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MTs, play key roles in neuronal function. In addition, synaptic biphasic fluctuations of MT instability/stability and tubulin post-translational modifications (PTMs) are associated with memory formation and are disrupted in aging, indicating a primary role for the regulation of MT dynamics and tubulin PTMs in the maintenance of synaptic plasticity. In support of this model, we recently found that stabilization of dynamic MTs and induction of tubulin PTMs by the formin mDia1 contribute to oligomeric Aβ1-42 synaptotoxicity, and inhibition of MT dynamics alone is sufficient to promote tau hyperphosphorylation and tau dependent synaptotoxicity (Qu et al., J Cell Biol, 2017). To test whether these changes occur at synapses and are directly responsible for synapse loss, we have further developed microscopy assays that measure MT invasions into dendritic spines and MT contacts with single presynaptic boutons of hippocampal neurons in culture. Surprisingly, we found that dynamic MT plus ends preferentially grow near presynaptic boutons (Qu et al., Curr Biol, 2019), and rescue/nucleation at boutons is enhanced by neurotransmitter release or when neurons are challenged with oligomeric Aβ1-42, an activity mediated by tau. Our data underscore the existence of a previously uncharacterized formin-mediated pathway of synaptotoxicity and a subset of tau-dependent presynaptic dynamic MTs that respond to neurotransmission and excitotoxicity.