21 March 2006

Alzheimer's, Beta Amyloid, and the Choroid Plexus



The Choroid Plexus is a complex of capillary rich cells located in the ventricles of the brain, which produce cerebral spinal fluid, and perform other functions protective of the brain. This Purdue University newsrelease discusses a recent research finding that links the choroid plexus to the function of filtering beta amyloid from brain fluid and CSF.

The researchers found that the choroid plexus acts as a sort of "fishnet" that captures the protein, called beta-amyloid, and prevents it from building up in the cerebrospinal fluid, which surrounds and bathes the brain and spinal cord. Moreover, tissue in the organ is able to soak up large amounts of the protein and may contain enzymes capable of digesting beta-amyloid, said Wei Zheng (pronounced Way Zsheng), an associate professor in the School of Health Sciences at Purdue University.

The findings represent the first time that researchers have identified the potential existence of a natural mechanism in the brain for removing beta-amyloid.

"This newly uncovered pathway may help explain how normal brains balance this protein and how an imbalance caused by aging, genetic or environmental factors may lead to or worsen Alzheimer's disease," Zheng said.

Researchers had already known that the cerebrospinal fluid in the brains of Alzheimer's patients contains abnormally high quantities of beta-amyloid fragments. Beta-amyloid deposits accumulate over a period of years, resulting in abnormal clumps, or plaque, typical of Alzheimer's disease. Scientists do not yet know whether the disease is caused by the plaque formations or beta-amyloids themselves.

The discovery suggests that a malfunctioning choroid plexus could allow too much of the protein to build up in the brain.


Read the rest here. For further study, this helpful article further details choroid plexus malfunction and breakdown in ageing and Alzheimer's disease.

In this article, I discussed some recent research evidence linking beta amyloid to memory loss and neuron death in Alzheimer's. Today's Purdue report adds more information to the overall picture.

It is important to understand the complete dynamic story of beta amyloid, from its formation to its action on neurons, to its breakdown and removal, if we are to understand all of our potential therapeutic choices in reducing the detrimental effect of this protein.

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2 Comments:

Blogger al fin said...

You are right. Thanks for the links.
It is nice when the pieces fall together and make sense.

Thursday, 23 March, 2006  
Blogger Unknown said...

One must look primarily now on the role of dysfunctional choroidal cell mitochondria. Before any amyloid deposits can be seen in transgenetic animal models of "AD", it is the mitochondria that shows signs of damage with diminished ETC and increased production of free radicals.
I suspect the primary process is mitochondrial DNA errors (please recall such MiDNA have no protective histones as does Nuclear DNA. Joel Ross

Saturday, 05 February, 2011  

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