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A new study published in the journal Nature Medicine shows that a protein present in the blood can be used to accurately monitor the progression of Alzheimer's disease well before the appearance of the first clinical signs.
Colored cortical neuron with an antibody against the NF-L neurofilament subunit in green. Image Credit: Gerry Shaw / CC BY-SA 3.0.
"It's something that would be easy to integrate into a screening test in a neurology clinic," said Dr. Brian Gordon, a researcher at the Mallinckrodt Institute of Radiology. the University of Washington.
"We have validated it in people with Alzheimer's disease because we know that their brain is undergoing significant neurodegeneration, but this marker is not specific to Alzheimer's disease. High levels could be a sign of many neurological diseases and injuries. "
"The fact that there is still no effective treatment for Alzheimer's disease is partly due to the fact that current treatments start far too late," said Dr. Mathias Jucker, senior researcher at the German Disease Center. neurodegenerative and the Hertie Institute for Clinical Research on the Brain.
The new test detects the neurofilament light chain (NfL), a structural protein that is part of the inner skeleton of neurons.
When brain neurons are damaged or dying, the protein escapes into the cerebrospinal fluid that bathes the brain and spinal cord and then into the bloodstream.
The discovery of high levels of protein in a person's cerebrospinal fluid has been shown to be strong evidence that some of his brain cells have been damaged. But getting cerebrospinal fluid requires a spinal tap, which many people are reluctant to undergo.
Dr. Gordon, Dr. Jucker, and their colleagues investigated whether NfL levels in the blood also reflected neurological damage.
Scientists have turned to a group of families with rare genetic variants responsible for Alzheimer's disease at a young age – usually between 50 and 40 or even 30 years of age. Families constitute the study population of the Alzheimer Network with Hereditary Prevalence (DIAN).
A parent carrying this mutation has a 50% chance of pbading genetic error to a child, and any child who inherits a variant is almost certain to develop dementia symptoms the same age as his or her parent. This timeline gives researchers an opportunity to study what is happening in the brain in the years preceding the onset of cognitive symptoms.
The researchers studied more than 400 people participating in the DIAN study, including 247 carriers of an early-onset genetic variant and 162 of their unaffected relatives. Each participant had already visited a DIAN clinic to donate blood, brain tests and cognitive tests. About half had been evaluated more than once, usually two or three years apart.
In patients with the defective gene variant, NfL protein levels were higher initially and increased with time. In contrast, protein levels were low and largely stable in individuals with the healthy form of the gene. This difference was detectable 16 years before the probable appearance of cognitive symptoms.
In addition, when the team examined participants' brain scans, they found that the rate at which protein levels increased was a function of the rate at which the precuneus – a part of the brain involved in memory – had been thinned and narrowed.
"Sixteen years before the onset of symptoms, it's really early enough in the process of the disease, but we still could see some differences. This could be a good preclinical biomarker to identify those who will develop clinical symptoms, "said Stephanie Schultz, a graduate student at the University of Washington.
All kinds of neurological damage can cause the NfL protein to spill neurons into the blood.
Protein levels are high in people with Lewy body dementia and Huntington's disease; they occur dramatically in people with multiple sclerosis during a push and in football players immediately after a blow to the head.
A commercial kit is available to test protein levels in the blood, but it has not been approved by the FDA to diagnose or predict the risk of brain damage to an individual. Before being able to use such a test for patients with Alzheimer's disease or any other neurodegenerative disorder, researchers will need to determine how much protein in the blood is too much and how quickly protein levels can increase. before becoming a subject of concern.
"I could see that this would be used at the clinic in a few years to identify signs of brain injury in individual patients," said Dr. Gordon.
"We are not up to the point of telling people," In five years, you will suffer from dementia. "We are all working in this direction."
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Oliver Preische et al. The dynamics of serum neurofilaments predicts the neurodegeneration and clinical progression of presymptomatic Alzheimer's disease. Nature Medicine, published online 21 January 2019; doi: 10.1038 / s41591-018-0304-3
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