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>We additionally show that HCQ exerts dose-dependent effects on late long-term potentiation (LTP) and rescues impaired hippocampal synaptic plasticity prior to significant accumulation of amyloid plaques and neurodegeneration in APP/PS1 mice.

iirc (I am not qualified!!) Alzheimers relates to plaques in our brain, and this sounds to me like it fixes a precursor to the plaque accumulation (the loss of plasticity?)

The plaques are a side effect of something we don't understand yet. Treating the plaque or slowing it is not a solution, we need to find and fix the cause.

Quite apart from the validity of this study, isn’t a purely palliative measure still valuable?

Literally billions of dollars has been spent, futilely, on the idea that removing plaques would stop/reverse the symptoms of Alzheimer's Disease.

This "amyloid hypothesis" has not been a smashing success, to put in mildly.

It's not clear that treating amyloid plaque is actually palliative for Alzheimer's patients.

> some anti-inflammatory properties

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6214864/

Lots of literature 1 google/ddg search away for you, but there's an example.

Being anti-inflammatory?