While the cause and progression of Alzheimer's disease remains unknown, scientists widely accept that amyloid beta plaque buildup leads to cognitive dysfunction associated with the disease.
Now, researchers at the Max Planck Florida Institute for Neuroscience may have stumbled upon a potential cause of Alzheimer's based on a newly discovered signaling pathway in cellular models of the disease. They found that the presence of the amyloid beta peptide triggers increased levels of a signaling protein, CentA1, and this protein appears to create cognitive dysfunction. The finding could open the door for new therapies to treat the debilitating disease.
The Institute, which opened in Jupiter, FL, in December 2012, is the first U.S. extension of the Munich, Germany-based Max Planck Society for the Advancement of Science.
Conducting tests on rat brain slices, researchers identified the signaling protein--called centaurin-α1, or CentA1--and measured its effects on neurons. They observed that the presence of amyloid beta triggered higher levels of CentA1, which seems to cause neuronal dysfunction.
The researchers used RNA silencing to reduce the production of CentA1 in the rat brain samples, which caused the neurons exposed to amyloid beta to return to normal functioning--that is, the neurons no longer showed signs of Alzheimer's--even though the amyloid beta was still present.
When they increased CentA1, a series of proteins was activated, and these proteins formed a signaling pathway from CentA1 to neuronal dysfunction. The researchers found that by inhibiting other proteins along the pathway, they were, in effect, able to "cure" the affected neurons. The research was published in the Journal of Neuroscience.
The scientists have already started to conduct studies in mouse models of Alzheimer's disease.
- here's the study abstract
- read the press release