Alzheimer’s disease begins decades before any symptoms, such as memory loss, appear. Therefore, early diagnosis increases the chances of stopping the disease with drugs. A new study on an inherited form of the disease shows that a protein called GFAP it is a possible biomarker of very early stages of the disease. The study, carried out by researchers at the Karolinska Institutet (Sweden) and published in the journal “Brain”, could one day lead to earlier detection of this serious and frequent disease.
“Our results suggest that GFAP, a putative biomarker of activated immune cells in the brain, reflects changes in the brain due to Alzheimer’s disease that occur before tau protein accumulation and measurable neuronal damage,” says the The study’s first author, Charlotte Johansson. “In the future it could be used as a non-invasive biomarker of early activation of immune cells such as astrocytes in the central nervous system, which may be valuable for the development of new drugs and the diagnosis of cognitive diseases.”
Alzheimer’s disease causes 60 to 70 percent of all dementia cases, according to the Swedish Brain Foundation. In Alzheimer’s disease, nerve cells in the brain degenerate as a result of the abnormal buildup of the proteins beta-amyloid and tau. As more brain neurons are damaged, this manifests itself in dysfunctions of cognitive functions such as memory and speech.
The disease progresses insidiously, and biological changes in the brain begin as early as 20 to 25 years before memory loss and other cognitive symptoms become apparent. The sooner a patient is correctly diagnosed, the sooner appropriate treatment can be offered. This is one of the many reasons why more research is needed on accurate and easy-to-use methods for early diagnosis.
Researchers at the Karolinska Institutet and colleagues at Iceland’s Landspitali University Hospital, the University of Gothenburg and University College London (UK) have studied biomarkers in blood to detect very early pathological changes in a rare and inherited form of Alzheimer’s disease. which represents less than one percent of all cases. People with a parent with Alzheimer’s caused by a mutation have a 50% risk of developing the disease.
People with a parent with Alzheimer’s caused by a mutation have a 50% risk of developing the disease
For their study, the researchers analyzed 164 blood plasma samples from 33 mutation carriers and 42 relatives without the inherited pathogenic predisposition. The data was collected between 1994 and 2018.
Their results reveal clear changes of various blood protein concentrations in mutation carriers.
“The first change we observed was an increase in GFAP (glial fibrillary acidic protein) approximately ten years before the first symptoms of the disease,” says the study’s last author, Caroline Graff, a professor in the Department of Neurobiology, Life Sciences. Attention and Society of Instituto Karolinska. “This was followed by an increase in the concentrations of P-tau181 and, later, of NfL (neurofilament light protein), which we already know is directly associated with the extent of neuronal damage in the Alzheimer’s brain. This finding on GFAP improves the chances of early diagnosis.”