Agree. I liked these exerpts, for example:
<<We have summarized on Figure 12 a possible mechanism of action for anatabine that highlights its potential therapeutical application in AD. Further mechanistic work will be required to precisely identify the mode of action of anatabine responsible for the prevention of tau phosphorylation and determine whether it is mainly mediated via a reduction of microgliosis/neuroinflammation, an inhibition of the kinases responsible for tau phosphorylation or a combination of both.
Our data provide in vivo evidence that a chronic oral treatment with anatabine reduces pathological tau hyperphosphorylation and the formation of pathological tau conformers/oligomers leading to a reduction of tau-related functional deficits in Tg Tau P301S mice. These data support further exploration of anatabine as a possible disease modifying agent for tau-associated neurodegenerative conditions and, in particular AD, since we have shown that anatabine also displays Aß lowering properties [22].>>
And cooperation with/from other scientists:
<<Acknowledgements
We are grateful to Dr. Peter Davies (Albert Einstein College of Medecine, Bronx, NY, USA) for the gift of the DA9, PHF-1, CP13, RZ3 and MC1 antibodies and to Dr. Lester Binder (Feinberg School of Medicine, Northwestern University, Chicago, IL, USA) for providing the TOC1 antibody. AER is the recipient of an NIA grant: RO1 AG-19795. We thank Mr. Thomas Guengant for his help during the behavioral testing.>>
