How brain amyloid protein turns toxic in Alzheimer's disease
 

So, will they now test to see if this "long-suspected link between Alzheimer's disease and abnormalities in the way amyloid protein is processed in the brain" is also true in the PD brain. I suppose we should assume this to be true even before it is proved. The similarities between PD and Alzheimer's are constant.

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How brain protein turns toxic in Alzheimer's disease

09:00 21 January 2007
From New Scientist Print Edition.
http://www.newscientist.com/article/...s-disease.html

The long-suspected link between Alzheimer's disease and abnormalities in the way amyloid protein is processed in the brain has been confirmed at last.

Usually harmless, the amyloid protein is thought to trigger neurological damage when it is broken down and transformed into toxic fragments of beta-amyloid. Previous studies have shown that people with Alzheimer's have reduced levels of several proteins involved in processing amyloid.

To find out whether low levels of any of these proteins could cause the production of toxic beta-amyloid, Peter St George-Hyslop at the University of Toronto in Canada and colleagues studied the DNA of 6861 people, 46 per cent of whom had Alzheimer's (Nature Genetics, DOI: 10.1038/ng1943).

Those with the disease proved significantly more likely to have variants of the gene SORL1, which usually produces a protein that binds amyloid and transports it to an area of the cell where it can be harmlessly recycled.

To demonstrate that mutations in SORL1 could trigger the disease, the researchers treated cells in the lab to deactivate the gene. This led to a substantial increase in the production of toxic beta-amyloid. "Where SORL1 is absent or defective, it allows the amyloid to float off into other areas where it is degraded," says St George-Hyslop.

The team have identified two regions of SORL1 they believe harbour the disease-causing mutations, but have not yet found the mutations themselves.

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WHAT IS PARKINSON'S DISEASE AND WHAT CAUSES IT?

University of Maryland Medical Center
http://www.umm.edu/patiented/article...t_000051_1.htm

Excerpts from webpage:
"Proteins Involved in Parkinson's Disease Important research now suggests that three molecules are critical in the development of inherited PD: parkin, alpha synuclein (specifically alphaSp22), and ubiquitin, which all interact in the normal brain. AlphaSp22 is produced in the nerve cells involved with the dopamine pathway. Parkin normally causes alpha synuclein to bind with a molecule called ubiquitin, which then triggers apoptosis causing this compound to self-destruct. In many cases of inherited Parkinson's disease, however, parkin is abnormal and fails to bind alpha synuclein to ubiquitin. Apoptosis does not take place and, instead of dying, synuclein accumulates in Lewy bodies , deposits of fibrous tissue found in all patients with PD.

"Another protein that may be critical in the disease process is beta amyloid, which builds up in the brains of Alzheimer's patients and is a major factor in that disease. Beta amyloid also increases the build-up of synuclein and may help explain the connection between Alzheimer's and Parkinson's disease in many patients."