Rudolph Tanzi is a Harvard professor and he earlier worked a lot with PBT2 studies and with Masters et al. from Australia. His team published an interesting study with nicotinamide riboside (NR) demonstrating that pTau217 decreased by giving early AD patients 1 g of NR, a precursor of NAD+, nicotinamide adenine dinucleotide.
The interesting thing to me as an ATH investor is that "NAD+ acts as the primary electron donor in the mitochondrial respiratory chain and regulates various enzymes involved in key metabolic pathways such as glycolysis, the Krebs cycle, and fatty acid oxidation". This is very similar to what ATH 434 does on the mitochondrial level according to Kosman's poster last autumn ( https://alteritytherapeutics.com/wp-content/uploads/DB-sfn-2024-poster-10Oct24.pdf).
434 improves energy production by normalizing the iron Fe2+/fe3+ balance but NR improves energy production by being a precursor to NAD+. Both the Fe2+/Fe3+ ratio and NAD+ synthesis become worse in AD.
Another issue may be important as well: Tanzi's study used the p217T as a quantitative measure of AD progression.
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