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Christopher J. H. Elliott

Researcher at University of York

Publications -  80
Citations -  7479

Christopher J. H. Elliott is an academic researcher from University of York. The author has contributed to research in topics: Dopaminergic & Lymnaea stagnalis. The author has an hindex of 27, co-authored 79 publications receiving 6854 citations. Previous affiliations of Christopher J. H. Elliott include Max Planck Society & University of Warwick.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Comparative neuroethology of feeding control in molluscs

TL;DR: The conclusions derived from studies on gastropod feeding are generally consistent with those from other systems, but often provide more detailed information on the behavioural function of a particular property of the nervous system.
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Neuromuscular organization and aminergic modulation of contractions in the Drosophila ovary

TL;DR: A new model of tissue-specific actions of octopamine is proposed, in which strengthening of peritoneal sheath contractions, coupled with relaxation of the oviduct, eases ovulation in female flies with mutations in the octopaminergic system.
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Loss and gain of Drosophila TDP-43 impair synaptic efficacy and motor control leading to age-related neurodegeneration by loss-of-function phenotypes

TL;DR: Data suggest that dysfunction of Drosophila TDP-43 triggers a cascade of events leading to loss-of-function phenotypes whereby impaired synaptic transmission results in defective motor behavior and progressive deconstruction of neuronal connections, ultimately causing age-related neurodegeneration.
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UDCA exerts beneficial effect on mitochondrial dysfunction in LRRK2G2019S carriers and in vivo

TL;DR: There is clear preclinical impairment of mitochondrial function in NM-LRRK2G 2019S that is distinct from the mitochondrial impairment observed in parkin-related PD, and the beneficial effect of UDCA on mitochondrial function as well as on the function of dopaminergic neurons expressing LRRK 2G2019S suggests that UDCA is a promising drug for future neuroprotective trials.