[lurkingforacure]

Just saw this and it's one big claim, this drug "stops Parkinson's 100 percent of the time"...here's the link:

http://wjz.com/local/parkinsons.dise...2.1877151.html

Anyone know anything about this?

[reverett123]

1. Nat Med. 2010 Aug 22. [Epub ahead of print]

Inhibitors of leucine-rich repeat kinase-2 protect against models of Parkinson's
disease.

Lee BD, Shin JH, Vankampen J, Petrucelli L, West AB, Ko HS, Lee YI, Maguire-Zeiss
KA, Bowers WJ, Federoff HJ, Dawson VL, Dawson TM.

[1] Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering,
Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2]
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore,
Maryland, USA.

Leucine-rich repeat kinase-2 (LRRK2) mutations are a common cause of Parkinson's
disease. Here we identify inhibitors of LRRK2 kinase that are protective in in
vitro and in vivo models of LRRK2-induced neurodegeneration. These results
establish that LRRK2-induced degeneration of neurons in vivo is kinase dependent
and that LRRK2 kinase inhibition provides a potential new neuroprotective
paradigm for the treatment of Parkinson's disease.


PMID: 20729864 [PubMed - as supplied by publisher]

[bluedahlia]

Originally Posted by lurkingforacure

Just saw this and it's one big claim, this drug "stops Parkinson's 100 percent of the time"...here's the link:

http://wjz.com/local/parkinsons.dise...2.1877151.html

Anyone know anything about this?

Do you think, if i get myself some "mickey mouse" ears and a long tail, that maybe I won't have to wait the "elusive" five years?

[lurkingforacure]

Originally Posted by reverett123

1. Nat Med. 2010 Aug 22. [Epub ahead of print]

Inhibitors of leucine-rich repeat kinase-2 protect against models of Parkinson's
disease.

Lee BD, Shin JH, Vankampen J, Petrucelli L, West AB, Ko HS, Lee YI, Maguire-Zeiss
KA, Bowers WJ, Federoff HJ, Dawson VL, Dawson TM.

[1] Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering,
Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2]
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore,
Maryland, USA.

Leucine-rich repeat kinase-2 (LRRK2) mutations are a common cause of Parkinson's
disease. Here we identify inhibitors of LRRK2 kinase that are protective in in
vitro and in vivo models of LRRK2-induced neurodegeneration. These results
establish that LRRK2-induced degeneration of neurons in vivo is kinase dependent
and that LRRK2 kinase inhibition provides a potential new neuroprotective
paradigm for the treatment of Parkinson's disease.


PMID: 20729864 [PubMed - as supplied by publisher]

Does this mean it works only if you have the LRKK2 PD? We were tested and dont' have that gene...I've been told a lot of PWP don't. What about the non Larkers?

[paula_w]

if we are to contribute, we must not speak different languages. Let's start issung tickets for nothing speak, meaning it says nothing, because the speaker intends it not to +be deceptive, and hopes many will think they are satisfied with the statement.

somewhere maybe it's Johns Hopkins , don't remember which article but they referred to it as the Parkinson Paradigm. i met them [ slow down .......breathe in, breathe out. stretch a leg, be proactive, physicallly too. they don'tt know who' they' are you are five thought minimum ahead of your writing. furthermore, haha - like i'm in shape. if i could easily deep breathe and stretch out a leg without crashing to the floor it would be a picture i could easily let you think is true for awhile, anyway , because we do worry about meeting new pwp and knowing fulll well how we can look under our poorer functioning periods it's best not to bs.

truth is.....'THEY' are the mayo clinic in Jacksonville and I think i met two of the reserachers there at an AAN . One was named Owen Ross and the other a Danish name i think. i orignally misread the article and thought it might be them until i again read johns hopkins. iT's a logical rabbit to chase without any more need to explain. lol

anyway i think theirs could be similar and i can't think of something that would be described with more confidence than alpha synuclein. the wpc is stirring up activity like a busy beehive that comes before the harvest. I have no idea if the activiity around a beehive comes before the harvest, or even if there is a harvest. We are stilll just as busy no matter whether there is a harvest or not. ha!

important tho.....
A sitcom writer is talking with us about writing for the book and he also has a song you can download from amazon or itunes.The PD Song. Many of you may know him from plm....if i had to choose another profession it would be comedy writer , which doesn't mean i'm any good at it, but i sure do like playing with it. we should make our own language and see to it that it is included in the paradigm. that's what will change the paradigm the most.....we will be in it. Does anyone want to strart out with it? we have to do it quickly and you will have people on it immediately so it can be considered for the book.

we need a new glossary. they already came up with a good description of this dysfunction [pd paradigm]and what it will take to make this real for everyone not just people trying to make a liviing.

If someone tries to hide it with political correctness like alpha synuclein challenged i will scream.


ok i'm getting too many ideas have to stop - a few suggestions below but we can't take this on until it's organized = i think it's a killer idea.

we have to change our concept of measuring end points. they are mixing apples with oranges. we need to replace the names and real job functions on the name tag of the person working with you .

so what is the parkinson paradigm. are we just going to let them define it, write papers on it, then preclinical research, look at what the monkey paradigm is and jump it over to human, you Darwinians just won't quit making that jump...lol.... stop it!!

that was a joke so just leave it be.

i think you get my drift

Google needs to check in once in awhile . Lots of people need to begin standing up for what would work and we should be able to define some of it ourselves

[zimmer127]

the mouse study
It has probably the most immediate relevance for people with LRRK2 but they also hope it will help others as well. Nobody seems sure exactly what the function for LRRK2 is anyway. (not that most of us would understand it if they did!) My husband does have the LRRK2 mutation so we are really hopeful.

[Jaye]

Regardless of my views on bedside manner of a few, Dr. Ted Dawson is a very nice man who speaks regularly to local support groups and answers patient questions in English for as long as it takes. He is also stunningly brilliant. With his wife, neuroscientist Valina Dawson, PhD, he guides some of the most amazing neurotrophic research around. I would not take their findings lightly.

And yes, the mice are dancing in the streets again.

Jaye
In my car 171 miles from Portland, OR

[zimmer127]

I recently attended a lecture about genetics and mental illness. Don't know if I can explain how this lecture relates to genetics and PD but I will try. They have discovered around 100 genetic variations already that make a person more vulnerable to some mental illnesses - schizophrenia, autism spectrum disorder and bipolar disorder. Depending on the person, some of these mutations can cause different manifestations in different people. So a family may have one of these known mutations but some of the family members are normal, some may have autisms, some schizophrenia, etc. The reason is that all 3 illnesses can be caused by disruptions in several different processes, and each mutation will affect one of the processes. The mutations overlap in what illnesses they can help cause. But of the 100 known mutations, many effect the same systems, so some may effect GABA, some glutamate, etc. So in Parkinson's disease, they know of at least 8 genes that can affect vulnerability to PD. They are not sure yet how each one does that, but by studying one like LRRK2, they may get insight into how some of the other ones disrupt things and increase the chances for PD. That's probably as clear as mud. It made sense when the expert was explaining it and helped me understand why the symptoms of autism spectrum disorders, schizophrenia and bipolar disorder often overlap, and why having a person with one of these in a family can increase the chances of someone else having one of the other related disorders.

[Sasha]

Can someone please explain if they actually have bred mice with "leucine-rich repeat kinase-2 (LRRK2) mutations"? Or are we are looking at some proxy?

What I mean is that it seems to me that Parkinsons research is mostly done on animals that have been given a stand-in for the disease. This is achieved by destroying the mices' movement abilities with a toxin. Thus many research findings don't necessarily apply to us unless we picked up our movement disorders at an Ecstacy party (or similar drug-related event). I'm not sure that any animals get Parkinsons in the sense we do. (PLEASE correct me if I'm wrong in this conclusion)

I hope this research is really based on something that applies to people as well as mice. Like the same genetic mutation, similarlily acquired or something similar.
Sasha

[zimmer127]

The mouse is genetically engineered to have the same mutation that some PWP have. Here is part of an article that explains that:
"While the mice are not at the stage where they experience the typical symptoms of Parkinson's, like tremors or reduced movement, we are able to study the potential root cause of the disease in these mice," said Dr. Yue. "Importantly, as we have developed assays that allow us to measure the enzymatic activity of LRRK2 in the brain, the mouse models provide valuable tools in the preclinical development of drug compounds that target aberrant LRRK2 activity. This research may translate to non-familial Parkinson's disease as well."
In the study, Dr. Yue developed two mouse models with the normal or mutant LRRK2 using an advanced form of genetic engineering called bacterial artificial chromosome genetics (BAC). BAC gives scientists more control over where and when a foreign gene is expressed in the target animal. Dr. Yue and his team genetically engineered a fragment of genomic DNA containing a human Parkinson's disease mutation of LRRK2 and injected it into the mice.
How LRRK2 functions is unknown, but Dr. Yue and his team showed that the mutant LRRK2 produces too much so-called kinase activity in the brain. They are now pursuing the question whether the increased kinase activity accounts for the reduced dopamine levels, subsequently leading to neurodegeneration.
"Not having a mouse model has been a significant barrier to bringing the LRRK2 breakthrough from bench to bedside," said Dr. Yue. "The new model likely replicates the earliest stage of Parkinson's disease, giving us the opportunity to understand the biochemical and molecular events that cause the disease."