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Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPV SIP Q, which shares SIP motif with SALLR SIP A – a peptide derived from activity-dependent neurotrophic factor (ADNF). Mechanistically, both NAPV SIP Q and SALLR SIP A contain a SIP motif that is identified as a variation of SxIP domain, providing direct interaction with microtubule end-binding proteins (EBs). The peptide SKIP was shown before to provide neuroprotection  in vitro  and protect against Adnp-related axonal transport deficits  in vivo . Here we show, for the first time that SKIP enhanced microtubule dynamics, and prevented Tau-microtubule dissociation and microtubule disassembly induced by the Alzheimer’s related zinc intoxication. Furthermore, we introduced, CH 3 CO-SKIP-NH 2  (Ac-SKIP), providing efficacious neuroprotection. Since microtubule – Tau organization and dynamics is central in axonal microtubule cytoskeleton and transport, tightly related to aging processes and Alzheimer’s disease, our current study provides a compelling molecular explanation to the  in vivo  activity of SKIP, placing SKIP motif as a central focus for MT-based neuroprotection in tauopathies with axonal transport implications.

A Novel Microtubule-Tau Association Enhancer and Neuroprotective Drug Candidate: Ac-SKIP