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Andrew N. Clarkson

Researcher at University of Otago

Publications -  98
Citations -  3802

Andrew N. Clarkson is an academic researcher from University of Otago. The author has contributed to research in topics: Stroke & Neuroprotection. The author has an hindex of 28, co-authored 82 publications receiving 2908 citations. Previous affiliations of Andrew N. Clarkson include University of California, Los Angeles & University of Sydney.

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Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke

TL;DR: This work shows that after a stroke in mice, tonic neuronal inhibition is increased in the peri-infarct zone, and identifies new pharmacological targets that provide the rationale for a novel strategy to promote recovery after stroke and possibly other brain injuries.
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Current and novel polymeric biomaterials for neural tissue engineering

TL;DR: Most of neural tissue engineering applications are in pre-clinical study, in particular for use in the central nervous system, however collagen polymer conduits aimed at regeneration of peripheral nerves have already been successfully tested in clinical trials.
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AMPA Receptor-Induced Local Brain-Derived Neurotrophic Factor Signaling Mediates Motor Recovery after Stroke

TL;DR: Findings indicate that the role of glutamate signaling through the AMPAR changes over time in stroke: early potentiation of AMPAR signaling worsens stroke damage, whereas later potentiated of the same signaling system improves functional recovery.
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A role for ephrin-A5 in axonal sprouting, recovery, and activity-dependent plasticity after stroke.

TL;DR: Combined blockade of ephrin-A5 and forced use of the affected limb promote new and surprisingly widespread axonal projections within the entire cortical hemisphere ipsilateral to the stroke, indicating that stroke activates a newly described membrane-bound astrocyte growth inhibitor to limit neuroplasticity, activity-dependent axonal sprouting, and recovery in the adult.
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Neuroprotective effects of (–)-epigallocatechin gallate following hypoxia-ischemia-induced brain damage: novel mechanisms of action

TL;DR: The in vivo neuroprotective effects of EGCG are not exclusively due to its antioxidant effects but involve more complex signal transduction mechanisms, including modulation of NOS isoforms and preservation of mitochondrial complex activity and integrity.