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John Dunlop

Researcher at AstraZeneca

Publications -  99
Citations -  4705

John Dunlop is an academic researcher from AstraZeneca. The author has contributed to research in topics: Agonist & Receptor. The author has an hindex of 37, co-authored 98 publications receiving 4276 citations. Previous affiliations of John Dunlop include Princeton University.

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High-throughput electrophysiology: an emerging paradigm for ion-channel screening and physiology

TL;DR: This Review provides an update on the current state-of-the-art for the various automated electrophysiology platforms that are now available and critically evaluates their impact in terms of ion-channel screening, lead optimization and the assessment of cardiac ion- channel safety liability.
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Protein misfolding in neurodegenerative diseases: implications and strategies

TL;DR: Therapeutic options are currently being explored that target different steps in the production and processing of proteins implicated in neurodegenerative disease, including synthesis, chaperone-assisted folding and trafficking, and degradation via the proteasome and autophagy pathways.
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Improving and Accelerating Drug Development for Nervous System Disorders

TL;DR: To accelerate nervous system drug development, the Institute of Medicine's Forum on Neuroscience and Nervous System Disorders has hosted a series of public workshops that brought together representatives of industry, government, academia, and patient groups to discuss these challenges and offer potential strategies to improve the translational neuroscience.
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A cog in cognition: How the α7 nicotinic acetylcholine receptor is geared towards improving cognitive deficits

TL;DR: Efficacy of alpha7 nAChR agonists across a range of cognitive processes ranging from pre-attentive to attentive states and working and recognition memory provides a solid basis for their pro-cognitive effects.
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Impaired Spinal Cord Glutamate Transport Capacity and Reduced Sensitivity to Riluzole in a Transgenic Superoxide Dismutase Mutant Rat Model of Amyotrophic Lateral Sclerosis

TL;DR: Estimation of synaptosomal glutamate transport activity in a recently developed transgenic rat model of amyotrophic lateral sclerosis overexpressing the G93A Cu2+/Zn2+ superoxide dismutase (SOD1) mutation revealed a loss of GLT-1 as well as qualitative changes in GLAST but no measurable changes in EAAC1, indicating that deficits in glutamate transporters in this rat model may be glial specific.