Hanna E. Stevens

ORCID: 0000-0002-3906-0786
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About
Contact & Profiles
Research Areas
  • Neuroendocrine regulation and behavior
  • Stress Responses and Cortisol
  • Birth, Development, and Health
  • Autism Spectrum Disorder Research
  • Child and Adolescent Psychosocial and Emotional Development
  • Tryptophan and brain disorders
  • Genetics and Neurodevelopmental Disorders
  • Maternal Mental Health During Pregnancy and Postpartum
  • Attention Deficit Hyperactivity Disorder
  • Neurogenesis and neuroplasticity mechanisms
  • Anesthesia and Neurotoxicity Research
  • Neonatal and fetal brain pathology
  • Heavy Metal Exposure and Toxicity
  • Congenital heart defects research
  • Pesticide Exposure and Toxicity
  • Toxic Organic Pollutants Impact
  • Parkinson's Disease Mechanisms and Treatments
  • Pregnancy and preeclampsia studies
  • Pluripotent Stem Cells Research
  • Telomeres, Telomerase, and Senescence
  • Family and Disability Support Research
  • Reproductive System and Pregnancy
  • Neurotransmitter Receptor Influence on Behavior
  • Hearing Loss and Rehabilitation
  • Adolescent and Pediatric Healthcare

University of Iowa
2016-2025

Intel (United States)
2024

Yale University
2008-2023

Carilion Clinic
2023

University at Buffalo, State University of New York
2023

University College London
2023

Virginia Tech
2023

Jacobs (United Kingdom)
2023

Carver Bible College
2020

Universidade Estadual Paulista (Unesp)
2018

Natalia Dominik Stefania Magri Riccardo Currò Elena Abati Stefano Facchini and 95 more Marinella Corbetta Hannah Macpherson Daniela Di Bella Elisa Sarto Igor Stevanovski Sanjog R. Chintalaphani Fulya Akçimen Arianna Manini Elisa Vegezzi Ilaria Quartesan Kylie-Ann Montgomery Valentina Pirota Emmanuele Crespan Cecilia Perini Glenda Paola Grupelli Pedro José Tomaselli Wilson Marques John C. Ambrose Prabhu Arumugam Emma L. Baple Marta Bleda F. Boardman-Pretty J. M. Boissiere C. R. Boustred Helen Brittain Mark J. Caulfield Gary C.W. Chan C.E.H. Craig Louise C. Daugherty Anna de Burca A. Devereau Greg Elgar Rebecca E. Foulger Tom Fowler Pedro Furió‐Tarí Emil K. Gustavsson Janna M. Hackett Dina Halai Angela Hamblin S Henderson J. Holman Tim Hubbard Kristina Ibáñez Robert W. Jackson J. Louise Jones Dalia Kasperavičiūtė Melis Kayikci L. Lahnstein Keith A. Lawson S. E. A. Leigh I. U. S. Leong Fernando López F. Maleady-Crowe James Mason Ellen M. McDonagh Loukas Moutsianas Michael Mueller Nirupa Murugaesu Anna C. Need Chris A. Odhams Christine Patch D. Perez-Gil Dimitris Polychronopoulos J. Pullinger T. Rahim Augusto Rendon Pablo Riesgo-Ferreiro Thomas R. Rogers Mina Ryten Bianca Rugginini K Savage K. Sawant Richard H. Scott Afshan Siddiq A. Sieghart Damian Smedley Katherine R. Smith Alona Sosinsky W. Spooner Hanna E. Stevens Ashley Stuckey Rukhsana Sultana Ellen Thomas Simon R. Thompson Carolyn Tregidgo Arianna Tucci Edward E. Walsh Scott Watters M. J. Welland Eleanor Williams Kate Witkowska Scott Wood Magdalena Zarowiecki Joseph Shaw James M. Polke

Cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS) is an autosomal recessive neurodegenerative disease, usually caused by biallelic AAGGG repeat expansions in RFC1. In this study, we leveraged whole genome sequencing data from nearly 10 000 individuals recruited within the Genomics England project to investigate normal pathogenic variation of RFC1 repeat. We identified three novel motifs, AGGGC (n = 6 five families), AAGGC 2 one family) AGAGG 1), associated with CANVAS...

10.1093/brain/awad240 article EN cc-by Brain 2023-07-14

There is increasing appreciation for the neurodevelopmental underpinnings of many psychiatric disorders. Disorders that begin in childhood such as autism, language disorders or mental retardation well adult-onset may have origins early neurodevelopment. Neural stem cells (NSCs) can be defined self-renewing, multipotent are present both embryonic and adult brain. Several recent research findings demonstrate illness with abnormal specification, growth, expansion differentiation NSCs. For...

10.3389/fnins.2010.00059 article EN cc-by Frontiers in Neuroscience 2010-01-01

ABSTRACT Prenatal stress is associated with altered behavioral, cognitive, and psychiatric outcomes in offspring. Due to the importance of GABAergic systems normal development disorders, prenatal effects on these neurons have been investigated animal models. delays progenitor migration, but significance early developmental disruptions for continued cells juvenile brain unclear. Here, we examined populations adult medial frontal cortex (mFC) hippocampus through stereological counting, gene...

10.1002/dneu.22376 article EN Developmental Neurobiology 2016-01-02

Highlights•Postpartum liver circulates NAD metabolites to increase mammary NAD+ and NADP+ >20-fold•NR supplementation superinduces prolactin, biosynthetic programs, lactation•Weanlings of NR-fed mothers are hypoglycemia resistant advanced in motor learning•Adult offspring retain striking physical behavioral advantagesSummaryConditions metabolic stress dysregulate the metabolome. By restoring NAD, nicotinamide riboside (NR) provides resistance such conditions. We tested hypotheses that...

10.1016/j.celrep.2019.01.007 article EN cc-by Cell Reports 2019-01-01

To understand the role of specific fibroblast growth factor receptors (FGFRs) in cortical development, we conditionally inactivated Fgfr2 or both Fgfr1 and [ conditional knock-out (cKO) double mice, respectively] radial glial cells dorsal telencephalon. are necessary for attainment a normal number excitatory neurons cerebral cortex. The action FGF appears to be through increasing self-renewal neuronal precursors within ventricular zone. Volume measurements, assessments neuron number, areal...

10.1523/jneurosci.5837-09.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-04-21

Prenatal stress, a risk factor for neurodevelopmental disorders (NDDs), leads to immune alterations, including offspring neuroimmune cells. Differences in outcomes may arise from whether the extent of prenatal stress crosses "thresholds" effects on specific outcomes. Therefore, we sought determine using models with different extents stress. We focused striatal outcomes, because their relevance NDDs. Pregnant CD1 mice were assigned four groups (each: N=6): no (NoS) or one following stressors...

10.1101/2025.01.30.635666 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-01-30

Pyrethroid insecticides represent a broad class of chemicals used widely in agriculture and household applications. Human studies show mixed effects maternal pyrethroid exposure on fetal growth neurodevelopment. Assessment shared metabolites as biomarker for obscures specific within this broader class. To better characterize development, we investigated to permethrin, type I pyrethroid, α-cypermethrin, II development mice. Pregnant CD1 mice were exposed permethrin (1.5, 15, or 50 mg/kg),...

10.1101/2025.03.16.643434 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-03-17

Insulin-like growth factor 1 (IGF1) is produced primarily in the placenta utero and an essential hormone for neurodevelopment. Specifically, how placental IGF1 production persistently influences brain unclear. This study evaluated effects of Igf1 overexpression on embryonic postnatal development, particularly striatum, a region highly linked to neurodevelopmental disorders. Placental was overexpressed via placental-targeted CRISPR manipulation. altered structure function distinctly females...

10.1101/2025.03.27.644829 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-03-29

Maternal stress during pregnancy is associated with an increased risk of psychopathology in offspring. Resident immune cells the brain, microglia, may be mediators prenatal and altered neurodevelopment. Here, we demonstrate that neither exogenous pro-inflammatory cytokine, interleukin-1β (IL-1β), nor glucocorticoid hormone, corticosterone, recapitulated full effects on morphology microglial cortical plate embryonic mice; IL-1β showed greater similarity to microglia. Unexpectedly, oil vehicle...

10.1186/s12974-018-1079-7 article EN cc-by Journal of Neuroinflammation 2018-02-16
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