I suppose it could be that neuroprotection happens along many pathways. Imagine someone has 3 different bills to pay, A, B, C, each bill the same amount. If a grant comes along (SGLT2i) and pays bill A, the indebted individual will report that they were financially protected, even if B, C, were not paid, as we don’t know the extent of any neuroprotection from any drug, none are probably 100% anyway. If a different grant institution (lithium) pays bill B, then even if A and C are unpaid, the debtor will report that they were financially protected, same as in the case of the SGLT2i grantor. Now, if the SGLT2i grantor said, I’ll pay for A, but only if you don’t accept the grant from “lithium” (who pays B), and the debtor agrees, then the situation doesn’t change insofar as financial protection. In either case, one of the pathways is protected, therefore overall, neuroprotection is maintained under allthe scenarios I outlined.
Now imagine that there is only one bill to pay. It won’t matter whether SGLT2i pays it or Lithium pays it, it gets paid - protection is maintained. And if SGLT2i says: I’ll pay your bill as long as you don’t accept the grant from Lithium, the bill still gets paid, no difference (assuming both pay the same amount!).
To sum up:
-
Neuroprotection is likely acting along different axis and pathways. If lithium acts along one set of pathways and SGLT2i along a different set of pathways, you might be still protected by either interventions and it would take specific measurements to determine if SGLT2i protects more overall, or lithium more - we don’t know.
-
If both SGLT2i act along the same pathway(s) of protection as lithium, then if SGLT2i displaces lithium, and provides the same protection, then SGLT2i acts as a replacement and substitution, therefore any loss of lithium in the process is irrelevant insofar as neuroprotection.
The overlap of protection pathways need not even occur. Imagine that there’s a field that’s being flooded. We can put the dam downstream close to the field, or much further up the stream, but in either case, we no longer are flooded. It might not matter how you lower LDL, whether closer or further upstream (f.ex. LDL lowering by statins or by BA), what matters is that LDL is lowered, because the active damaging agent is LDL, and removing it by any means is what matters. We don’t care if it’s lithium or SGLT2i in this scenario, if both are addressing some mechanism through the same or different pathways.
And so on. The possibilities are many, it seems to me. But in general, I think the concept of “neuroprotection” is a bit fuzzy - how do we measure that, by specific outcomes or biomarkers or what. Knowing that, we could examine what SGLT2i and lithium do exactly and to see whether they’d be additive, mildly subtractive or what.
