There is clearly something wrong with pharmaceutical innovation.
...the economics of the drug development, argues Professor Kinch, who in July was appointed associate vice chancellor of Washington University in St. Louis, are not conducive to creating the highest levels of public health.
Some argue that the patent system governing drug innovation is not up to the task, and suggest handing over most drug research and development to the National Institutes of Health, which already spend tens of billions on basic research.
http://www.nytimes.com/2014/07/23/business/a-dearth-of-investment-in-much-needed-drugs.html?mabReward=RI%3A15&action=click&pgtype=Homepage®ion=CColumn&module=Recommendation&src=rechp&WT.nav=RecEngine&_r=0
Friday, July 25, 2014
Thursday, May 1, 2014
Nicotinamide useful for Chronic Fatigue Syndrome?
Futurepundit has an old article that suggests that nicotinamide helps MS. http://www.futurepundit.com/archives/003738.html#reply20140429084955
The original abstract:
Axonal damage is a major morphological alteration in the CNS of patients with multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the underlying mechanism for the axonal damage associated with MS/EAE and its contribution to the clinical symptoms remain unclear. The expression of a fusion protein, named “Wallerian degeneration slow” (Wlds), can protect axons from degeneration, likely through a β-nicotinamide adenine dinucleotide (NAD)-dependent mechanism. In this study, we find that, when induced with EAE, Wlds mice showed a modest attenuation of behavioral deficits and axon loss, suggesting that EAE-associated axon damage may occur by a mechanism similar to Wallerian degeneration. Furthermore, nicotinamide (NAm), an NAD biosynthesis precursor, profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits in EAE models. Finally, we demonstrate that delayed NAm treatment is also beneficial to EAE models, pointing to the therapeutic potential of NAm as a protective agent for EAE and perhaps MS patients.
http://www.jneurosci.org/content/26/38/9794.abstract?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=multiple+sclerosis&searchid=1&FIRSTINDEX=0&volume=26&issue=38&resourcetype=HWCIT
Other articles at the Journal of Neuroscience suggest that this has been replicated - has it?
I wonder if MS is sufficiently similar to Chronic Fatigue Syndrome for this to be meaningful to CFS patients?
The original abstract:
Axonal damage is a major morphological alteration in the CNS of patients with multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the underlying mechanism for the axonal damage associated with MS/EAE and its contribution to the clinical symptoms remain unclear. The expression of a fusion protein, named “Wallerian degeneration slow” (Wlds), can protect axons from degeneration, likely through a β-nicotinamide adenine dinucleotide (NAD)-dependent mechanism. In this study, we find that, when induced with EAE, Wlds mice showed a modest attenuation of behavioral deficits and axon loss, suggesting that EAE-associated axon damage may occur by a mechanism similar to Wallerian degeneration. Furthermore, nicotinamide (NAm), an NAD biosynthesis precursor, profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits in EAE models. Finally, we demonstrate that delayed NAm treatment is also beneficial to EAE models, pointing to the therapeutic potential of NAm as a protective agent for EAE and perhaps MS patients.
http://www.jneurosci.org/content/26/38/9794.abstract?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=multiple+sclerosis&searchid=1&FIRSTINDEX=0&volume=26&issue=38&resourcetype=HWCIT
Other articles at the Journal of Neuroscience suggest that this has been replicated - has it?
I wonder if MS is sufficiently similar to Chronic Fatigue Syndrome for this to be meaningful to CFS patients?
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