Laura M Huckins on Muck Rack

Laura M Huckins

New York
As seen in: Nature, Cell Press, Cell Reports, EBioMedicine, The Lancet, medRxiv, The Journal of Clinical Investigation, Psiquiatria.com, Biological Psychiatry
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Articles

Single-nucleus epigenomic dysregulation unmasks genetic risk-associated neurodegenerative glia states

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By Xia Han, Gregory Rosenberg, Tao Zhang, Chia-Yi Lee, Ashvin Ravi, Mikhail Melnik, Salvatore Spina, Alissa L. Nana, Lea T. Grinberg, William W. Seeley, Karen H. Gylys, Laura M Huckins, Towfique Raj, Jessica Rexach, Vivianne M. Kisling, Tina Bilousova
| Nature Verified
Abstract The accumulation of abnormal tau protein selectively affects distinct brain regions and specific populations of neurons and glial cells in tau-related dementias, such as Alzheimer’s disease, Pick’s disease and progressive supranuclear palsy. Although the three disorders share the feature of tau protein pathology, the regulatory circuitry of non-coding genetic variants underlying risk-associated cell states remains to be elucidated.
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Transcriptomic and phenotypic convergence of neurodevelopmental disorder risk genes in vitro and in vivo

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By Meilin Fernandez Garcia, Kayla G Retallick-Townsley, April Pruitt, Elizabeth Davidson, Novin Balafkan, Jonathan Warrell, Zhiyuan Chu, Yi Dai, Sarah Fitzpatrick Verified, Ran Meng, Annabel Sen, Sophie Cohen, Suha Khan, Charlotte Becker, Jenny Liu, Susanna Liu, Sadaf Ghorbani, Marisa DeCiucis, Prashant Emani, Huanyao Gao, Hongying Shen, Mark Gerstein, Zuoheng Wang, Laura M Huckins, Ellen Hoffman, Kristen J. Brennand, Tzu-Chieh Huang, Alfred Kibowen, Olivia Livoti, Grace Dossou, Jen Cheung, P. J. Michael Deans
| Nature Verified
Abstract Diverse risk genes have been identified for neurodevelopmental disorders (NDDs), but how these genes converge on similar biological pathways in neurons, and thus give rise to similar phenotypes, is unclear.
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Functional implications of polygenic risk for schizophrenia in human neurons - Nature Communications

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By Aiqun Li, Judit González, Georgios Voloudakis, Minghui Wang, John F. Fullard, Kiran Girdhar, Eli A Stahl, Schahram Akbarian, Panos Roussos, Paul F. O’Reilly, Laura M Huckins
| Nature Verified
Abstract Genome wide association studies of schizophrenia reveal a complex polygenic risk architecture comprised of hundreds of risk variants; most are common in the population, non-coding, and act by genetically regulating the expression of one or more gene targets (“eGenes”). It remains unclear how the myriad genetic variants that are predicted to confer individually small effects combine to yield substantial clinical impacts in aggregate.
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