Scientists shed new light on memory loss

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Washington, March 13 : Researchers at the Buck Institute say that the normal process of forgetting day to day happenings is much heavily present in Alzheimer's disease (AD) sufferers, and it is perhaps key to the profound memory loss associated with the incurable neurodegenerative disorder.

The researchers say that their suggestion is based on a study that builds on previous animal research, wherein they could completely prevent Alzheimer's disease in mice genetically engineered with a human Alzheimer's gene, Mouzheimer's, by blocking a single site of cleavage of a molecule called APP for amyloid precursor protein.

Normally, this site on APP is attacked by molecular scissors called caspases, but blocking that process prevented the disease.

In their latest study, the researchers studied human brain tissue, and found that patients suffering from AD showed more of the cleavage process than people of the same age who did not have the disease.

However, upon extending their study to much younger people without Alzheimer's disease, they were astonished to find that younger subjects displayed as much as ten times the amount of the same cleavage event as the AD patients.

The researchers say that their study implicates a biochemical "switch" associated with that cleavage of APP, causing AD brains to become stuck in the process of breaking memories.

The study also points to AD as a syndrome affecting the plasticity or malleability of the brain, they add.

Published in the Journal of Alzheimer's Disease, the new study provides new insight into a molecular event resulting in decreased brain plasticity, a central feature of AD.

"Young brains operate like Ferraris - shifting between forward and reverse, making and breaking memories with a facility that surpasses that of older brains, which are less plastic. We believe that in aging brains, AD occurs when the 'molecular shifting switch' gets stuck in the reverse position, throwing the balance of making and breaking memories seriously off kilter," said Dr. Dale Bredesen, Buck Institute faculty member and leader of the research group.

In their previous work, the researchers prevented the cleavage in mice genetically engineered to develop the amyloid plaques and deposits associated with AD.

The mice had normal memories and showed no signs of brain shrinkage or nerve cell damage, despite the fact that their brains were loaded with the sticky A-beta plaques that are otherwise associated with Alzheimer's disease.

"A-beta is produced throughout the brain throughout life; we believe that it is a normal regulator of the synapses, the connections between neurons," said lead author of that study Dr. Veronica Galvan, who added that just like cancer, AD is a disease in which imbalanced cell signalling plays an important role.

"The fact that many people develop A-beta plaques yet show no symptoms of AD tells us that the downstream signalling of A-beta-not just A-beta itself-is critical, and these pathways can be targeted therapeutically. Simply put, we can restore the balance," said Bredesen.

Continuing research at the institute focuses on nerve signalling and efforts to "disconnect" the molecular mechanism that throws memory-making in the reverse direction, as well as understanding mechanisms that support brain cell connections that are crucial to the process of memory making.

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