Susanne Frykman Group
Check out SyDAD, a Marie Curie European Training Network.
Please see www.sydad.eu for further information.
Synaptic Degeneration in Alzheimer Disease
Synaptic degeneration is one of the first hallmarks to occur during Alzheimer disease (AD) pathogenesis and the one that correlates best with cognitive decline. However, the molecular mechanisms behind this degeneration remain largely elusive. In this project, we are focusing on one of the potential key players in AD synaptic degeneration, namely the amyloid beta-peptide (Abeta), but we are also aiming to identify novel pathways behind synaptic degeneration in AD.
Questions that we aim to answer include:
- How is Abeta released from the neurons?
- Is the precursor APP-CTF-beta even more toxic than Abeta?
- What are the synaptic targets for Abeta and APP-CTF-beta?
- Which other pathways underlie synaptic degeneration in AD?
|Susanne Frykman||PhD, Associate professor|
|Jolanta Lundgren||PhD student|
ADAM10 and BACE1 are localized to synaptic vesicles.
J. Neurochem. 2015 Nov;135(3):606-15
Activity-independent release of the amyloid β-peptide from rat brain nerve terminals.
Neurosci. Lett. 2014 Apr;566():125-30
Identification of two novel synaptic γ-secretase associated proteins that affect amyloid β-peptide levels without altering Notch processing.
Neurochem. Int. 2012 Jul;61(1):108-18
Minor contribution of presenilin 2 for γ-secretase activity in mouse embryonic fibroblasts and adult mouse brain.
Biochem. Biophys. Res. Commun. 2011 Jan;404(1):564-8
Synaptic and endosomal localization of active gamma-secretase in rat brain.
PLoS ONE 2010 Jan;5(1):e8948
Karolinska Institutet, Department of Neurobiology, Care Sciences and Society, KI Alzheimer's Disease Research Center
Novum, floor 5
SE-141 86 Stockholm