[olsen]

Alzheimer’s Research Finds Clue For Parkinson-Like Diseases


May 16, 2011



...Scientists have suspected exposure to viruses and other environmental factors may trigger symptoms associated with Parkinson-like diseases, but why such exposure would actually destroy certain areas of the brain has been mysterious.

New research suggests a pathway located at the base of the brain that is essential for the execution of smooth, coordinated movements may be selectively damaged by the friendly fire of the body’s immune response, according to University of Florida and Mayo Clinic Florida scientists writing today in Nature Neuroscience.

“In the movie ‘Awakenings,’ it was suggested that people who previously suffered from an infection like the flu developed Parkinsonism, probably because of degeneration in a brain pathway known as the nigrostriatal tract. But the links between infection and subsequent Parkinsonism have always been controversial,” ...“Our data show that when a certain master protein that stimulates the immune system and antiviral response is expressed at high levels, it causes neuronal loss primarily in the nigrostriatal tract, thereby creating vulnerability to Parkinson’s and similar movement disorders.”

The master protein is known as interferon gamma, which regulates the activity of genes important to the human immune system, and coordinates the body’s immune defenses against many types of infection. In their study, high levels of interferon gamma resulted in widespread brain inflammation in model systems. Yet, most of the brain did not degenerate — only the nigrostriatal tract...


The symptoms of impaired movement in the disorders that are collectively called Parkinsonism are the result of degeneration and death of nerve connections that produce dopamine. But nothing yet satisfactorily explains what causes neural damage.

“Epidemiological studies and anecdotal observations aside, previous studies have never shown a direct link between chronic inflammation and Parkinson’s pathology,” said Paramita Chakrabarty, a postdoctoral fellow in Golde’s laboratory. “We have shown that a small protein produced by our bodies in response to infections, called interferon-gamma, can directly lead to the loss of cells in the brain regions that are selectively targeted in Parkinson’s patients. More importantly, these changes were age-progressive, thus giving us an opportunity to initiate treatment in an early therapeutic window when the disease pathology is minimal.”...



“In general, we have had few clues as to why certain people are at risk for Parkinsonism, and this gives us an interesting possibility to explore,” said Golde, who is a professor in the department of neuroscience at UF’s McKnight Brain Institute. “Namely, that infection or other factors that cause certain type of brain inflammation and high levels of interferon gamma can predispose one to Parkinsonism or even cause it outright.”

http://www.ahaf.org/alzheimers/newsu...h-finds-1.html

[paula_w]

more on this subject. Interferon gamma is a cytokine.

http://en.wikipedia.org/wiki/Interferon-gamma

[reverett123]

Go to the most incredibly informative and amazing site on the Web explaining it - Mine!
A Matter of Balance

[olsen]

and for those with DNA results from 23andme, the interferon gamma (IFN-y)
protein is encoded by the IFNG gene. I have no idea if any SNPs in this gene are important/pathogenic. do not have time at present to try to determine if any problems identified

[GerryW]

Andrographis is apparently useful for microglial inflammation. I have recently added it to my armamentarium. http://jpet.aspetjournals.org/content/308/3/975.full

"Therefore, inhibition of only one or two factors by selective inhibitors may not be sufficient to halt the degenerative process. Thus, searching for drugs that have widespectrum anti-inflammatory effects and that remain effective after the initiation of the inflammatory process may be most promising. In this study, we reported that ANDRO exhibited a neuroprotective effect in both pretreatment and post-treatment schemes and was effective in attenuating LPS-induced production of several proinflammatory factors, including superoxide, TNF-α, NO, and PGE2."

[olsen]

http://www.pdonlineresearch.org/node/17112