[lurkingforacure]

If I read this right, researchers have developed a mouse model of PD using the LRRK2 gene, which allows them to study, as the mouse ages, what happens in the brain...there are several siginificant findings I noted in the article, but read for yourself:

http://www.healthnewsdigest.com/news...eatments.shtml

[imark3000]

is the following:
" Dr. Robert Burke, the Alfred and Minnie Bressler Professor of Neurology (in Pathology) at Columbia University Medical Center, and his colleague Ms. Tinmarla Francis Oo, senior staff associate at Columbia University Medical Center, further discovered that the dopamine deficit came from disintegration, not of the dopamine neurons themselves, but of their axons, the long, filament-like structures responsible for transmitting dopamine to distant targets in the brain. Their insights, says Dr. Li, are helping us understand the disease at a deeper level -- something that will lead us to better treatments and possibly even a cure for Parkinson's disease.

"

[girija]

Ceregene CEO in his interview with mJFF said pretty much the same. They found their gene product at the site of injection but not getting transported thru axons. Now it looks like there is a defect in the transport of dopamine and so probably there is accumulation of dopamine in neurons. Another recent paper says excess dopamine is toxic to neurons........The more we know about PD, the harder it gets to swallow all those pills that increase dopamine/its effects.

girija

Originally Posted by imark3000

is the following:
" Dr. Robert Burke, the Alfred and Minnie Bressler Professor of Neurology (in Pathology) at Columbia University Medical Center, and his colleague Ms. Tinmarla Francis Oo, senior staff associate at Columbia University Medical Center, further discovered that the dopamine deficit came from disintegration, not of the dopamine neurons themselves, but of their axons, the long, filament-like structures responsible for transmitting dopamine to distant targets in the brain. Their insights, says Dr. Li, are helping us understand the disease at a deeper level -- something that will lead us to better treatments and possibly even a cure for Parkinson's disease.

"

[Debi Brooks]

An important side note..we are among those who provided funding for this mouse model and have been pressing very hard to get this model more widely available (in a time and cost-effective manner) so that a researchers in other labs (academic and industry) can benefit from this model and advance our LRRK2 knowledge more efficiently.

Debi

[lurkingforacure]

Originally Posted by Debi Brooks

An important side note..we are among those who provided funding for this mouse model and have been pressing very hard to get this model more widely available (in a time and cost-effective manner) so that a researchers in other labs (academic and industry) can benefit from this model and advance our LRRK2 knowledge more efficiently.

Debi

Debi, I saw that MJFF was one of the funders of this and am very grateful. From what I have read, the current disease model has left researchers with a less than ideal situation with which to work, and I and others are hoping this new mouse model will really propel the understanding of PD forward. Thanks so much for helping with this huge improvement in the way research will hopefully be conducted.

[girija]

Lurkingforacure,

This is taken from PDonline research: an interview with the senior author of this paper. Very good questions and honest answers. I highly recommend it.

Quoted as is.
"KC: How does your model mimic human PD?

CL: It recapitulates the progressive reduction of movement at the behavioral level, dopamine release deficit at the circuitry level, and DA neuron atrophy and neurite degeneration at the histopathological level. Hyperphosphorylation of tau is another feature ....................

KC: What features of human PD are missing from your model?

CL: Overt and robust DA neuronal death. Although there is statistically significant DA cell body atrophy and a striking DA neurite degeneration, cell death is not yet significant at the age of 10 months. It will be important to examine for this at a later time point.

Another missing feature is robust Lewy body pathology. This might be due to the fact that there is no human alpha-synuclein in these mice. Mice have endogenous alpha-synuclein which is not prone to aggregation. We are currently examining whether ................"