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Abstract
Slow axonal transport is a multivariate phenomenon implicated in several neurodegenerative disorders. Recent reports have unraveled the molecular basis of the transport of certain slow component proteins, such as the neurofilament subunits, tubulin, and certain soluble enzymes such as Ca2+/calmodulin-dependent protein kinase IIa (CaM kinase IIa), etc., in tissue cultured neurons. In addition, genetic analyses also implicate microtubule-dependent motors and other housekeeping proteins in this process. However, the biological relevance of this phenomenon is not so well understood. Here, the authors have discussed the possibility of adopting neurogenetic analyses in multiple model organisms to correlate molecular level measurements of the slow transport phenomenon to animal behavior, thus facilitating the investigation of its biological efficacy.
ACKNOWLEDGEMENTS
We express our deep gratitude to Prof. Obaid Siddiqi for his insights and engagement with our research; to Prof. K. S. Krishnan for inviting us to compose the thoughts expressed in this review; and we apologize to all those whose work could not be cited here due to limitations of our knowledge. K.R. is supported by an intramural grant from Tata Institute of Fundamental Research (TIFR) and A.S. is a final-year research scholar of TIFR.
Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.