SOLNA, Sweden — Alzheimer’s disease often progresses silently for decades before symptoms start to sneak up on older adults. This means that early detection is crucial for the quality of life of those at risk. A new Swedish study may make this easier to achieve as scientists demonstrated that a protein called GFAP could serve as a prospective biomarker for catching Alzheimer’s a decade before symptoms emerge.
“Our results suggest that GFAP, a presumed biomarker for activated immune cells in the brain, reflects changes in the brain due to Alzheimer disease that occur before the accumulation of tau protein and measurable neuronal damage,” says study first author Charlotte Johansson, a doctoral student at the Department of Neurobiology, Care Sciences and Society at the Karolinska Institutet, in a media release. “In the future it could be used as a non-invasive biomarker for the early activation of immune cells such as astrocytes in the central nervous system, which can be valuable to the development of new drugs and to the diagnostics of cognitive diseases.”
Alzheimer’s progresses gradually as nerve cells lose function due to an abnormal accumulation of two proteins — beta-amyloid and tau. It can take anywhere from 20 to 25 years for this to start showing its effects through worsening memory and speech functions.
GFAP could be the first sign of Alzheimer’s
So far, the researchers from Karolinska Institutet, as well as Landspitali University Hospital in Iceland, Gothenburg University, and University College London, have been working together to study blood biomarkers to catch early changes that appear in an inherited form of Alzheimer disease. This form is exceedingly rare, accounting for fewer than one percent of all cases. Those with a parent with Alzheimer’s disease triggered by a mutation have a 50-percent risk of developing the degenerative condition as well.
To delve into this, the researchers analyzed 164 blood plasma samples from 33 mutation carriers and 42 relatives not predisposed from data collected between 1994 and 2018. Their findings displayed significant changes in blood protein concentrations among those carrying the mutation.
“The first change we observed was an increase in GFAP (glial fibrillary acidic protein) approximately ten years before the first disease symptoms,” says study author Caroline Graff, professor at the Department of Neurobiology, Care Sciences and Society. “This was followed by increased concentrations of P-tau181 and, later, NfL (neurofilament light protein), which we already know is directly associated with the extent of neuronal damage in the Alzheimer brain. This finding about GFAP improves the chances of early diagnosis.”
Alzheimer’s continues to impact the lives of millions around the world. As such, the authors hope that their work makes detecting early signs of neurological deterioration a simpler process.
The findings are published in the journal Brain.
