broad reappraisal of the way that drugs are tested in animal
models of neurodegenerative disease. Jim Schnabel reports.
Scott and his colleagues con-
cluded that the previous positive drug trials in
ALS mice were likely to have been so plagued
by non-drug-related variations in mouse
lifespan that this ‘noise’ was really all they had
measured. In the context of small sample sizes
and a bias against negative results, they noted,
a high degree of noise could easily have led to
the appearance of positive results even when
no drug effect had existed.
mouse was not excluded appropriately from
a study. Such an exclusion should have hap-
pened if, for example, an animal died young of
non-ALS causes — Scott came to believe that
mouse colonies in some academic labs were
“filthy” with infections — or failed to express
enough copies of the mutant SOD1 gene.
“People will do
an experiment once with ten animals and get
a result, and if it’s the right result it gets pub-
lished in a high-profile journal,” says Duff
The wrong model?
Mouse models could therefore end up being
not only more difficult and expensive to use
with acceptable rigour, but at the same time
more narrowly predictive of the human con-
dition.
http://www.nature.com/nature/journal/v454/n7205/edsumm/e080807-02.html
One of the newly identified genetic variants, SCARB2, is associated with a known Parkinson's disease pathway involving protein degradation.
The other, SREBF1, is not associated with any known Parkinson's pathway.
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