Kaitlyn
@Crambberriee
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Junior Research Fellow at St. John's College, Oxford Vancouver, BC 🇨🇦
Oxford, England
Joined October 2011
Check out ASAPs team Craggs latest preprint on the selective vulnerability of Anxa1+ dopamine neurons in PD! . @CraggASAP @meletislab @WadeMartinsLab.
Anxa1+ dopamine neuron vulnerability defines prodromal Parkinson's disease bradykinesia and procedural motor learning impairment #biorxiv_neursci.
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RT @biorxiv_neursci: Anxa1+ dopamine neuron vulnerability defines prodromal Parkinson's disease bradykinesia and procedural motor learning….
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RT @gsgothard: 🚨new preprint alert!🚨 very excited to share the story of my PhD work :) including: development of excitatory-inhibitory circ….
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RT @WadeMartinsLab: Delighted that @quyentbd paper “Early deficits in an in vitro striatal microcircuit model carrying the #Parkinson's GBA….
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Very excited to share that our preprint is online now! @Andrea_Loreto1 and I show that SARM1 neurotoxicity is reversible and can be prevented in human neurons using ASOs. Massive thanks to the whole team! @WadeMartinsLab @Lab_Coleman @KavliOxford.
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RT @biorxiv_neursci: SARM1 activation induces reversible mitochondrial dysfunction and can be prevented in human neurons by antisense oligo….
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RT @Andrea_Loreto1: Our latest preprint is out! We developed ASOs targeting human SARM1, and report exciting mechanistic insights showing t….
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RT @BryanNgZH: Happy to share my 2nd iPSC paper from my PhD studies with @WadeMartinsLab at We showed that depleti….
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RT @CCSF_Scholar: Thank you to @CanUKFoundation @MapleTrust @CanadianUK @RobertRAFry and @RalphGoodale for celebrating our scholars with us….
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RT @hmg_journal: SEPT 15 2023 Issue: Cover: Mitochondrial dysfunction and mitophagy defects in LRRK2-R1441C Parkin….
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RT @BVahsen: Delighted to share our paper @NatureComms. We show that C9orf72-#ALS iPSC microglia are pro-inflammatory and toxic to co-cultu….
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RT @BRyanLab2: Our new paper is out in @hmg_journal! We show impaired mitophagy in LRRK2 R1441C iPSC-derived dopaminergic neurons from peo….
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Check out new work from our lab exploring mitochondrial dysfunction in Parkinson's disease. Congrats to all authors, especially @Marta_Madureira on her first first author paper! 🥳.
New research from @WadeMartinsLab & colleagues explores mitochondrial dysfunction & mitophagy defects in LRRK2-R1441C-associated #Parkinsons models; Also shows LRRK2 interaction with MIRO1 occurs at mitochondria, in a genotype-independent manner.
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RT @Brain1878: Cramb et al. review the evidence for dopamine release deficits prior to neurodegeneration in Parkinson’s disease, and highli….
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RT @MichaelOkun: Dopamine release deficits in #Parkinsons there is actually dysfunction or dysregulation of axonal dopamine release before….
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RT @ScienceofPD: New review from @Crambberriee @DayneBeccano @StephCragg & @WadeMartinsLab explores the question (& evidence) of whether th….
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Finally a massive thank you to funding bodies @ASAP_Research @NSERC_CRSNG @StJohnsOx and @CCSF67 for supporting this work!.
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Cell death and loss of DA are often used interchangeably to explain motor symptoms in PD. We highlight a critical distinction between these two concepts: is synaptic dysfunction an innocent bystander indicating imminent cellular demise or does it contribute to symptom onset?.
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These questions include: how do other neuronal and non-neuronal cell types drive or protect from DA release defects in PD? How might co-transmission of other neurotransmitters from DA neurons contribute to disease pathogenesis?.
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Here, we explore the evidence that dopamine (DA) release defects are consistently observed early in a broad range of genetic models of Parkinson’s disease (PD). We discuss the known mechanisms by which they occur and remaining questions we should aim to address as a field.
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