Alzheimer’s disease is a debilitating and progressive neurological disorder that primarily affects short-term memory. As the condition worsens, patients may experience difficulty finding the right words, disorientation, a decline in social abilities, and emotional changes.

While the disease itself is not typically fatal, those in advanced stages of Alzheimer’s are at a higher risk of life-threatening complications, such as severe infections. With no cure currently available, early detection and management are crucial in slowing the progression of this heartbreaking illness.

The onset of Alzheimer’s disease can occur years before any visible symptoms, such as memory loss, appear. Therefore, an early diagnosis can greatly improve the chances of delaying the progression of the disease through medication.

According to a recent study on a genetic form of Alzheimer’s, a protein known as GFAP may serve as a biomarker for the disease’s earliest stages.

In a breakthrough study published in the prestigious journal Brain, researchers at Karolinska Institutet have uncovered a promising avenue for the early detection of Alzheimer’s disease.

According to the study’s lead author, Charlotte Johansson, a doctoral student at Karolinska Institutet’s Department of Neurobiology, Care Sciences and Society, their findings suggest that GFAP, a protein previously believed to signal activation of immune cells in the brain, may actually be an early indicator of changes in the brain caused by Alzheimer’s disease, preceding the build-up of tau protein and detectable neuronal damage.

In the future, GFAP could potentially be used as a “non-invasive biomarker for early detection of immune cell” activation in the central nervous system, which could aid in the development of new treatments and in diagnosing cognitive diseases.

According to the Swedish Brain Foundation, anywhere between 60% and 70% of all instances of dementia may be attributed to Alzheimer’s disease.

In Alzheimer’s disease, beta-amyloid and tau proteins build up in the brain in a strange way, which kills nerve cells.

As more neurons in the brain get hurt, cognitive functions like memory and speech start to break down.

Memory loss and other cognitive symptoms don’t appear for 20 to 25 years until the illness has already subtly changed the brain biologically.

The sooner a patient gets a correct diagnosis, the sooner the right treatment can be given. This is only one of many factors that call for additional investigation into accurate, practical early detection techniques.

Researchers at the Karolinska Institutet, along with their colleagues at the Landspitali University Hospital in Iceland, Gothenburg University, and University College London in the United Kingdom, have been analyzing biological markers in blood for very early pathological changes in a rare and inherited form of Alzheimer disease. This form of the disease accounts for less than one percent of all cases.

People who have a parent with Alzheimer’s disease caused by a mutation have a 50% chance of also getting the disease.

The researchers analyzed 164 plasma samples from the blood of 33 people who had the mutation and 42 of their relatives who did not have the inherited pathogenic tendency. The information was gathered from 1994 to 2018.

Their results show that the mutation carriers have different levels of several proteins in their blood.

“The first change we observed,” as explained by the last author Caroline Graff, “was an increase in GFAP (glial fibrillary acidic protein) approximately ten years before the first disease symptoms.”

According to the author, “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’s brain.”

“This finding about GFAP improves the chances of early diagnosis,” the author adds.

Source: 10.1093/brain/awac399 

Image Credit: Shutterstock


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