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Volume 8 Journal of Alzheimers Disease & Parkinsonism
ISSN: 2161-0460 Euro Dementia 2018
May 24-25, 2018
May 24-25, 2018 | Vienna, Austria
11th International Conference on
Alzheimers Disease & Dementia
Distribution pattern of amyloid beta peptides and aquaporin 4 proteins in Alzheimer’s disease and
associated transgenic mouse models
Magdalena Temmel1, 2, Karin Lanegger 3, Johannes Attems4, Jörg Neddens2 , Heinz Hutter5 and Birgit Hutter-Paier 2
1Karl-Franzens-Universität Graz, Austria
2QPS Austria GmbH, Austria
3FH Joanneum Graz, Austria
4Newcastle University, UK
5Medical University of Graz, Austria
The amyloid cascade hypothesis postulates that accumulation of Aβ is an initial event in the pathology of Alzheimer’s
disease (AD) and represents overall one of the two main histopathological features. This study aimed at investigating the
distribution and clearance of amyloid beta peptides in AD brain tissue as well as in two associated mouse models — APPSL
and 5xFAD. We histologically quantified various parameters: first, we evaluated the absolute distribution pattern of amyloid
beta peptides; second, we investigated the occurrence of cerebral amyloid angiopathy (CAA) and third, we examined the
localization of aquaporin 4 (AQP4) water channels. We immunofluorescently labelled sections from human AD patients at
different Braak stages (I/II, III/IV and V/VI) and brain sections from the two transgenic mouse lines across different time
points. Quantifications of labelled tissues revealed that overall amyloid-beta intensity, significantly increased in humans at
advanced Braak stages and both transgenic mice during aging. Evaluation of CAA, which is defined as amyloid-β deposition
in vascular walls, was technically challenging in human tissue. However, APPSL and 5xFAD transgenic mice developed severe
CAA with increasing age. Finally, studying AQP4 protein distribution as a major participant of the glymphatic system involved
in the clearance of amyloid beta revealed that in AD, parenchymal AQP4 increased with disease progression, while perivascular
AQP4 was decreased at early AD stages and returned back to baseline levels at late stages. Furthermore, AQP4 protein was
accumulated in close proximity to amyloid beta plaques. A similar result was observed in APPSL and 5xFAD mouse brain
tissue. Together, these data show that these two mouse models are valuable to study amyloid-beta related pathways in AD.
Biography
Magdalena Temmel is currently a PhD student of Natural Sciences at the Karl-Franzens University of Graz, Austria. In her PhD thesis, she focuses on investigating
high-fat diet induced changes in the A53T-mutated alpha-synuclein expressing mouse model of Parkinson’s disease. She is performing all her project-associated
works at QPS Austria Neuropharmacology, which is a leading CRO focusing on central nervous system, orphan and mental disorders. The research presented here
was part of her Master’s thesis that was performed as a cooperation project between several universities.
Magdalena Temmel et al., J Alzheimers Dis Parkinsonism 2018, Volume 8
DOI:10.4172/2161-0460-C3-043