Author

Mandi E. Schmidt

University of British Columbia

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Neuroscience· 5

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Organism:mouse· 5 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Assay:electronic health records· 1 Assay:protein structure· 1

Frequent Co-Authors

Michael R. HaydeniD· 5 shared Dale D. O. MartiniD· 3 shared Nicholas S. CaroniD· 3 shared Amber L. SouthwelliD· 2 shared Yen T.N. Nguyen· 2 shared Amy Smith-DijakiD· 1 shared Caodu Buren· 1 shared Colton M. Tom· 1 shared

Activity by Year

2018-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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5 shared papersNeuroscience

Michael R. HaydenORCID

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5 papers

Recent·Most cited

Rescue of aberrant huntingtin palmitoylation ameliorates mutant huntingtin-induced toxicity

Fanny L. Lemarié, Nicholas S. Caron, Shaun S. Sanders, Mandi E. Schmidt, Yen T.N. Nguyen, Seung‐Hyun Ko, Xiaohong Xu, Mahmoud A. Pouladi, Dale D. O. Martin, Michael R. Hayden

This study investigates the role of HTT palmitoylation in Huntington disease by assessing its dysregulation in models and showing that modulating palmitoylation reduces mHTT toxicity.

Neurobiology of Disease · Aug 11, 2021Peer-reviewedNeuroscience

The interaction of aging and oxidative stress contributes to pathogenesis in mouse and human Huntington disease neurons

Emily Machiela, Ritika Jeloka, Nicholas S. Caron, Shagun Mehta, Mandi E. Schmidt, Helen J. E. Baddeley, Colton M. Tom, Nalini Polturi, Yuanyun Xie, Virginia B. Mattis, Michael R. Hayden, Amber L. Southwell

This study investigates how aging and oxidative stress interact in Huntington disease neurons from mice and humans, finding that aging accelerates mutant HTT accumulation and increases oxidative stress sensitivity.

Frontiers in Aging Neuroscience · Sep 18, 2020Peer-reviewedNeuroscience

Spontaneous Axonal ER Ca2+ Waves Mediate a Shift From Action Potential-Dependent to Independent Glutamate Release in the YAC128 HD-Model

James P. Mackay, Amy Smith-Dijak, Ellen T. Koch, Peng Zhang, Evan Fung, Wissam B. Nassrallah, Caodu Buren, Mandi E. Schmidt, Michael R. Hayden, Lynn A. Raymond

The paper shows that spontaneous axonal ER Ca2+ waves increase miniature glutamate release while reducing AP-dependent release in YAC128 HD-model neurons.

bioRxiv · Jan 31, 2020 · PreprintNeuroscience

Identification of a novel caspase cleavage site in huntingtin that regulates mutant huntingtin clearance.

Dale D. O. Martin, Mandi E. Schmidt, Yen Thi-Kim Nguyen, Nikola Lazic, Michael R. Hayden

The paper identifies a new caspase-1 cleavage site in mutant huntingtin that promotes its clearance and reduces aggregation.

The FASEB Journal · Nov 13, 2018Peer-reviewedNeuroscience

Feeding Schedule And Proteolysis Regulate Autophagic Clearance Of Mutant Huntingtin

Dagmar E. Ehrnhoefer, Dale D. O. Martin, Mandi E. Schmidt, Xiaofan Qiu, Safia Ladha, Nicholas S. Caron, Niels Henning Skotte, Yen T.N. Nguyen, Kuljeet Vaid, Amber L. Southwell, Sabine Engemann, Sonia Franciosi, Michael R. Hayden

This study shows that scheduled feeding and prevention of caspase-6 cleavage enhance autophagic clearance of mutant huntingtin in HD models and patients.

Acta Neuropathologica Communications · Feb 26, 2018Peer-reviewedNeuroscience