Blood biomarker could identify Alzheimer’s disease 10 years before symptoms begin

Reetfeed
Blood biomarker could identify Alzheimer's disease 10 years before symptoms begin
Aditya Chaudhary

Alzheimer’s Disease Symptoms: Although more than 55 million people worldwide are affected by Alzheimer’s disease, there is no cure for it – and treatment options are limited. While there has been some recent progress in efforts to find a cure for the disease, and this has led to the development of two drugs that may delay the progression of the disease, their benefits are debated. In such a situation, it is not necessary to tell that in most of the clinical trials, considering the effectiveness of these drugs, the treatment starts only after the symptoms arise. This means that the damage from the disease has already happened.

It is believed that if treatment is started earlier – before symptoms start – the damage can be prevented. But the problem is that the clinical signs that doctors look for to diagnose a patient with Alzheimer’s disease appear only after neurodegeneration has occurred. Our recent study argues for using a different biomarker than those currently used to diagnose Alzheimer’s.

Good News: Artificial pancreas will give relief to diabetes patients, now Britain has also adopted this technique

We found that this biomarker, which can be found in a person’s blood, can detect disease up to ten years before symptoms begin. This provides an opportunity to stop the inflow of the disease before the symptoms of the disease appear in the body. Our study was conducted using data from Swedish families who had a form of Alzheimer’s disease caused by a genetic mutation. Whereas autosomal dominant Alzheimer’s disease (ADAD) has symptoms similar to diffuse Alzheimer’s disease (the most common form of Alzheimer’s, which is a combination of genetic, lifestyle, and environmental factors) and these symptoms occur much earlier—usually before a person’s age. In the 40s or 50s of age.

Since the mutation is inherited, if a parent has ADAD, their child will have a 50 percent chance of inheriting the mutation. Although this form occurs in less than one percent of all people with Alzheimer’s disease, research studies in these families provide valuable information about how Alzheimer’s disease normally progresses.

Our study looked at 75 people from three different families who had a history of ADAD. Participants provided a total of 164 blood samples, all collected between 1994 and 2018. Levels of four different blood-based biomarkers with known links to Alzheimer’s disease were analyzed. We also did other tests like MRI imaging and cognitive tests to look for signs of disease. Our main finding was that the level of a particular protein, called GFAP, increased in the study before other known prognostic blood-based biomarkers were analyzed. This increase started ten years before the first noticeable signs of Alzheimer’s disease.

GFAP is a protein released by astrocytes of the brain. These are specialized cells that, among other functions, participate in the immune system of the brain. While we know that GFAP is involved in brain immune system processes, we do not know its exact function. Our results are consistent with other recent studies on genetic forms of Alzheimer’s, which have shown higher GFAP levels before disease onset.

Research has also shown that GFAP levels are higher in people who have preclinical Alzheimer’s disease without a genetic cause, who have other symptoms of Alzheimer’s disease but are not yet showing symptoms. This suggests that our findings may also apply to more common forms of Alzheimer’s disease. The results of our study are also important to support our general understanding of Alzheimer’s disease – specifically the early disease processes in the brain.

Combined with other recent findings, it is clear that more investigation is needed regarding GFAP and its function in the brain – including in the progression of Alzheimer’s disease. Perhaps future treatments for Alzheimer’s disease will be more successful if they aim to target both the brain’s astrocytes and other common hallmarks of Alzheimer’s disease – such as the accumulation of beta-amyloid in the brain.

(Caroline Graf and Charlotte Johansson, Karolinska Institutet, Solnavegan, Sweden)