Kinesin gene variability may affect tau phosphorylation in early Alzheimer's disease
(2007) In International Journal of Molecular Medicine 20(2). p.233-239- Abstract
- 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... (More)
- 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 hyper-phosphorylated 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/648422
- author
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- apolipoprotein, biomarkers, polymorphism, Alzheimer's disease, kinesin, E, axonal transport
- in
- International Journal of Molecular Medicine
- volume
- 20
- issue
- 2
- pages
- 233 - 239
- publisher
- Spandidos Publications
- external identifiers
-
- wos:000248282800013
- scopus:34347242354
- ISSN
- 1791-244X
- language
- English
- LU publication?
- yes
- id
- c5bdf762-c147-4165-8b65-dc982c370b73 (old id 648422)
- date added to LUP
- 2016-04-01 17:02:44
- date last changed
- 2022-03-15 04:43:46
@article{c5bdf762-c147-4165-8b65-dc982c370b73, abstract = {{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 hyper-phosphorylated 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.}}, author = {{Andersson, Malin E. and Sjolander, Annica and Andreasen, Niels and Minthon, Lennart and Hansson, Oskar and Bogdanovic, Nenad and Jern, Christina and Jood, Katarina and Wallin, Anders and Blennow, Kaj and Zetterberg, Henrik}}, issn = {{1791-244X}}, keywords = {{apolipoprotein; biomarkers; polymorphism; Alzheimer's disease; kinesin; E; axonal transport}}, language = {{eng}}, number = {{2}}, pages = {{233--239}}, publisher = {{Spandidos Publications}}, series = {{International Journal of Molecular Medicine}}, title = {{Kinesin gene variability may affect tau phosphorylation in early Alzheimer's disease}}, volume = {{20}}, year = {{2007}}, }