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Early disturbances in axonal transport, before the onset of Background: gross neuropathology, occur in a spectrum of neurodegenerative diseases including Alzheimer’s disease. Kinesin superfamily motor proteins (KIFs) are responsible for anterograde protein transport within the axon of various cellular cargoes, including synaptic and structural proteins. Dysregulated KIF expression has been associated with AD pathology and genetic polymorphisms within kinesin-light chain-1 (KLC1) have been linked to AD susceptibility. We examined the expression of KLC1 in AD, in relation to that of the KLC1 motor complex (KIF5A) and to susceptibility genotypes. We analysed KLC1 and KIF5A gene and protein expression in Methods: midfrontal cortex from 47 AD and 39 control brains. We found that gene expression of both and Results: KIF5A KLC1 increased with Braak tangle stage (0-II vs III-IV and V-VI) but was not associated with significant change at the protein level. We found no effect of KLC1 SNPs on KIF5A or KLC1 expression but KIF5A SNPs that had previously been linked to susceptibility in multiple sclerosis were associated with reduced mRNA expression in AD cortex. KIF5A The findings raise the possibility that genetic polymorphisms Conclusions: within the gene locus could contribute to disturbances of axonal KIF5A transport, neuronal connectivity and function across a spectrum of neurological conditions, including AD.

KIF5A and KLC1 expression in Alzheimer’s disease: relationship and genetic influences