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Kinesin gene variability may affect tau phosphorylation in early Alzheimer's disease.

Journal article
Authors Malin E Andersson
Annica Sjölander
Niels Andreasen
Lennart Minthon
Oskar Hansson
Nenad Bogdanovic
Christina Jern
Katarina Jood
Anders Wallin
Kaj Blennow
Henrik Zetterberg
Published in International journal of molecular medicine
Volume 20
Issue 2
Pages 233-9
ISSN 1107-3756
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Health and Care Sciences
Pages 233-9
Language en
Keywords Aged, Aged, 80 and over, Alzheimer Disease, genetics, metabolism, pathology, Apolipoproteins E, genetics, Case-Control Studies, Disease Progression, Female, Gene Frequency, Humans, Male, Microtubule-Associated Proteins, genetics, Middle Aged, Phosphorylation, Polymorphism, Single Nucleotide, Protein Kinases, metabolism, Variation (Genetics), physiology, tau Proteins, metabolism
Subject categories Medical and Health Sciences


Kinesin is a microtubule-associated motor protein that transports Alzheimer-associated amyloid precursor protein (APP) in neurons. In animal models, impaired kinesin-mediated APP transport seems to enhance formation of the neurotoxic 42 amino acid fragment of beta-amyloid (A beta 42). In man, one study suggests that a polymorphism (rs8702, 56,836G>C) in the kinesin light chain 1 gene (KNS2) may affect the risk of Alzheimer's disease (AD). To further assess KNS2 as a susceptibility gene for AD we analyzed 802 patients with sporadic AD and 286 controls, 134 longitudinally followed patients with mild cognitive impairment (MCI) and 39 cognitively stable controls for the rs8702 polymorphism. The rs8702 polymorphism did not influence risk of AD (p=0.46). However, rs8702 interacted with APOE epsilon 4 carrier status in AD (p=0.006) and influenced cerebrospinal fluid levels of hyperphosphorylated tau in MCI patients who converted to AD during follow-up (p=0.018). These findings support earlier indications that genetic variability in the KNS2 gene may play a role during early stages of AD pathogenesis.

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