Can we modify amyloid accumulation in the retina?

This study will investigate the potential for modifying a specific enzyme inhibitor
(Neuroserpin) in the retina that we hypothesise is involved in the regulation of neurotoxic
amyloid protein - a feature of Alzheimers disease (AD). We have also seen deposition of
amyloid in the retina in glaucoma patients. In our pilot study we showed that neuroserpin
co-localises with amyloid beta plaques. We will now investigate whether modulating
neuroserpin expression at both the protein level and the gene level is beneficial to clearance
of amyloid from the tissues. This may in turn improve the retinal function in a mouse model
of AD. We will use a particular strain of mouse that manifests AD like changes in the retina,
and we will modify the neuroserpin levels via antibody neutralisation and by viral vector
gene therapy techniques. If this approach is successful it could lead to new treatment
options for these neurodegenerative disorders