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Study breaks blood-brain barriers to understanding Alzheimer's
Date:12/13/2013

ases in beta-amyloid lead to nerve cell damage in the brain. This is supported by genetic studies that link familial forms of the disease to mutations in amyloid precursor protein (APP), the larger protein from which plaque-forming beta-amyloid molecules are derived. Nonetheless, previous studies on mice showed that increased beta-amyloid levels reproduce some of the problems associated with Alzheimer's. The animals have memory problems, beta-amyloid plaques in the brain and vascular damage but none of the neurofibrillary tangles and neuron loss that are hallmarks of the disease.

In this study, the researchers show that pericytes may be a key to whether increased beta-amyloid leads to tangles and neuron loss.

Pericytes are cells that surround the outside of blood vessels. Many are found in a brain plumbing system called the blood-brain barrier. It is a network that exquisitely controls the movement of cells and molecules between the blood and the interstitial fluid that surrounds the brain's nerve cells. Pericytes work with other blood-brain barrier cells to transport nutrients and waste molecules between the blood and the interstitial brain fluid.

To study how pericytes influence Alzheimer's disease, Dr. Zlokovic and his colleagues crossbred mice genetically engineered to have a form of APP linked to familial Alzheimer's with ones that have reduced levels of platelet-derived growth factor beta receptor (PDGFR-beta), a protein known to control pericyte growth and survival. Previous studies showed that PDGFR-beta mutant mice have fewer pericytes than normal, decreased brain blood flow, and damage to the blood-brain barrier.

"Pericytes act like the gatekeepers of the blood-brain barrier," said Dr. Zlokovic.

Both the APP and PDGFR-beta mutant mice had problems with learning and memory. Crossbreeding the mice slightly enhanced these problems. The mice also had increased beta-amyloid plaque deposition near brain cel
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Contact: Christopher G Thomas
nindspressteam@ninds.nih.gov
301-496-5751
NIH/National Institute of Neurological Disorders and Stroke
Source:Eurekalert  

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