The current theory doesn't seem to be working out well, for the patients. What if the chronic inflammation, and cell decay, was addressed? Then, the healthier cells could do their own housekeeping. Leronlimab does not focus on a narrow mechanism of action. Leronlimab's mechanism of action starts with returning the immune system to homeostasis, and halting the chronic inflammation. A healthier system should take care of those Tau and Amyloid plaques. That seems like a more productive clinical to run.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4779179/

"A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in mitochondria function contributes to aging. In particular, we discuss how mitochondria contribute to specific aspects of the aging process including cellular senescence, chronic inflammation and the age-dependent decline in stem cell activity. Signaling pathways regulating the mitochondrial unfolded protein response and mitophagy are also reviewed with particular emphasis placed on how these pathways might in turn regulate longevity."