@Crambberriee

Junior Research Fellow at St. John's College, Oxford Vancouver, BC 🇨🇦

 Oxford, England
Joined October 2011
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  • Followers216
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Check out ASAPs team Craggs latest preprint on the selective vulnerability of Anxa1+ dopamine neurons in PD! @CraggASAP @meletislab @WadeMartinsLab
bioRxiv Neuroscience@biorxiv_neursci22 Dec 2024
Anxa1+ dopamine neuron vulnerability defines prodromal Parkinson's disease bradykinesia and procedural motor learning impairment biorxiv.org/cgi/content/shor… #biorxiv_neursci
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Anxa1+ dopamine neuron vulnerability defines prodromal Parkinson's disease bradykinesia and procedural motor learning impairment biorxiv.org/cgi/content/shor… #biorxiv_neursci
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Delighted that @quyentbd paper “Early deficits in an in vitro striatal microcircuit model carrying the #Parkinson's GBA-N370S mutation” is now published pubmed.ncbi.nlm.nih.gov/3860… @norabv139 @OxfordDPAG @KavliOxford @DPAGAthenaSwan

Early deficits in an in vitro striatal microcircuit model carrying the Parkinson's GBA-N370S...

Understanding medium spiny neuron (MSN) physiology is essential to understand motor impairments in Parkinson's disease (PD) given the architecture of the basal ganglia. Here, we developed a custom...

pubmed.ncbi.nlm.nih.gov
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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 biorxiv.org/cgi/content/shor…
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SARM1 activation induces reversible mitochondrial dysfunction and can be prevented in human neurons by antisense oligonucleotides biorxiv.org/cgi/content/shor… #biorxiv_neursci
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Our latest preprint is out! We developed ASOs targeting human SARM1, and report exciting mechanistic insights showing that neurotoxicity and mitochondrial dysfunction are reversible, even hours after SARM1 activation! In human neurons! Key implications for SARM1 therapies #SARM1
bioRxiv Neuroscience@biorxiv_neursci4 Apr 2024
SARM1 activation induces reversible mitochondrial dysfunction and can be prevented in human neurons by antisense oligonucleotides biorxiv.org/cgi/content/shor… #biorxiv_neursci
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Happy to share my 2nd iPSC paper from my PhD studies with @WadeMartinsLab at nature.com/articles/s41380-0…! We showed that depleting tau in human iPSC-derived neurons is protective against Abeta. It was a collaborative effort, extremely thankful to the team. #research #Alzheimer

Tau depletion in human neurons mitigates Aβ-driven toxicity

Molecular Psychiatry - Tau depletion in human neurons mitigates Aβ-driven toxicity

nature.com
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Thank you to @CanUKFoundation @MapleTrust @CanadianUK @RobertRAFry and @RalphGoodale for celebrating our scholars with us this evening. We wish you all the best with your exciting work.
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SEPT 15 2023 Issue: academic.oup.com/hmg/issue/3… Cover: Mitochondrial dysfunction and mitophagy defects in LRRK2-R1441C Parkinson’s disease models doi.org/10.1093/hmg/ddad102
Cover: These images illustrate the impairment of mitophagy caused by LRRK2 R1441C mutations in rat BAC-transgenic primary cortical neuronal cultures and human iPSC-derived dopaminergic neurons. Mitophagy has been assessed using two mitophagy reporters MitoQC and mtKeima) that show different fluorescent profiles when in neutral or acidic environments. The ability of cells to induce mitophagy was assessed by induction of mitophagy with CCCP.

ALT Cover: These images illustrate the impairment of mitophagy caused by LRRK2 R1441C mutations in rat BAC-transgenic primary cortical neuronal cultures and human iPSC-derived dopaminergic neurons. Mitophagy has been assessed using two mitophagy reporters MitoQC and mtKeima) that show different fluorescent profiles when in neutral or acidic environments. The ability of cells to induce mitophagy was assessed by induction of mitophagy with CCCP.

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Delighted to share our paper @NatureComms. We show that C9orf72-#ALS iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9. Special thanks to all the amazing people from @MNDOxford who contributed! @NDCNOxford @KavliOxford nature.com/articles/s41467-0…
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Our new paper is out in @hmg_journal! We show impaired mitophagy in LRRK2 R1441C iPSC-derived dopaminergic neurons from people with Parkinson's and primary cortical neurons. academic.oup.com/hmg/article… Some of Matt's cortical cultures even made the front cover!
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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! 🥳
The Science of Parkinson's@ScienceofPD30 Jun 2023
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 academic.oup.com/hmg/advance…
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Kaitlyn retweeted
Brain@Brain187816 Apr 2023
Cramb et al. review the evidence for dopamine release deficits prior to neurodegeneration in Parkinson’s disease, and highlight mechanisms by which these deficits can occur. bit.ly/3GOTw2d
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Dopamine release deficits in #Parkinsons there is actually dysfunction or dysregulation of axonal dopamine release before cell loss. Blows your mind right, think about it, and read this @Brain1878 and it will make sense. academic.oup.com/brain/advan…
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New review from @Crambberriee @DayneBeccano @StephCragg & @WadeMartinsLab explores the question (& evidence) of whether there is impaired dopamine release in #Parkinsons before there is any cell loss academic.oup.com/brain/advan…
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Very excited to finally share our review on dopamine release defects in Parkinson’s disease now available open access at Brain! @WadeMartinsLab @DayneBeccano @StephCragg @KavliOxford @ASAP_Research academic.oup.com/brain/advan…

Impaired dopamine release in Parkinson’s disease

Cramb et al. review the evidence for dopamine release deficits prior to neurodegeneration in Parkinson’s disease. They highlight the mechanisms by which th

academic.oup.com
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more replies
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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Finally a massive thank you to funding bodies @ASAP_Research @NSERC_CRSNG @StJohnsOx and @CCSF67 for supporting this work!
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