Protein linked to Alzheimer's plays critical role in brain development

Washington, Oct 19 (ANI): The amyloid precursor protein, or APP, associated with the development of Alzheimer's disease, has also been found to play a critical role in brain development, say researchers.

The study led by Georgetown University Medical Center scientists suggests that a balance of APP is critical.

Abeta is one of many proteins found to be associated with the disease. It is released when APP, a larger protein, is cut by several enzymes. This occurs when APP is abnormally processed, possibly due to trauma, cholesterol levels or oxidative stress.

When Abeta is released, it can form plaque, a contributing factor in AD. Thus, Abeta and APP are involved in the early process of AD development.

APP is also known to be present at the synapses between neurons though its molecular action is not understood. Synapse loss is thought to be one of the main contributors to the cognitive decline seen in AD.

Previous studies have shown that the importance of synapses and dendritic spines, the protrusions that allow communication between brain neurons, in learning and memory.

In this new research, scientists found decreased spine density in mice that have been genetically modified to not produce APP.

The scientists then looked at four-week-old mice that over produced APP and found a significant increase in spine density.

After one year, however, these mice have Abeta plaques, as well as a decrease in spine density due to the effect of Abeta, which is known to be neurotoxic.

"Our work suggests that APP balance is critical for normal neuronal development, connection of synapses, and dendritic spine development, all of which have implications for the extensive synapse loss and cognitive decline seen in Alzheimer's disease," said the study's author, Dr Hyang-Sook Hoe, a research scientist in the department of neuroscience.

"One strategy to counteract development of Alzheimer's disease is to maintain balance in APP protein expression in order to prevent production of Abeta," Hoe added.

The study was presented at 39th annual meeting of the Society for Neuroscience. (ANI)