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Scientists offer hope to ALS sufferers

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flashl Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Feb-03-08 09:45 PM
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Scientists offer hope to ALS sufferers
SAN DIEGO, Feb. 3 (UPI) -- Scientists in San Diego have found a way to slow the progression of amyotrophic lateral sclerosis in mice, offering hope to those with Lou Gehrig's disease.

Don Cleveland of the University of California's San Diego School of Medicine said the new technique involved specifically targeting neuronal support cells known as astrocytes, Nature Neuroscience reported Sunday.

"Mutant genes that cause ALS are expressed widely, not just in the motor neurons," the professor of medicine said. "Targeting the partner cells like astrocytes, which live in a synergistic environment with the neuron cells, helps stop the 'cascade of damage.' Therapeutically, this is the big news."

By removing the mutant gene from those atrocytes, Cleveland and his fellow researchers found mice with ALS lived twice as long as those who kept the offending gene.

UPI
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midnight Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Feb-03-08 09:55 PM
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1. For those who are surrering with this terrible disease this
sounds like a beautiful discovery. I would love to hear from those here with a science understanding of what this discovery actually means.
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aquart Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Feb-03-08 10:31 PM
Response to Reply #1
2. So would I.
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Steven_S Donating Member (810 posts) Send PM | Profile | Ignore Sun Feb-03-08 11:43 PM
Response to Reply #1
3. They didn't give very much information
I'll keep an eye out for more, thanks for the link. There's also exciting developments coming from a study in Italy where using a combination of Rilutek and Lithium Carbonate kept almost all of the participants from progressing further in their disease.


Nov 23, 2007

Italy. Lithium effective against ALS

Lithium "to slow down, with a certainty in excess of 95%, the progression of ALS". These exceptional results came out from an Italian study on 48 ALS patients, 32 treated with standard therapy of riluzol, 16 treated with riluzol and lithium. These results have already been submitted to a well-known international journal that is now verifying the data and may publish the report shortly. "15 months after the start of the study, 30% of the patients treated only with riluzol died. In the second group there were no deaths, even though half of the patients in the group had the most aggressive form of ALS, that is bulbar". This is what one of the Italian researchers, experimenting with the use of lithium against ALS, Francesco Fornai, associate professor of the department of Human Morphology and applied biology at the University of Pisa, stated. Furthermore, utilizing parameters from the neurological scale to measure progression, there was no significant deterioration of the ALSFRS-R, while the decline was evident within 3 months in the other group. At the end of the study the decline was measured at 50%. A preview of this study was given on Nov 8, 2007 during the XXXIV LIMPE Congress, the Italian league in the fight against Parkinson's disease.
The neurodegenerative pathology and ALS, explain the researchers, have many common elements. Funds permitting, lithium will also be studied against Parkinson's disease. In the meantime, the Italian study may obscure patient's expectation of the other study due in January 2008, that is the US study on the Igf-1.
The attention on therapies against ALS has intensified in Italy since the Ministry of Health decided against the treatment of patients with the drug Igf-1 or the combination Igf-1/Igf-Bp3.
Fornai started to study medications not provided by the Healthcare system in Italy, which patients have had to go through the Courts to obtain. Fornai started to study the effect of lithium 2 years ago on mice genetically modified to develop ALS, starting with the capacity of this substance to intervene on certain cellular degenerative processes. "As I proceeded with the research I noticed how lithium would slow down other cellular damaging mechanisms."
The Italian researcher explains how, with appropriate distinctions, ALS and Parkinson are similar in the effect they have on cells. " In the first a slight compromise of the damaged neurons in Parkinson, in the latter we noticed spinal damage as in ALS". Lithium, known as a treatment for bipolar conditions, "accelerates mechanism to remove proteins and altered mitochondrion. It also increases the speed that cells dispose of signs of the decease, practically freeing themselves.
Lithium always promotes the birth of new mitochondrion. Therefore, it does not block the gene that triggers the decease but it accelerates at that point the replacement to stop the progression, a process that the third characteristic of lithium contributes to, i.e. neurogenesi. In some stem cell studies, it was observed how this substance increases the survival in the bone marrow."
Since the first tests were concluded, one hundred more patients are now under treatment, under a new protocol established with the Italian Drugs agency (AIFA). "If the positive results are confirmed by this new study, the sampling will be even larger. Likely, colleagues in the rest of the world will do the same".
The Italian scientist will continue his research in this area but adds: "we have to try other molecules such as Rapamycin (sirolimus) that in contrast to lithium is more expansive" Although the road is clearer, the hunt is not over. It is a project that the University of Pisa is undertaking with IRCCS Neuromed, the west Piedmont University, the IRCCS Santa Lucia and the teaching polyclinic Sant'Andrea in Rome.

The link to the Italian publication is as follows:
http://staminali.aduc.it/php_newsshow_0_6473.html

This article was published in a publication called
Stem Cells
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lizerdbits Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Feb-04-08 01:29 PM
Response to Reply #1
4. They don't give many details
And I'm not sure if that would help me since I'm not knowledgeable about neurology. :) It just says they changed a mutation in the astrocytes which are 'support cells.' They don't even say anything about what the gene does. Maybe astrocytes interact with motor neurons via extracellular signaling somehow and if those connections aren't functioning properly the motor neurons will degenerate due to not getting proper signals.

I suppose for treatment it would mean suppressing a mutant protein since we've got the genes we've got and can't fix that. Maybe intake of some neurotransmitter or other chemical that's not produced in sufficient quantity? :shrug:
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