Research Traces Link Between Beta Amyloid Protein, PirB/LilrB2 Protein And Alzheimer's Disease

PirB (red) is heavily concentrated on the surface of growing nerve cells.
Credit: Dr. Carla Shatz, Stanford University.

Stanford University School of Medicine researchers suggest that a link between the beta-amyloid protein and the PirB/LilrB2 protein may be a strong factor in the development of Alzheimer's Disease. The LilrB2 protein found in humans and its counterpart, the PiirB protein found in mice controls the visual system development in the brain. Research show that these class of proteins bind with the beta-amyloid protein which triggers the onset of Alzheimer's disease.

The research also shows that depleting PirB in the brain of the mouse model prevented the chain reaction and reduced memory loss. This discovery can lead to the development of treatments that can delay, treat or even prevent this this disease.

Alzheimer's disease causes brain cells to die and damages brain affecting its functions such as cognition, memory, and the control of the body's processes. Protein fragments, called plaques and tangles, stick together to form the Alzheimer's protein which stats to kill brain cells. The disease starts at the Hippocampus and ultimately destroys the whole brain.

The slow progression of the disease takes around eight to ten years from beginning to end which starts with memory loss. It then starts to spread and affect the part of the brain that controls balance and mobility. Ultimately, the disease starts attacking the area where breathing and heart functions are controlled.

Alzheimer's disease is a form of dementia that affects more than 5 million Americans. Currently there is no cure for the disease.