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"Axonal transport dysfunction in Alzheimer's disease"
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PhD
in Clinical neuroscience, Dept. of Psychiatry and Neurochemistry, Göteborg University.
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PhD
student - MALIN ANDERSSON
malin.andersson@clinchem.gu.se
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supervisor
- HENRIK ZETTERBERG
henrik.zetterberg@clinchem.gu.se |
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PROJECT DESCRIPTION AND AIM |
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The aim of this project is to study axonal transport dysfunction in
Alzheimer’s disease (AD) by combining clinical genetic association
analysis of a gene variant in the kinesin gene (KNS2) in humans with
basic analysis of kinesin 1 expression and function using zebrafish
as a model organism.
Alzheimer’s disease is the most common form of dementia and a
very painful disease for patients as well as their relatives. The causing
events of sporadic Alzheimer’s disease are still unsolved, but
aggregation of ß-amyloid1-42 in the brain seems important. Axonal
transport dysfunction, especially defective kinesin-mediated transport
of the amyloid precursor protein may increase ß-amyloid1-42 production.
Thus kinesin and axonal transport are of high interest in the area of
AD pathogenesis.
We are in the process of establishing a zebrafish laboratory in which
we will be able to genetically manipulate and study gene knockdown in
vivo in living zebrafish. After finishing the first genetic part of
the project I will use this system and dose-dependently knockdown our
gene of interest and do analysis of the general effects on development
of the central nervous system using gross microscopy and effect on ß-amyloid1-42
production using mass spectroscopy. Further, I will perform micro array
analysis to study the effect of KNS2 knockdown on general gene expression
in the zebra fish in order to get guidance in the selection of relevant
proteins for further experiments.
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CONTACT INFORMATION
Henrik Zetterberg
Dep. of Neurokemi,
V-huset
Sahlgrenska Universitetssjukhuset/Mölndal
431 80 Mölndal
E-mail: henrik.zetterberg@clinchem.gu.se
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