Hello Annesse and welcome to Neuro-talk.
While there are many theories with respect to the cause of MS and other auto-immune diseases, I had not heard of the protease and DNase1 connection; although similar claims were and are made with respect to lipase, the enzyme that helps to metabolize fats, cholesterol and essential fatty acids.
While these theories may have some validity, as with other diseases involving immune system dysfunction, like cancer and allergies, it seems that metabolic errors of this sort may be a contributing factor or condition, rather than a singular cause. Despite the extensive search for a single common cause, one has yet to be established; although I sincerely wish you all the best in your endeavor to do so.
Typically when we look at any result there is a process and protocol as it were to be followed; at least with respect to scientific research. The theory behind that protocol has stood the test of time and is as follows.
'When a cause and condition come together there is a predictable result. Therefore both the causes and conditions must be discovered if one is to gain a full understanding of the result.'
In this case the result is auto-immune disease, including MS.
The difference between cause, condition and result can most easily be appreciated if the three are examined rather simplistically.
For example, in the case of a bean sprout, we can see that the cause of the sprout is the bean seed; for if that cause did not exist, there could be no sprout. Yet the bean seed does not become a sprout until it meets with certain conditions. So it can also be appreciated that the conditions alone will not produce a bean sprout if the cause is not also present in the form of a bean seed.
It is only when both the cause (the bean seed) and the conditions (moisture, warmth, fertile soil and light) come together that the resultant effect (a bean sprout) is produced.
Getting back to auto-immune disease, despite extensive research to find a common cause, one has yet to be established, but many theories have gained popular acceptance; at least as far as propensity goes. This propensity theory simply means that there may be a common causation for how certain diseases manifest in individuals. In the case of auto-immune disease, the propensity is an alteration of the immune system function that is often accompanied by inflammation.
The proposed 'common propensity cause theory' seems to be leaning primarily toward genetics.
If it turns out that genetics is the cause of auto-immune disease, we are still left to figure out what the conditions are that might 'turn on' the gene cause; or to promote the seed to become a sprout, if we use the example given.
Research to date indicates that these conditions seem to be many and include stress, climate, vaccination, immune challenges, infections, nutritional deficiencies and metabolic errors.
What you are proposing, specifically that of a metabolic error as a cause of auto-immune disease, may actually fall into the latter category of conditions; things that may meet with the cause to produce the effect of auto-immune disease.
It seems that just like the process of a bean seed turning into a sprout, in the case of auto-immune disease, it is likely that more than one condition might also be needed to produce the resultant effect. Thus in keeping with your mention of a protease and DNase1 connection, it is also likely that more of the other conditions mentioned above, or even some, as of yet unknown conditions, must also be present along with such a deficiency to produce the resultant disease.
By supporting, cooperating and sharing ideas with each other, as well as with researchers and those who treat the symptoms of disease, just as you have, eventually it will be figured out. We must also remain open to the different theories of others as they present, so that all things are taken into consideration and carefully analyzed.
Then we will be in a better position to do so again when it comes time to figure out how best to interfere with either the cause or the conditions in order to prevent the resultant effect of disease.
As it is now however, just trying to figure out what the causes and conditions are and how they combine to produce the result of MS (and other disease as well), is the sort of thing that drives those involved in research nuts.
On a more personal level, this has been my struggle too.
With love, Erika