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Article: Neonatal Subarachnoid Hemorrhage Disrupts Multiple Aspects of Cerebellar Development.

Butler, David F / Skibo, Jonathan / Traudt, Christopher M / Millen, Kathleen J

bioRxiv : the preprint server for biology

2023

Abstract: Over the past decade, survival rates for extremely low gestational age neonates (ELGANs; <28 weeks gestation) has markedly improved. Unfortunately, a significant proportion of ELGANs will suffer from neurodevelopmental dysfunction. Cerebellar hemorrhagic ...

Abstract	Over the past decade, survival rates for extremely low gestational age neonates (ELGANs; <28 weeks gestation) has markedly improved. Unfortunately, a significant proportion of ELGANs will suffer from neurodevelopmental dysfunction. Cerebellar hemorrhagic injury (CHI) has been increasingly recognized in the ELGANs population and may contribute to neurologic dysfunction; however, the underlying mechanisms are poorly understood. To address this gap in knowledge, we developed a novel model of early isolated posterior fossa subarachnoid hemorrhage (SAH) in neonatal mice and investigated both acute and long-term effects. Following SAH on postnatal day 6 (P6), we found significant decreased levels of proliferation with the external granular layer (EGL), thinning of the EGL, decreased Purkinje cell (PC) density, and increased Bergmann glial (BG) fiber crossings at P8. At P42, CHI resulted in decreased PC density, decreased molecular layer interneuron (MLI) density, and increased BG fiber crossings. Results from both Rotarod and inverted screen assays did not demonstrate significant effects on motor strength or learning at P35-38. Treatment with the anti-inflammatory drug Ketoprofen did not significantly alter our findings after CHI, suggesting that treatment of neuro-inflammation does not provide significant neuroprotection post CHI. Further studies are required to fully elucidate the mechanisms through which CHI disrupts cerebellar developmental programming in order to develop therapeutic strategies for neuroprotection in ELGANs.
Language	English
Publishing date	2023-02-10
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.10.528048
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Article: Neonatal subarachnoid hemorrhage disrupts multiple aspects of cerebellar development.

Butler, David F / Skibo, Jonathan / Traudt, Christopher M / Millen, Kathleen J

Frontiers in molecular neuroscience

2023 Volume 16, Page(s) 1161086

Abstract	Over the past decade, survival rates for extremely low gestational age neonates (ELGANs; <28 weeks gestation) has markedly improved. Unfortunately, a significant proportion of ELGANs will suffer from neurodevelopmental dysfunction. Cerebellar hemorrhagic injury (CHI) has been increasingly recognized in the ELGANs population and may contribute to neurologic dysfunction; however, the underlying mechanisms are poorly understood. To address this gap in knowledge, we developed a novel model of early isolated posterior fossa subarachnoid hemorrhage (SAH) in neonatal mice and investigated both acute and long-term effects. Following SAH on postnatal day 6 (P6), we found significant decreased levels of proliferation with the external granular layer (EGL), thinning of the EGL, decreased Purkinje cell (PC) density, and increased Bergmann glial (BG) fiber crossings at P8. At P42, CHI resulted in decreased PC density, decreased molecular layer interneuron (MLI) density, and increased BG fiber crossings. Results from both Rotarod and inverted screen assays did not demonstrate significant effects on motor strength or learning at P35-38. Treatment with the anti-inflammatory drug Ketoprofen did not significantly alter our findings after CHI, suggesting that treatment of neuro-inflammation does not provide significant neuroprotection post CHI. Further studies are required to fully elucidate the mechanisms through which CHI disrupts cerebellar developmental programming in order to develop therapeutic strategies for neuroprotection in ELGANs.
Language	English
Publishing date	2023-04-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2023.1161086
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Article ; Online: Human Cerebellar Development and Transcriptomics: Implications for Neurodevelopmental Disorders.

Haldipur, Parthiv / Millen, Kathleen J / Aldinger, Kimberly A

Annual review of neuroscience

2022 Volume 45, Page(s) 515–531

Abstract: Developmental abnormalities of the cerebellum are among the most recognized structural brain malformations in human prenatal imaging. Yet reliable information regarding their cause in humans is sparse, and few outcome studies are available to inform ... ...

Abstract	Developmental abnormalities of the cerebellum are among the most recognized structural brain malformations in human prenatal imaging. Yet reliable information regarding their cause in humans is sparse, and few outcome studies are available to inform prognosis. We know very little about human cerebellar development, in stark contrast to the wealth of knowledge from decades of research on cerebellar developmental biology of model organisms, especially mice. Recent studies show that multiple aspects of human cerebellar development significantly differ from mice and even rhesus macaques, a nonhuman primate. These discoveries challenge many current mouse-centric models of normal human cerebellar development and models regarding the pathogenesis of several neurodevelopmental phenotypes affecting the cerebellum, including Dandy-Walker malformation and medulloblastoma. Since we cannot model what we do not know, additional normative and pathological human developmental data are essential, and new models are needed.
MeSH term(s)	Animals ; Cerebellar Neoplasms ; Cerebellum ; Female ; Humans ; Macaca mulatta ; Mice ; Neurodevelopmental Disorders/genetics ; Neurodevelopmental Disorders/pathology ; Pregnancy ; Transcriptome
Language	English
Publishing date	2022-04-19
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	282459-0
ISSN	1545-4126 ; 0147-006X
ISSN (online)	1545-4126
ISSN	0147-006X
DOI	10.1146/annurev-neuro-111020-091953
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Article ; Online: Association between dietary patterns and periodontal disease: The OsteoPerio cohort study.

Yue, Yihua / Hovey, Kathleen M / LaMonte, Michael J / Wactawski-Wende, Jean / Andrews, Chris A / Millen, Amy E

Journal of clinical periodontology

2024

Abstract: Aim: To examine the association of dietary patterns with periodontal disease (PD) and its progression over 5 years.: Materials and methods: Analyses involved 1197 post-menopausal women from the OsteoPerio cohort. Dietary patterns assessed include ... ...

Abstract	Aim: To examine the association of dietary patterns with periodontal disease (PD) and its progression over 5 years. Materials and methods: Analyses involved 1197 post-menopausal women from the OsteoPerio cohort. Dietary patterns assessed include Healthy Eating Index-2015 (HEI), Alternative HEI (AHEI), Dietary Approaches to Stop Hypertension (DASH) and alternate Mediterranean Diet (aMed) at baseline (the average of two food frequency questionnaires administered between 1993 and 2001). At baseline and the 5-year follow-up, periodontal assessments evaluated alveolar crestal height (ACH), probing pocket depth (PPD), clinical attachment loss (CAL), percentage of gingival sites bleeding on probing (%BOP) and missing teeth due to PD. Linear and logistic regression were used to examine the associations. Results: Cross-sectionally, HEI and aMed were associated with smaller CAL and %BOP; along with DASH, they were associated with a decreased odds of teeth missing due to PD. AHEI and aMed were associated with a decreased odds of severe PD. Prospectively, AHEI was associated with greater ACH progression. This association was attenuated to the null after loss of ACH was imputed for teeth lost due to PD over follow-up, or after excluding participants with diabetes, osteoporosis, hypertension or heart disease at baseline. Conclusions: Better adherence to healthy dietary patterns was associated with better PD measures cross-sectionally but greater progression of ACH over 5 years. The latter might be explained by incident tooth loss due to PD and pre-existing comorbidities.
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	188647-2
ISSN	1600-051X ; 0303-6979
ISSN (online)	1600-051X
ISSN	0303-6979
DOI	10.1111/jcpe.13979
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Zs.A 1003: Show issues

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Article: ZIC1 Function in Normal Cerebellar Development and Human Developmental Pathology.

Aruga, Jun / Millen, Kathleen J

Advances in experimental medicine and biology

2018 Volume 1046, Page(s) 249–268

Abstract: Zic genes are strongly expressed in the cerebellum. This feature leads to their initial identification and their name "zic," as the abbreviation of "zinc finger protein of the cerebellum." Zic gene function in cerebellar development has been investigated ...

Abstract	Zic genes are strongly expressed in the cerebellum. This feature leads to their initial identification and their name "zic," as the abbreviation of "zinc finger protein of the cerebellum." Zic gene function in cerebellar development has been investigated mainly in mice. However, association of heterozygous loss of ZIC1 and ZIC4 with Dandy-Walker malformation, a structural birth defect of the human cerebellum, highlights the clinical relevance of these studies. Two proposed mechanisms for Zic-mediated cerebellar developmental control have been documented: regulation of neuronal progenitor proliferation-differentiation and the patterning of the cerebellar primordium. Clinical studies have also revealed that ZIC1 gain of function mutations contribute to coronal craniosynostosis, a rare skull malformation. The molecular pathways contributing to these phenotypes are not fully explored; however, embryonic interactions with sonic hedgehog signaling, retinoic acid signaling, and TGFβ signaling have been described during mouse cerebellar development. Further, Zic1/2 target a multitude of genes associated with cerebellar granule cell maturation during postnatal mouse cerebellar development.
MeSH term(s)	Animals ; Cerebellum/growth & development ; Cerebellum/physiology ; Craniosynostoses/genetics ; Craniosynostoses/metabolism ; Craniosynostoses/pathology ; Dandy-Walker Syndrome/genetics ; Dandy-Walker Syndrome/metabolism ; Dandy-Walker Syndrome/pathology ; Humans ; Mice ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neural Stem Cells/metabolism ; Neural Stem Cells/pathology ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Nerve Tissue Proteins ; Transcription Factors ; ZIC1 protein, human ; ZIC4 protein, human
Language	English
Publishing date	2018
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-981-10-7311-3_13
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Article ; Online: What cerebellar malformations tell us about cerebellar development.

Haldipur, Parthiv / Millen, Kathleen J

Neuroscience letters

2018 Volume 688, Page(s) 14–25

Abstract: Structural birth defects of the cerebellum, or cerebellar malformations, in humans, have long been recognized. However, until recently there has been little progress in elucidating their developmental pathogenesis. Innovations in brain imaging and human ... ...

Abstract	Structural birth defects of the cerebellum, or cerebellar malformations, in humans, have long been recognized. However, until recently there has been little progress in elucidating their developmental pathogenesis. Innovations in brain imaging and human genetic technologies over the last 2 decades have led to better classifications of these disorders and identification of several causative genes. In contrast, cerebellar malformations in model organisms, particularly mice, have been the focus of intense study for more than 70 years. As a result, many of the molecular, genetic and cellular programs that drive formation of the cerebellum have been delineated in mice. In this review, we overview the basic epochs and key molecular regulators of the developmental programs that build the structure of the mouse cerebellum. This mouse-centric approach has been a useful to interpret the developmental pathogenesis of human cerebellar malformations. However, it is becoming apparent that we actually know very little regarding the specifics of human cerebellar development beyond what is inferred from mice. A better understanding of human cerebellar development will not only facilitate improved diagnosis of human cerebellar malformations, but also lead to the development of treatment paradigms for these important neurodevelopmental disorders.
MeSH term(s)	Animals ; Cerebellar Diseases/pathology ; Cerebellum/abnormalities ; Cerebellum/growth & development ; Humans ; Neurogenesis/genetics ; Neurogenesis/physiology
Language	English
Publishing date	2018-05-23
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2018.05.032
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Zs.A 1166: Show issues

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Article ; Online: Hippocampal granule cell dispersion: a non-specific finding in pediatric patients with no history of seizures.

Roy, Achira / Millen, Kathleen J / Kapur, Raj P

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 54

Abstract: Chronic epilepsy has been associated with hippocampal abnormalities like neuronal loss, gliosis and granule cell dispersion. The granule cell layer of a normal human hippocampal dentate gyrus is traditionally regarded as a compact neuron-dense layer. ... ...

Abstract	Chronic epilepsy has been associated with hippocampal abnormalities like neuronal loss, gliosis and granule cell dispersion. The granule cell layer of a normal human hippocampal dentate gyrus is traditionally regarded as a compact neuron-dense layer. Histopathological studies of surgically resected or autopsied hippocampal samples primarily from temporal lobe epilepsy patients, as well as animal models of epilepsy, describe variable patterns of granule cell dispersion including focal cell clusters, broader thick segments, and bilamination or "tram-tracking". Although most studies have implicated granule cell dispersion as a specific feature of chronic epilepsy, very few "non-seizure" controls were included in these published investigations. Our retrospective survey of 147 cadaveric pediatric human hippocampi identified identical morphological spectra of granule cell dispersion in both normal and seizure-affected brains. Moreover, sections across the entire antero-posterior axis of a control cadaveric hippocampus revealed repetitive occurrence of different morphologies of the granule cell layer - compact, focally disaggregated and bilaminar. The results indicate that granule cell dispersion is within the spectrum of normal variation and not unique to patients with epilepsy. We speculate that sampling bias has been responsible for an erroneous dogma, which we hope to rectify with this investigation.
MeSH term(s)	Adolescent ; Child ; Child, Preschool ; Female ; Hippocampus/cytology ; Hippocampus/pathology ; Humans ; Infant ; Infant, Newborn ; Male ; Neurons/cytology ; Neurons/pathology ; Retrospective Studies ; Seizures/pathology ; Young Adult
Language	English
Publishing date	2020-04-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-00928-3
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Article: The IFIH1-A946T risk variant promotes diabetes in a sex-dependent manner.

Stock, Amanda J / Gonzalez-Paredes, Pierina / Previato de Almeida, Luciana / Kosanke, Stanley D / Chetlur, Srinivaas / Budde, Hannah / Wakenight, Paul / Zwingman, Theresa A / Rosen, Aaron B / Allenspach, Eric / Millen, Kathleen J / Buckner, Jane H / Rawlings, David J / Gorman, Jacquelyn A

bioRxiv : the preprint server for biology

2024

Abstract: Type 1 diabetes (T1D) is an autoimmune disease in which pancreatic islet β-cells are attacked by the immune system, resulting in insulin deficiency and hyperglycemia. One of the top non-synonymous single-nucleotide polymorphisms (SNP) associated with T1D ...

Abstract	Type 1 diabetes (T1D) is an autoimmune disease in which pancreatic islet β-cells are attacked by the immune system, resulting in insulin deficiency and hyperglycemia. One of the top non-synonymous single-nucleotide polymorphisms (SNP) associated with T1D is in the interferon-induced helicase C domain-containing protein 1 (
Language	English
Publishing date	2024-01-23
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.20.576482
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Article ; Online: The IFIH1-A946T risk variant promotes diabetes in a sex-dependent manner.

Stock, Amanda J / Gonzalez Paredes, Pierina / de Almeida, Luciana Previato / Kosanke, Stanley D / Chetlur, Srinivaas / Budde, Hannah / Wakenight, Paul / Zwingman, Theresa A / Rosen, Aaron B I / Allenspach, Eric J / Millen, Kathleen J / Buckner, Jane H / Rawlings, David J / Gorman, Jacquelyn A

Frontiers in immunology

2024 Volume 15, Page(s) 1349601

Abstract	Type 1 diabetes (T1D) is an autoimmune disease in which pancreatic islet β-cells are attacked by the immune system, resulting in insulin deficiency and hyperglycemia. One of the top non-synonymous single-nucleotide polymorphisms (SNP) associated with T1D is in the interferon-induced helicase C domain-containing protein 1 (
MeSH term(s)	Female ; Animals ; Mice ; Interferon-Induced Helicase, IFIH1/genetics ; Diabetes Mellitus, Type 1 ; DEAD-box RNA Helicases/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Genetic Predisposition to Disease ; Mice, Inbred NOD ; Autoimmune Diseases/genetics ; Interferons/genetics
Chemical Substances	Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13) ; DEAD-box RNA Helicases (EC 3.6.4.13) ; Interferons (9008-11-1)
Language	English
Publishing date	2024-02-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1349601
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Article: Embryology.

Haldipur, Parthiv / Dang, Derek / Millen, Kathleen J

Handbook of clinical neurology

2018 Volume 154, Page(s) 29–44

Abstract: With the growing recognition of the extent and prevalence of human cerebellar disorders, an understanding of developmental programs that build the mature cerebellum is necessary. In this chapter we present an overview of the basic epochs and key ... ...

Abstract	With the growing recognition of the extent and prevalence of human cerebellar disorders, an understanding of developmental programs that build the mature cerebellum is necessary. In this chapter we present an overview of the basic epochs and key molecular regulators of the developmental programs of cerebellar development. These include early patterning of the cerebellar territory, the genesis of cerebellar cells from multiple spatially distinct germinal zones, and the extensive migration and coordinated cellular rearrangements that result in the formation of the exquisitely foliated and laminated mature cerebellum. This knowledge base is founded on extensive analysis of animal models, particularly mice, due in large part to the ease of genetic manipulation of this important model organism. Since cerebellar structure and function are largely conserved across species, mouse cerebellar development is highly relevant to humans and has led to important insights into the developmental pathogenesis of human cerebellar disorders. Human fetal cerebellar development remains largely undescribed; however, several human-specific developmental features are known which are relevant to human disease and underline the importance of ongoing human fetal research.
MeSH term(s)	Animals ; Cerebellum/cytology ; Cerebellum/embryology ; Cerebellum/growth & development ; Embryology ; Humans ; Neurons/physiology
Language	English
Publishing date	2018-06-18
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-444-63956-1.00002-3
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