Affiliations: [a] MS and Stem Cell Group, Translational Health Sciences, Bristol Medical School, University of Bristol, UK | [b] Dementia Research Group, Translational Health Sciences, Bristol Medical School, University of Bristol, UK
Correspondence:
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Correspondence to: Kelly Hares, PhD, MS and Stem Cell Group, 1st Floor, Clinical Neurosciences Office, Learning and Research Building, Southmead Hospital, Bristol, BS10 5NB, UK. Tel.: +44 0117 414 7804; Fax: +44 0117 4147838; E-mail: kelly.hares@bristol.ac.uk.
Abstract: Defects in motor protein-mediated neuronal transport mechanisms have been implicated in a number of neurodegenerative disorders but remain relatively little studied in Alzheimer’s disease (AD). Our aim in the present study was to assess the expression of the anterograde kinesin superfamily motor proteins KIF5A, KIF1B, and KIF21B, and to examine their relationship to levels of hyperphosphorylated tau, amyloid-β protein precursor (AβPP), and amyloid-β (Aβ) in human brain tissue. We used a combination of qPCR, immunoblotting, and ELISA to perform these analyses in midfrontal cortex from 49 AD and 46 control brains. Expression of KIF5A, KIF1B, and KIF21B at gene and protein level was significantly increased in AD. KIF5A protein expression correlated inversely with the levels of AβPP and soluble Aβ in AD brains. Upregulation of KIFs may be an adaptive response to impaired axonal transport in AD.
Keywords: Alzheimer’s disease, amyloid, kinesin, tau
