize the state of health with the help of samples of cerebrospinal liquid and brain scans. Some participants were even investigated several times, so that their condition could be followed for several years. Ultimately, the different data gave a picture of how the blood levels of beta-synuclein changed during Alzheimer’s disease. “The concentration of beta-synuclein in the blood starts to rise for about 11 years before the first symptoms of dementia are expected. In other words, there are early signs of synaptic degeneration,” says Otto. “Loss of brain masses and other pathological changes that also occur in Alzheimer’s disease do not place until later. And after the start of the symptoms, the more serious the cognitive disorders, the higher the science synuclein level in the blood. Thus this is reflected in both the pre-symptoms of the pre-sympto-stadia.”

Perspectives

DZNE researcher Öckkl expects that similar effects will also take place in the sporadic form of Alzheimer’s disease: “Given the agreements with the hereditary variant, I consider this very likely. But of course this must still be verified in studies. If confirmed, this biomarker can be used in the context of extensive diagnostostic.” And he also sees potential: “In addition to early detection, this marker may also be useful to assess whether a therapy will take effect, so that synaptic loss and therefore disease progression slows down.” Such a monitoring tool would be equally important for the development of therapies in clinical examinations and for treatment in routine care. “In the future we will probably have a whole series of biomarkers available to assess the status of Alzheimer’s disease. I can well imagine that beta-synuclein will play a role in this repertoire,” says Öckl.