"Axonal transport dysfunction in Alzheimer's disease"
PhD in Clinical neuroscience, Dept. of Psychiatry and Neurochemistry, Göteborg University.

PhD student - MALIN ANDERSSON

malin.andersson@clinchem.gu.se

 

supervisor - HENRIK ZETTERBERG

henrik.zetterberg@clinchem.gu.se



PROJECT DESCRIPTION AND AIM

 

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.


CONTACT INFORMATION

Supervisor

Henrik Zetterberg

Dep. of Neurokemi,

V-huset

Sahlgrenska Universitetssjukhuset/Mölndal

431 80 Mölndal

E-mail: henrik.zetterberg@clinchem.gu.se