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Published on: July 8, 2012
by Kristi Davis for Daily Rx:
Memory loss is thought to result from brain cell damage, but how the damage happens is not totally clear.
One suspect for brain cell damage is beta amyloid, which is a protein that builds up in AD and causes plaques in the brain.
New research showed that beta amyloid interfered with brain cell function and spread from cell to cell. This information helps scientists to understand the role beta amyloid plays in AD, which may someday lead to better treatments.
A series of studies led by Sangeeta Nath, PhD, at Linköping University in Sweden, sought to understand the role of beta amyloid in brain cells.
Beta amyloid is naturally occurring in the brain and it serves many functions. However, in AD it builds-up to form plaques, and these plaques can interfere with brain functions.
The researchers looked at brain cells of both rats and humans in a laboratory. They injected beta amyloid into a single neuron then took pictures of the neurons using powerful microscopes.
In the first phase of their studies, they found that, in rat brain cells, the injection of beta amyloid caused the cells to have a break-down in their structure. These changes in structure caused the cell to lose function.
The second phase of the studies used human cells. They found that, when they injected beta amyloid into one neuron, the beta amyloid was passed along to other neurons – specifically the ones that it was touching.
The authors conclude that beta amyloid can be harmful to individual cells, even when there are no plaques, because beta amyloid interferes with the cell structure.
Additionally, the authors showed that beta amyloid can transfer from one cell to another, and this might help to explain how AD progresses through the brain.
This information helps scientists to better understand the role that betaamyloid plays in AD. However, these cells were outside of the brain in a laboratory, so more research is needed to understand how beta amyloid might transfer in intact brain networks.
This research report was published in the June 27 issue of the Journal of Neuroscience. The studies were funded by the Linköping University Neurobiology Centre, the Swedish Alzheimer’s Foundation, Swedish Research Council, among others.
The authors of this study report no financial conflicts of interest.
Picture Source: Businessweek
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