Lawrence Moon

ORCID: 0000-0001-9622-0312
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About
Contact & Profiles
Research Areas
  • Nerve injury and regeneration
  • Spinal Cord Injury Research
  • Neurogenesis and neuroplasticity mechanisms
  • Virus-based gene therapy research
  • Animal testing and alternatives
  • RNA Interference and Gene Delivery
  • Nerve Injury and Rehabilitation
  • Axon Guidance and Neuronal Signaling
  • Proteoglycans and glycosaminoglycans research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenetic and Muscular Disorders Research
  • Parkinson's Disease Mechanisms and Treatments
  • CRISPR and Genetic Engineering
  • Cerebral Palsy and Movement Disorders
  • Botulinum Toxin and Related Neurological Disorders
  • Neurological Disease Mechanisms and Treatments
  • RNA regulation and disease
  • Calpain Protease Function and Regulation
  • Computational Drug Discovery Methods
  • Meta-analysis and systematic reviews
  • Wound Healing and Treatments
  • Transcranial Magnetic Stimulation Studies
  • Neurological Disorders and Treatments
  • Pain Mechanisms and Treatments
  • Sports injuries and prevention

King's College London
2014-2023

University College London
2016-2023

University of London
2016-2023

Spark Therapeutics (United States)
2022

John Wiley & Sons (United States)
2019

Hudson Institute
2019

Age UK
2018

École Polytechnique Fédérale de Lausanne
2018

British Pharmacological Society
2015

Wolfson Medical Center
2006-2013

ABSTRACT While neuroimmune interactions are increasingly recognized as important in nociceptive processing, the nature and functional significance of these is not well defined. There multiple reports that activation spinal microglia a critical event generation neuropathic pain behaviors but mediators this remain disputed. Here we show chemokine CCL2, produced by both damaged undamaged primary sensory neurons states rats, released an activity dependent manner from central terminals fibres. We...

10.1016/j.ejpain.2008.04.017 article EN European Journal of Pain 2008-06-13

Stroke is the dominant cause of sensorimotor disability that primarily affects elderly. We now show neuroplasticity and functional recovery after stroke constrained by inhibitory chondroitin sulphates. In two blinded, randomized preclinical trials, degradation sulphate using chondroitinase ABC reactivated promoted in elderly rats. Three days stroke, was microinjected into cervical spinal cord to induce localized plasticity forelimb circuitry. Chondroitinase effectively removed from...

10.1093/brain/aws027 article EN Brain 2012-03-06

Addressing the common problems that researchers encounter when designing and analysing animal experiments will improve reliability of in vivo research. In this article, Experimental Design Assistant (EDA) is introduced. The EDA a web-based tool guides researcher through experimental design analysis process, providing automated feedback on proposed generating graphical summary aids communication with colleagues, funders, regulatory authorities, wider scientific community. It have an important...

10.1371/journal.pbio.2003779 article EN cc-by PLoS Biology 2017-09-28

After a spinal cord injury, axons fail to regenerate in the adult mammalian central nervous system, leading permanent deficits sensory and motor functions. Increasing neuronal activity after an injury using electrical stimulation or rehabilitation can enhance plasticity result some degree of recovery; however, underlying mechanisms remain poorly understood. We found that placing mice enriched environment before enhanced proprioceptive dorsal root ganglion neurons, lasting increase their...

10.1126/scitranslmed.aaw2064 article EN Science Translational Medicine 2019-04-10

Abstract Although transplanted Schwann cells (SCs) can promote axon regeneration and remyelination improve recovery in models of spinal cord injury, little is known about their survival how they interact with host tissue. Using labeled SCs from transgenic rats expressing human placental alkaline phosphatase (PLAP), SC a contusion lesion was assessed. Few PLAP survived at 2 weeks after acute transplantation. They died early due to necrosis apoptosis. Delaying transplantation until 7 days...

10.1002/glia.20287 article EN Glia 2005-11-02

Abstract In this study we investigated whether CNS axons regenerate following attenuation of scar formation using a combination antibodies against two isoforms transforming growth factor beta (TGFβ). Anaesthetized adult rats were given unilateral mechanical lesions the nigrostriatal tract. Implantation transcranial cannulae allowed wounds to be treated with TGFβ 1 and 2 once daily for 10 days postaxotomy. Eleven post‐transection brains from animals under terminal anaesthesia recovered...

10.1046/j.0953-816x.2001.01795.x article EN European Journal of Neuroscience 2001-11-01

There is an urgent need for a therapy that reverses disability after stroke when initiated in time frame suitable the majority of new victims. We show here intramuscular delivery neurotrophin-3 (NT3, encoded by NTF3 ) can induce sensorimotor recovery treatment 24 h stroke. Specifically, two randomized, blinded preclinical trials, we improved sensory and locomotor function adult (6 months) elderly (18 rats treated following cortical ischaemic with human NT3 delivered using clinically approved...

10.1093/brain/awv341 article EN cc-by Brain 2015-11-27

Growth of intact axons noninjured neurons, often termed collateral sprouting, contributes to both adaptive and pathological plasticity in the adult nervous system, but intracellular factors controlling this growth are largely unknown. An automated functional assay genes regulated sensory neurons from rat vivo spared dermatome model sprouting identified adaptor protein CD2-associated (CD2AP; human CMS) as a positive regulator axon growth. In non-neuronal cells, CD2AP, like other proteins,...

10.1523/jneurosci.2423-15.2016 article EN cc-by-nc-sa Journal of Neuroscience 2016-04-13

Brain and spinal injury reduce mobility often impair sensorimotor processing in the cord leading to spasticity. Here, we establish that complete transection of corticospinal pathways pyramids impairs locomotion leads increased spasms excessive mono- polysynaptic low threshold reflexes rats. Treatment affected forelimb muscles with an adeno-associated viral vector (AAV) encoding human Neurotrophin-3 at a clinically-feasible time-point after reduced normalized short latency Hoffmann reflex...

10.7554/elife.18146 article EN cc-by eLife 2016-10-19
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