That said, this study is cause for cautious optimism. The mechanism they've targeted cleared symptoms in 'two of these mouse models: One carried multiple human mutations in amyloid processing; the other carried a human mutation in the tau protein. ' Mosreso, it does it by modulating NAD+, long a target of interest in AD. From the paper

Nicotinamide adenine dinucleotide (NAD+) homeostasis is central to cellular resilience against oxidative stress, DNA damage, neuroinflammation, blood-brain barrier (BBB) deterioration, impaired hippocampal neurogenesis, synaptic plasticity deficits, and neurodegeneration.

As such it is not only of interest to sufferers of AD but the aging population in general.