Several years ago a major discovery was made by an ALS researcher at Northwestern University. It was discovered that the disease ALS was caused by a protein that was no longer controlled by the bodies regulation. This protein, whose name I cannot recall, is no longer marked for destruction and begins to pile up inside the nervous system, causing motor neuron damage. Has FAH joined in on any of this protein work? Has any FAH work be sited by these researchers working on a cure for ALS?
It seems that this massive breakthrough should be able to move forward progress on stopping this terrible, life wasting disease.
FAH and ALS
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Re: FAH and ALS
How to provide enough information to get helpful support
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Re: FAH and ALS
Hmm....nothing on ALS in there.
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Re: FAH and ALS
It could be possible that studies done here on F@H could be used in ALS since some project results can be used in a wide range of diseases. However, I was able to find a reference to ALS:
If there wasn't any ALS specific projects, then there might be the "generic" ones which can be used in different diseases.
Source -> http://folding.stanford.edu/home/faq/#ntoc55This is a central question of Folding@home and directly relates to our study of protein folding and misfolding, as it is related to misfolding-related diseases such as Alzheimer’s, ALS, and Huntington’s disease.
If there wasn't any ALS specific projects, then there might be the "generic" ones which can be used in different diseases.
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Re: FAH and ALS
The question which neither of us can answer is whether the ALS protein regulation process has anything to do with how a protein folds. FAH has done, and will continue to do, significant research in how the folding process relates to disease but that tends to divide diseases into two categories and it's not clear which category ALS falls into.
Posting FAH's log:
How to provide enough info to get helpful support.
How to provide enough info to get helpful support.
Re: FAH and ALS
OK. I am sure someone will answer these questions in the future!bruce wrote:The question which neither of us can answer is whether the ALS protein regulation process has anything to do with how a protein folds. FAH has done, and will continue to do, significant research in how the folding process relates to disease but that tends to divide diseases into two categories and it's not clear which category ALS falls into.
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Re: FAH and ALS
Hi! RMouse!
Feinberg scientists found the cause of ALS by discovering a protein, ubiquilin2, whose critical job is to recycle damaged or misfolded proteins in motor and cortical neurons and shuttle them off to be reprocessed.
In people with ALS, Feinberg researchers found ubiquilin2 isn't doing its job. As a result, the damaged proteins and ubiquilin2 loiter and accumulate in the motor neurons in the spinal cord and cortical and hippocampal neurons in the brain. The protein accumulations resemble twisted skeins of yarn – characteristic of ALS – and cause the degeneration of the neurons.
Researchers found ubiquilin2 in these skein-like accumulations in the spinal cords of ALS cases and in the brains of ALS/dementia cases.
The scientists also discovered mutations in ubiquilin2 in patients with familial ALS and familial ALS/dementia. But the skein-like accumulations were present in people's brains and spinal cords in all forms of ALS and ALS/dementia, whether or not they had the gene mutation.
Source: http://www.feinberg.northwestern.edu/ne ... rough.html
To Admins, please: Do research in the F@H of this trend?
Feinberg scientists found the cause of ALS by discovering a protein, ubiquilin2, whose critical job is to recycle damaged or misfolded proteins in motor and cortical neurons and shuttle them off to be reprocessed.
In people with ALS, Feinberg researchers found ubiquilin2 isn't doing its job. As a result, the damaged proteins and ubiquilin2 loiter and accumulate in the motor neurons in the spinal cord and cortical and hippocampal neurons in the brain. The protein accumulations resemble twisted skeins of yarn – characteristic of ALS – and cause the degeneration of the neurons.
Researchers found ubiquilin2 in these skein-like accumulations in the spinal cords of ALS cases and in the brains of ALS/dementia cases.
The scientists also discovered mutations in ubiquilin2 in patients with familial ALS and familial ALS/dementia. But the skein-like accumulations were present in people's brains and spinal cords in all forms of ALS and ALS/dementia, whether or not they had the gene mutation.
Source: http://www.feinberg.northwestern.edu/ne ... rough.html
To Admins, please: Do research in the F@H of this trend?
In memory of my friend Galina.