Manipulation of Reelin signaling offers hope for reversing cognitive function of Alzheimer’s patients
A new study from Cell Biology Department scientists at the University of Barcelona working with laboratory mice sheds new light on the role that the protein Reelin plays in preserving plasticity in adult brains and restoring lost cognitive function. These findings were recently published in the periodical, Nature Connections, and are critical to the efforts to prevent and treat Alzheimer’s disease.
In spite of years of research seeking to locate the cause of Alzheimer’s disease, scientists still do not know the cause of this neurodegenerative ailment. However there are some known structures that appear to have a significant role in causing loss of cognitive function, neuronal death and decrease in synaptic functioning. These structures are amyloid plaques and neurofibrillary tangles. The new study reveals that when levels of Reelin were increased in the brain of laboratory mice with Alzheimer’s, cognitive loss was reversed. Further, it was confirmed that Reelin diminishes amyloid deposits and postpones the development of amyloid-beta fibril in vitro.
The role of Reelin in controlling tau protein and the amyloid precursor protein was already known, but the full extent of Reelin’s role was undiscovered. So, the researchers focused their efforts on analyzing Reelin’s role. With this new study, researchers working on prevention and treatment methodologies have a new comprehension of the bond between these two proteins and Reelin’s role in regulating them. The study proves that an increase in Reelin is beneficial to reversing the effects of Alzheimer’s disease.
Researchers discovered the nature of the interaction between Reelin in vitro and the peptide AB42, a lethal peptide responsible for the accumulation of senile plaques and formation of fibril. In vitro tests on mouse models revealed that Reelin was functioning to reduce plaque and delaying fibril formation. With these findings, researchers offer Reelin as a promoter of adult brain plasticity and protective agent for neurons. Future research will concentrate on identifying chemical composites that can stimulate Reelin signaling.