[lurkingforacure]

...here's the link:

http://www.eurekalert.org/pub_releas...-pdm030211.php

[imark3000]

Originally Posted by lurkingforacure

...here's the link:

http://www.eurekalert.org/pub_releas...-pdm030211.php

So this research tells that dopamine cells die partly due to failure in microtubule:
" But why do these microtubule-disrupting drugs only kill dopaminergic neurons and not other types of nerve cells? "Microtubule disassembly impairs dopamine release, so dopamine accumulates in the cell," explains Xia. Excess cytoplasmic dopamine may then be oxidized, producing reactive oxygen species (ROS) that induce cell death. Taxol prevented rotenone from increasing dopamine and ROS levels, and drugs that inhibit either dopamine synthesis or ROS protected neurons from rotenone-induced death."
If this is true, one can only conclude that dopamine boosting treatment (i.e. l-dopa medication) will only speed up cell death through increasing dopamine in the cytoplasm in allready sick cells with faulty microtubule.
Let us hope that new drugs will be found targetting the real causes of the disease instead of 50 years drugs which only give short time relief followed by many years of side effects that may be worse than the natural untreated illness.
That is of course my humble "unscientific" opinion.
cheers
Imad

[RLSmi]

Originally Posted by imark3000

So this research tells that dopamine cells die partly due to failure in microtubule:
" But why do these microtubule-disrupting drugs only kill dopaminergic neurons and not other types of nerve cells? "Microtubule disassembly impairs dopamine release, so dopamine accumulates in the cell," explains Xia. Excess cytoplasmic dopamine may then be oxidized, producing reactive oxygen species (ROS) that induce cell death. Taxol prevented rotenone from increasing dopamine and ROS levels, and drugs that inhibit either dopamine synthesis or ROS protected neurons from rotenone-induced death."
If this is true, one can only conclude that dopamine boosting treatment (i.e. l-dopa medication) will only speed up cell death through increasing dopamine in the cytoplasm in allready sick cells with faulty microtubule.
Let us hope that new drugs will be found targetting the real causes of the disease instead of 50 years drugs which only give short time relief followed by many years of side effects that may be worse than the natural untreated illness.
That is of course my humble "unscientific" opinion.
cheers
Imad

Not so "unscientific", I think!

Robert

[VICTORIALOU]

Interesting article about this particular type of yew (pacific) that taxol is derived from and the original medicinal uses by native americans


http://www.richardpitt.com/index.php...ngs&Itemid=115

[olsen]

Was Gleevec being looked at for stabilizing microtubules in PD models? or is my memory faulty?

[VICTORIALOU]

"The mice were administered imatinib (trade name Gleevec, an FDA-approved cancer drug), a relatively new drug currently approved for treatment of chronic myelogenous leukemia and gastrointestinal tumors. The drug potently reduces the production of beta amyloid in neuroblastoma cells transfected by amyloid precursor protein (APP) and also in cell-free extracts prepared from the transfected cells. Importantly, Gleevec has poor penetration of the blood-brain barrier in both mice and humans.

"This characteristic of the drug is precisely why we chose to use it," Sutcliffe explained. "Because it doesn't penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease."

The mice were injected with Gleevec twice a day for seven days; then plasma and brain tissue were collected, and the amount of beta amyloid in the blood and brain was measured. The findings: the drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer's."

[lurkingforacure]

Originally Posted by VICTORIALOU

Interesting article about this particular type of yew (pacific) that taxol is derived from and the original medicinal uses by native americans


http://www.richardpitt.com/index.php...ngs&Itemid=115

This is really interesting but you gotta read to the bottom of this article to see what the "provers" (as named in the article, I guess a term used for participants in alleopathic trials of a remedy) reported experiencing while taking this yew brew. While it may help with some things, it definitely has a down side.

[VICTORIALOU]

You are so right!!! I didn't scroll down to read the side effects, holy cow and thanks.

[olsen]

Davunetide is derived from a naturally occurring neuroprotective brain protein known as activity dependent neuroprotective protein (ADNP). Allon's laboratory and animal studies have shown that davunetide restores the function of structures in the brain — known as microtubules — which are critical to communication between brain cells and the structure of individual cells.
In 2008, Allon reported Phase IIa clinical trial results showing that davunetide had a statistically significant positive impact on memory function in patients with amnestic mild cognitive impairment (aMCI), a precursor to Alzheimer's disease (AD). The data was presented July 28 and July 30, 2008 to the International Conference on Alzheimer's Disease and Related Disorders (ICAD 2008).

(and there is a nasal spray form of this product)

http://www.marketwire.com/press-rele...PC-1100469.htm

[lurkingforacure]

Originally Posted by olsen

Davunetide is derived from a naturally occurring neuroprotective brain protein known as activity dependent neuroprotective protein (ADNP). Allon's laboratory and animal studies have shown that davunetide restores the function of structures in the brain — known as microtubules — which are critical to communication between brain cells and the structure of individual cells.
In 2008, Allon reported Phase IIa clinical trial results showing that davunetide had a statistically significant positive impact on memory function in patients with amnestic mild cognitive impairment (aMCI), a precursor to Alzheimer's disease (AD). The data was presented July 28 and July 30, 2008 to the International Conference on Alzheimer's Disease and Related Disorders (ICAD 2008).

(and there is a nasal spray form of this product)

http://www.marketwire.com/press-rele...PC-1100469.htm

Thanks for this Olsen, we have such great researchers here! I just read that this drug was granted orphan drug status from the FDA for PSP (a PD+ syndrome, as they call it) so maybe a PWP could get it? We'll see.