Betaine ameliorates schizophrenic traits by functionally compensating for KIF3-based CRMP2 transport
Shogo Yoshihara, Xuguang Jiang, Momo Morikawa, T. Ogawa, Sotaro Ichinose, Hirooki Yabe, Akiyoshi Kakita, Manabu Toyoshima, Yasuto Kunii, Takeo Yoshikawa, Yosuke Tanaka, Nobutaka Hirokawa
Abstract
neurons as a cause of neurite hyperbranching. Betaine administration significantly decreases CRMP2 carbonylation, which enhances the F-actin bundling needed for proper lamellipodial dynamics and microtubule exclusion and may thus functionally compensate for KIF3 deficiency. Because the KIF3 expression levels tend to be downregulated in the human prefrontal cortex of the postmortem brains of SCZ patients, this mechanism may partly participate in human SCZ pathogenesis, which we hypothesize could be alleviated by betaine administration.
Topics & Concepts
BetaineSchizophrenia (object-oriented programming)NeuroscienceCell biologyPathogenesisNeuriteMediatorActinPrefrontal cortexMechanism (biology)BiologyMorphogenesisChemistryInternal medicineBiochemistryMedicineGeneCognitionPsychiatryIn vitroPhilosophyEpistemologyMicrotubule and mitosis dynamicsAxon Guidance and Neuronal SignalingNeurogenesis and neuroplasticity mechanisms