Researchers have discovered a key protein in the brain that appears to act as a “switch” to turn Alzheimer’s disease on and off, according to a study published in the Journal of Neuroscience. The study, conducted by scientists at the Max Planck Florida Institute, found that high levels of Amyloid beta in the brain triggers the production of a specific protein, called centaurin-alpha1 (CentA1), which then produces a cascade of proteins that damage nearby neurons.
The study team further discovered that when an RNA silencing technique was used to shut down the production of CentA1, the damaged neurons returned to their healthy state.
Amyloid beta has long been suspected of playing a role in the development of Alzheimer’s, but scientists had been unsure of how the neuron damage was occurring. The discovery of the CentA1 protein’s function as a “signalling pathway” may lead to treatments that can “turn off” the production of brain-damaging proteins.
"This study transforms our understanding of the direct cause of Alzheimer's disease," said the study’s lead investigator Ryohei Yasuda, in an institute statement. "With further research, we may open up an entirely new avenue for treatments to combat this disease."
The study was conducted on rats, but it is cautiously being hailed as a “stunning breakthrough” for possible treatments for the debilitating disease.
Get the latest information on Alzheimer's and dementia, and attend other valuable sessions at this two-day event making education on the research, innovations, and program approaches to memory care a priority.