This has the look of something that might lead to an intermediary therapy for Alzheimer's disease, one that allows patients to better function despite beta amyloid build up - but it will be compensatory only, and won't solve the underlying damage and dysfunction of aging that causes beta amyloid to accumulate in the first place.
The scientific community so far has widely accepted that Alzheimer's disease is caused by the accumulation of a peptide called Amyloid beta. When Amyloid beta is applied to neurons, neuronal morphology becomes abnormal and synaptic function is impaired. However, how Amyloid beta causes dysfunction is unknown. [New] research indicates that the presence of Amyloid beta triggers increased levels of a signaling protein, called centaurin alpha 1 (CentA1), that appears to cause neuronal dysfunction - a potentially groundbreaking discovery that uncovers an important intermediary step in the progression of the disease.
As part of the research, the scientists were able to identify CentA1 and measure its negative effects on neurons. Utilizing an RNA silencing technique, they turned down the cellular production of CentA1, and showed that affected neurons, exposed to Amyloid beta and exhibiting Alzheimer's related symptoms, returned to normal morphology and synaptic function, even with the continued presence of Amyloid beta. They further found that increased CentA1 activates a series of proteins, and these proteins form a signaling pathway from CentA1 to neuronal dysfunction. Thus, inhibiting other proteins in the pathway also "cured" affected neurons.
The initial tests reported were conducted on rat brain slices. [Researchers have] already started to expand their studies to mouse models of Alzheimer's disease and preliminary experiments show promising results.