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Alzheimer’s disease is a progressive brain disorder that slowly destroys memory, thinking skills and the ability to perform simple tasks. Researchers have long known that dementia sufferers have higher levels of a certain protein that leaks into the cerebrospinal fluid after brain cells die.
But they could not work out how to measure it without invasive, expensive spinal taps. In a new study, scientists say they can now detect this protein in the blood and that levels of it rise at the same speed that the brain loses neurons and begins shrinking.
The blood test that looks for the protein would be performed in middle-age, well before most are diagnosed with Alzheimer’s disease. The team, led by Washington University School of Medicine in St Louis, Missouri, says a blood test is easier, faster and cheaper and could lead to routine screenings for degenerative brain conditions being offered in clinics.
Sufferers experience a decline in cognitive, behavioral and physical abilities and there is no cure. For the study, the team recruited more than 400 people from the Dominantly Inherited Alzheimer’s Network (DIAN). Led by Washington University, the aim of DIAN is to identify potential biomarkers of Alzheimer’s in people who carry a gene mutation that causes the disease.
About 250 of the participants had a genetic mutation and the rest were relatives that did not carry it. The adults also underwent blood work, brain scans and cognitive tests every two to three years. The researchers used a blood test kit similar to others available commercially but not yet approved by the US Food and Drug Administration to diagnose or predict brain damage.
The test detects levels of a protein called neurofilament light chain, which leaks into the blood and cerebrospinal fluid after brain cells are damaged or die.
Previous studies have shown the levels of the protein structure in spinal fluid are a good predictor for dementia, but this requires invasive and expensive spinal taps. Participants with the genetic mutation had higher baseline protein levels that rose as the study period continued.
Researchers were able to notice a difference between the two groups about 16 years before symptoms were expected to appear. ‘Sixteen years before symptoms arise is really quite early in the disease process, but we were able to see differences even then,’ said co-first author Stephanie Schultz, a graduate student at Washington University.
‘This could be a good preclinical biomarker to identify those who will go on to develop clinical symptoms.’
Next, the team had about 40 people with the faulty gene variant undergo brain scans and cognitive tests two years after their previous visit to the clinic. Researchers found the participants with protein levels that had increased dramatically over those two years had fewer neurons in brain tissue and performed worse on cognitive and memory tests.
Next, the team had about 40 people with the faulty gene variant undergo brain scans and cognitive tests two years after their previous visit to the clinic. Researchers found the participants with protein levels that had increased dramatically over those two years had fewer neurons in brain tissue and performed worse on cognitive and memory tests.
Additionally, the increase in neurofilament light chain proteins precisely matched the speed at which the precuneus – which plays a role in memory – thinned and shrank. ‘This is something that would be easy to incorporate into a screening test in a neurology clinic,’ said co-author Dr Brian Gordon, an assistant professor of radiology at Washington University’s Mallinckrodt Institute of Radiology.
‘We validated it in people with Alzheimer’s disease because we know their brains undergo lots of neurodegeneration, but this marker isn’t specific for Alzheimer’s. High levels could be a sign of many different neurological diseases and injuries.’ People suffering from Lewy body dementia and Huntington’s disease – two progressive brain disorders – have high protein levels.
The levels also radically spike when people with multiple sclerosis have a sudden episode of symptoms and when football players are hit in the head.
The levels also radically spike when people with multiple sclerosis have a sudden episode of symptoms and when football players are hit in the head.
‘This is something that would be easy to incorporate into a screening test in a neurology clinic,’ said co-author Dr Brian Gordon, an assistant professor of radiology at Washington University’s Mallinckrodt Institute of Radiology. ‘We validated it in people with Alzheimer’s disease because we know their brains undergo lots of neurodegeneration, but this marker isn’t specific for Alzheimer’s. High levels could be a sign of many different neurological diseases and injuries.’