Parkinson's disease stopped in animal model !!
 

http://medicalxpress.com/news/2012-0...se-animal.html

...UCLA professor of neurology Jeff Bronstein and UCLA associate professor of neurology Gal Bitan, along with their colleagues, report the development of a novel compound known as a "molecular tweezer," which in a living animal model blocked α-synuclein aggregates from forming, stopped the aggregates' toxicity and, further, reversed aggregates in the brain that had already formed. And the tweezers accomplished this without interfering with normal brain function.

The research appears in the current online edition of the journal Neurotherapeutics...

:D:D

Thank you Sim00
 

Thank you Sim00 for your great posts and follow up of research that a l can understand!
This one certainly opens a window of hope but all I can say presently is "Eureka for for the zebrafish who are assured of a cure :)", as for rats and humans, they have to wait a while !
Imad

We shall overcome.
 

Many thanks Imad,
however, it's always beautiful to read this kind of news. I feel better, today. Placebo effect?
:wink:

Baikal Skullcap
 

While we are, as usual, waiting, there is always Baikal Skullcap.

http://onlinelibrary.wiley.com/doi/1...201000604/full

Researchers report potential new treatment to stop Alzheimer's disease (and PD)
 

http://newsroom.ucla.edu/portal/ucla...op-239289.aspx

Last March, researchers at UCLA reported the development of a molecular compound called CLR01 that prevented toxic proteins associated with Parkinson's disease from binding together and killing the brain's neurons.
Building on those findings, they have now turned their attention to Alzheimer's disease, which is thought to be caused by a similar toxic aggregation or clumping, but with different proteins, especially amyloid-beta and tau.
And what they've found is encouraging. Using the same compound, which they've dubbed a "molecular tweezer," in a living mouse model of Alzheimer's, the researchers demonstrated for the first time that the compound safely crossed the blood–brain barrier, cleared the existing amyloid-beta and tau aggregates, and also proved to be protective to the neurons' synapses — another target of the disease — which allow cells to communicate with one another........