The sustained search for a treatment for Alzheimer’s disease has created many experimental therapies that target the accumulation of a protein called Amyloid Beta in the patient’s brains. On one hand the clinical results with the available treatments have been mixed because the Abeta levels do not correlate well with the severity of symptoms and on the other hand some studies suggest that the loading of this protein begins two or three decades before the patients’ show symptoms, which makes an early prevention impractical.The deterioration of the patients’ clinical picture seems to correlate well with the loss of excitatory neurological synapses that allow connectivity of cells.
Dr. Margolis et al., researchers at the Gladstone Institute of Neurological Disease at the University of California at San Francisco, found in 2010, that a protein called EphB2, which regulates the NMDA function essential for the proper synaptic connectivity, was decreased in the brains of AD patients. The decay of the Ephexin 5 had the collateral of slowing the function of the excitatory synapses, which could explain Autism’s cognitive dysfunction. Recently that fortuitous finding has been used in some new studies.
When the researchers added Amyloid Beta to the brains of healthy mice, there is an increased production of Ephexin 5. The analysis of brain tissues from the autopsy of patients with AD showed increased levels of EphB2. The researchers hypothesized that if they could get rid of EphB2, the process of degeneration of excitatory synapses could be halted or at least slowed.After using genetic engineering techniques to destroy the gene controlling the production of EphN2, they discovered that the animals with severe damage did not lose their excitatory synapses, which spared their memories.
Even though Amyloidosis cannot be ultimately stopped, the preservation of synaptic function might prevent the onset of memory loss in AD patients. If the scientists can determine how the abnormal protein damages the neurons, they can provide therapeutic alternatives to make them “amyloid-resistant.” These preventive measures can be instituted in later stages of the disease, unlike the ones pertaining amyloid that must be started in the 40s or 50s. As there are no drugs that can be safely given for forty years to AD patients, researchers are now focusing on an earlier stage of the disease and the medical therapies that can help patients avoid the ravages of it.
What do you think? Please tell us.
Don’t leave me alone.