soooo......... article 1 is about lrrk2 inhibators.
article 2 is about the affects of lrrk2 on cell nuclear membrane.
lrrk2 also affect the microglia that kill of the cells with a-sync problems.
article 1 proposes stopping lrrk2 from working
article 2 proposes fixing lrrk2
interesting asides -
ldopa causes arythmias
the dopamine cells are only part of the problem
is my understanding correct?
treatment seems to be getting closer, yet further, as always still at the very early stage
Hi Turnip. Both papers are concerned with inhibiting mutant LRRK2 (by a drug in the first paper and by fixing it genetically in the second). The first reference makes the assumption (or is it the journalist?) that too much LRRK2 can also be a cause (or an inevitable member in a causal sequence) of PD even in those cases not carrying a LRRK2 mutation and so inhibition of unmutated LRRK2 would still be therapeutic. I know that some major pharmaceutical companies have taken on LRRK2 as a target in PD ..............but I'm not sure the assumption has been proven.