Rodent research.
1. ALS is a mixture of similar related illness but not having the same biological pathways.
2. Results from the animal studies should only be tested on those ALS patients with the same type of ALS. Failure to do so discards the evidence for selective potential ALS therapeutics for specific sub ALS types.
3. The SOD1 mutant rodents used only represents a very small percentage of the human ALS types but consumes most of the research. Biological pathways are different and specific to different types of ALS.
4. The SOD1 mutant rodents types does not match human type SOD1 ALS exactly.
5. Rodents are bred to be genetically the same, eat the same type of food and live in the same kind of environmental conditions. This does not apply to humans. Rodents also have higher metabolic rate than humans.
5. Rodents have different genetic makeup, in certain critical, pathways so do not correlate exactly with humans. Meaning certain test substances will do different things in rodents and humans.
6. Biological pathways change over time in ALS. What might be therapeutic at the start of symptom onset may be detrimental later on or the other way around. ALS is not a static illness but changes over time. Selection and testing of therapeutics must take this factor in hand when testing on humans.
7. Gender difference occur in the same types of ALS but testing in animals/rodents rarely takes this into consideration.
8. Sloppy mouse testing seems also to be common.
Oxidative stress in ALS is only one of several dysfunctional pathways in ALS
This paper is just one example of what I have said above.
Alterations in anti-oxidative defence enzymes in erythrocytes from sporadic amyotrophic lateral sclerosis (SALS) and familial ALS patients.
CONCLUSIONS:
Changes in erythrocyte ADE activities suggest that oxidative stress, involved in the motor neurone pathogenesis of SALS and FALS, also has systemic effects.
Differences in ADE systems between the study groups revealed the presence of different types of oxidative pressure, indicating the potential additional benefit of individually designed anti-oxidant cocktail therapies
Add to the above that genetic testing and blood sampling of all people with ALS is not routinely done and anecdotal evidence, is ignored and that's where we are.
No central data base collecting and analysing tissue, genetic and blood samples for all with ALS.
Another factor is the failure to follow up exactly and find out why certain substances have been beneficial is some but, when retested, not in others and you get an idea of the state of ALS research.
Just cure one human, no matter whatever type of ALS, then we may be able to move forward.
