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In Alzheimer’s disease (AD), the amyloid-# (A#)-associated aggregation of tau triggers neurodegeneration and cognitive decline; hence, preventing tau aggregation is a key therapeutic target.
Preclinical research found that i) A# precipitates neuronal hyperactivity, ii) neuronal hyperactivity promotes synaptic release of soluble hyperphosphorylated tau (p-tau) seeds, and iii) p-tau seeds spread across synapses, ensuing tau aggregation.
We hypothesize that A# drives neuronal hyperactivity, triggering p-tau increase, followed by connectivity mediated tau spreading in AD. Thus, attenuating A#-related neuronal hyperactivity may limit p-tau release, tau aggregation and cognitive decline.
What you will do
This post will be based in Dr Simon Bell’s lab and the research assistant will work closely with lab members from Dr Simon Bell’s and Dr Matt Livesey’s lab. You will focus on reprogramming AD patient-derived iNPC neuron cultures on multi-electrode array systems to monitor neuronal activity.
In these AD model systems, you will assess whether A# production relates to neuronal activity, and whether neuronal hyperactivity drives neuronal p-tau secretion and trans-neuronal tau spreading using tau seeding assays. Lastly, you will determine whether tau spreading can be attenuated by applying neuronal activity lowering drugs.
Additional information
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