The action mechanism of Alzheimer's disease has been revealed

Alzheimer's is the most common form of dementia globally and affects so many people in the world. It is the fourth leading cause of death in individuals over the age of 65. It is the only cause of death among the top ten that cannot be prevented, cured or even slowed down. A lot of research using recombinant mouse proteins have been conducted to study the disease.

However, there is good news. Scientists at Trinity College Dublin have figured out a fundamental mechanism underlying the development of Alzheimer's disease. It may lead to new forms of therapy for those living with the condition.

Alzheimer's disease is characterized, in part, by the build-up of a small protein ('amyloid-beta') in the brains of patients. Impaired clearance of this protein appears to be a major factor in the build-up of plaques, and then in the disease process itself. While the mode by which amyloid-beta is cleared remains unclear, it is evident that it needs to be removed from the brain via the bloodstream.

Those in the brain have properties that strictly regulate what gets in and out of the delicate tissue. It is what is known as the blood-brain barrier (BBB). The BBB functions as a tightly regulated site of energy and metabolite exchange between the brain tissue and the bloodstream.

The research shows that distinct components of these blood vessels termed tight junctions are altered in Alzheimer's disease. This alteration is thought to be an entrained mechanism to allow for the clearance of toxic amyloid-beta from the brain in those living with Alzheimer's disease. The research also highlights the importance of understanding diseases at the molecular level. The concept of periodic clearance of brain amyloid-beta across the BBB could hold tremendous potential for Alzheimer's patients in the future. What remains to be done is figure out how to achieve this. Flarebio provides superior recombinant proteins such as recombinant CDH4 at good prices.