More upcoming presentation on Zn and a-beta and AD - Bush, Finkelstein and Adlard

The interaction between ZnT3 and Amyloid-β in Alzheimer’s disease
Location: WCC Hall A-C
Presentation time: Monday, Nov 17, 2014, 1:00 PM - 5:00 PM
Presenter at Poster: Mon, Nov. 17, 2014, 4:00 PM - 5:00 PM
Topic: ++C.02.h. In vivo Abeta toxicity
Authors: *S. M. HANCOCK, D. I. FINKELSTEIN, A. I. BUSH, P. A. ADLARD;
The Florey Inst. of Neurosci. and Mental He, Parkville, Australia
Abstract: Introduction: Alzheimer’s disease (AD) is the most common form of dementia for which there is currently no treatment or cure. Zinc has been repeatedly linked to AD with alterations in Zn distribution suggested to have a key role in AD. Moreover, a high binding affinity of zinc to amyloid-β (Aβ) has been demonstrated, along with the presence of Aβ plaques around glutamatergic synapses. Zinc transporter 3 (ZnT3) is responsible for loading Zn ions into presynaptic vesicles and is prevalent at glutamatergic synapses within the cortex. Past studies have shown that both ZnT3 mRNA and protein expression levels are altered in AD. We have demonstrated that ZnT3 is present in primary cultured mouse cells (neurons and astrocytes) and expression levels can be influenced by treatments with zinc and copper. We have further examined the interaction between ZnT3 and Aβ in vivo. Method: Transgenic ZnT3 KO and WT mice at either 3 or 12 months of age were anaesthetised and Aβ was unilaterally injected (2ug/5µl in 0.02M PBS) into the right hippocampus (2.54mm from Bregma, lateral 2mm and 2mm depth). Behavioural testing was performed at 7 and 14 days post injection, with animals subsequently culled for biochemical and histological analysis. Conclusion: These analyses will further define the interaction between Aβ and ZnT3, providing insight into the pathogenesis of AD.