Overexpression of kinesin superfamily motor proteins in Alzheimer’s Disease

Kelly Hares, Scott Miners, Amelia Cook, Claire Rice, Neil Scolding, Seth Love, Alastair Wilkins

Research output: Contribution to journalArticle (Academic Journal)peer-review

12 Citations (Scopus)
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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 hyperphosphorlyated 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.
Original languageEnglish
Pages (from-to)1511-1524
Number of pages14
JournalJournal of Alzheimer's Disease
Issue number4
Publication statusPublished - 7 Nov 2017


  • Alzheimer’s disease
  • Kinesin
  • Amyloid
  • Tau


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