Re: New variant Creutzfeldt-Jakob disease: the critique that never was
The above article is a no-response to what Venters argues in his
paper.
And the stats of the CJD unit in Glacow do not seem to confirm what
Ironside et al have said in the 2000 annual report of the Glagow Unit
last year. They promised a new increase of deaths due to vCJD somewhere
around 36 deaths for 2001 ( up to 53 !).
The last stats issued last monday 3 december ( 18 deaths only for the
last 11 months ) do not seem to confirm the trend predicted and it is not
the unfortunate death of Rachel Forbes that will change my opinion on the
subject. Probably in ten years from now, vCJD will not deserve more than a
footnote in papers devoted to CJD.
It should be the right time to try a real etiological treatment of
the condition based on what other hypothesis than "official" one might
suggest : even if mepacrine is able to melt amyloid plaques, the toxicity
of the molecule prevents lengthy use. It should be possible to prevent
possible oxidation effect of modified prion at the synapses ( glutathion ?
, vitamin C , other molecules fighting free-radicals) , and perhaps try
to fight the possible involvement of a metal imbalance in the brain (
chelates or chelating agents ? ).
Rapid Response:
Re: New variant Creutzfeldt-Jakob disease: the critique that never was
The above article is a no-response to what Venters argues in his
paper.
And the stats of the CJD unit in Glacow do not seem to confirm what
Ironside et al have said in the 2000 annual report of the Glagow Unit
last year. They promised a new increase of deaths due to vCJD somewhere
around 36 deaths for 2001 ( up to 53 !).
The last stats issued last monday 3 december ( 18 deaths only for the
last 11 months ) do not seem to confirm the trend predicted and it is not
the unfortunate death of Rachel Forbes that will change my opinion on the
subject. Probably in ten years from now, vCJD will not deserve more than a
footnote in papers devoted to CJD.
It should be the right time to try a real etiological treatment of
the condition based on what other hypothesis than "official" one might
suggest : even if mepacrine is able to melt amyloid plaques, the toxicity
of the molecule prevents lengthy use. It should be possible to prevent
possible oxidation effect of modified prion at the synapses ( glutathion ?
, vitamin C , other molecules fighting free-radicals) , and perhaps try
to fight the possible involvement of a metal imbalance in the brain (
chelates or chelating agents ? ).
Maurice LEGOY
Competing interests: No competing interests