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The conversion of p35 to p25 has been implicated as the underlying cause of cdk5 hyperactivation in many neurodegenerative conditions. The mechanism governing formation of p25 needs to be elucidated, and the present paper provides one such clue in the possible involvement of microtubule stabilization. This finding is worth pursuing further. However, the idea that microtubule-stabilizing agents may have therapeutic utility in AD and tauopathies must await demonstration of a definite and reproducible neurodegenerative effect of Abeta in vivo, particularly with respect to its effects on cdk5 activation.
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