Stacey Anne GouldUniversity of Cambridge | Cam · Department of Clinical Neurosciences
Stacey Anne Gould
Doctor of Philosophy
About
9
Publications
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Introduction
Stacey Anne Gould currently works at the Department of Clinical Neurosciences, University of Cambridge. She is currently studying the role of SARM1 activation after a range of physical and neurotoxic triggers, and how subsequent axon degeneration can be prevented using compounds with therapeutic potential. Her earlier work in behavioural neuropharmacology focussed on mechanisms of pain generation and ways to improve preclinical predictability of analgesic efficacy in spontaneous pain assays.
Publications
Publications (9)
Neurones are highly polarized cells with extensive axonal projections that rely on transport of proteins, RNAs, and organelles in a bidirectional manner to remain healthy. This process, known as axonal transport, can be imaged in real time through epifluorescent imaging of fluorescently labeled proteins, organelles, and other cargoes. While this is...
Activation of the pro-degenerative protein SARM1 after diverse physical and disease-relevant injuries causes programmed axon degeneration. Original studies indicate that substantially decreased SARM1 levels are required for neuroprotection. However, we demonstrate, in Sarm1 haploinsufficient mice, that lowering SARM1 levels by 50% delays programmed...
Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting side effect of cancer treatment, often associated with degeneration of sensory axons or their terminal regions. Presence of the slow Wallerian degeneration protein (WLDS), or genetic deletion of sterile alpha and TIR motif containing protein 1 (SARM1), which strongly protec...
Programmed axon degeneration (Wallerian degeneration) can occur after physical injury, inhibition of axon transport, exposure to neurotoxic compounds, and in diseases involving mitochondrial or metabolic dysfunction. There is increasing evidence that this pathway can be activated in human painful neuropathies and preclinical evidence suggests it is...
In Alzheimer’s disease (AD) many indicators point to a central role for poor axonal transport, but the potential for stimulating axonal transport to alleviate the disease remains largely untested. Previously we reported enhanced anterograde axonal transport of mitochondria in 8-11 months old MAPTP301L knockin mice, a genetic model of FTDP-17T. In t...
Background:
Burrowing is a rodent behavior validated as a robust and reproducible outcome measure to infer the global effect of pain in several inflammatory pain models. However, less is known about the effect of analgesics on burrowing in neuropathic pain models and no studies have determined burrowing performance in models of diabetes-associated...
In Alzheimer’s disease (AD) many indicators point to a central role for poor axonal transport, but the potential for stimulating axonal transport to alleviate the disease remains largely untested. Previously we reported enhanced anterograde axonal transport of mitochondria in 8-11 months old MAPTP301L knockin mice, a genetic model of FTDP-17T. In t...
