tae-1 is an inhibitor of amyloid-β fibril formation and aggregation.alzheimer’s disease (ad), a progressive neurodegenerative disorder, is characterized by the cerebral accumulation of insoluble aggregates of amyloid-β peptides (aβ). although the precise mechanisms governing neuronal loss remains ambiguous, toxicity resulting from aβ-activated pathways is evident.
in a previous study, the authors examined the effects of tae-1 on differentiated human sh-sy5y neuronal cells grown in tissue culture. results showed that the stimulation of neuronal cellular process length and branching was noted. moreover, the increased synaptophysin suggested that tae-1 could stimulate synapse formation. increased expression of map2 was also observed, indicating that tae-1 promoted the differentiation of human neurons. in addition, targeted ache inhibition was evaluated by electrochemical quantification of the enzymatic product, thiocholine, on unmodified gold screen-printed electrodes. it was found that at increasing tae-1concentrations, there was a corresponding decrease in the ache activity resulting in reduced amount of oxidizable thiocholine. the ic50 value was found to be 0.465 μm for tae-1 [1].
0.3 ± 0.02 μm for ache; 3.9 ± 0.2 μm for buche
[1] veloso aj, chow am, dhar d, tang dw, ganesh hv, mikhaylichenko s, brown ir, kerman k. biological activity of sym-triazines with acetylcholine-like substitutions as multitarget modulators of alzheimer's disease. acs chem neurosci. 2013 jun 19;4(6):924-9.