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Kit Wu

Researcher at Imperial College London

Publications -  44
Citations -  3085

Kit Wu is an academic researcher from Imperial College London. The author has contributed to research in topics: Parkinson's disease & Serotonergic. The author has an hindex of 22, co-authored 35 publications receiving 2755 citations.

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Parkinson's Disease Symptoms: The Patient's Perspective

TL;DR: It is suggested that as the disease advances the most troublesome issues that patients perceive are the lack of response to medication and the nonmotor aspects of the disease, highlighting the importance of assessment and patient‐centered management in the follow-up of these patients.
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Serotonergic Neurons Mediate Dyskinesia Side Effects in Parkinson’s Patients with Neural Transplants

TL;DR: Two patients with Parkinson’s disease, successfully treated with fetal tissue transplants more than a decade ago, developed troublesome involuntary movements, which were determined to be a result of an overabundance of serotonin-using neurons that developed from the graft, and strategies for avoiding and treating graft-induced dyskinesias that result from cell therapies for Parkinson's disease are suggested.
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Cue-induced striatal dopamine release in Parkinson's disease-associated impulsive-compulsive behaviours

TL;DR: The heightened response of striatal reward circuitry to heterogeneous reward-related visual cues among a group of patients with different impulsive-compulsive behaviours is consistent with a global sensitization to appetitive behaviours with dopaminergic therapy in vulnerable individuals.
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Staging of serotonergic dysfunction in Parkinson's Disease: An in vivo 11C-DASB PET study

TL;DR: The results suggest that progressive non-linear serotonergic dysfunction occurs in PD but it does not determine levels of disability and chronic exposure to dopaminergic therapy does not appear to influence SERT binding.
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Serotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson’s disease patients

TL;DR: Striatal serotonergic terminals contribute to LIDs pathophysiology via aberrant processing of exogenous levodopa and release of dopamine as false neurotransmitter in the denervated striatum of PD patients with LIDs, which supports the development of selective serotonin receptor type 1A agonists for use as antidyskinetic agents in PD.