The ability to maintain human brain explants in tissue culture was a critical step in the use of these cells for the study of central nervous system disorders. Ross G. Harrison (1870-1959) was the first to successfully maintain frog medullary tissue in culture in 1907, but it took another 38 years before successful culture of human brain tissue was accomplished. One of the pioneers in this achievement was Mary Jane Hogue (1883-1962). Hogue was born into a Quaker family in 1883 in West Chester, Pennsylvania, and received her undergraduate degree from Goucher College in Baltimore, Maryland. Research with the developmental biologist Theodor Boveri (1862-1915) in Würzburg, Germany, resulted in her Ph.D. (1909). Hogue transitioned from studying protozoa to the culture of human brain tissue in the 1940s and 1950s, when she was one of the first to culture cells from human fetal, infant, and adult brain explants. We review Hogue's pioneering contributions to the study of human brain cells in culture, her putative identification of progenitor neuroblast and/or glioblast cells, and her use of the cultures to study the cytopathogenic effects of poliovirus. We also put Hogue's work in perspective by discussing how other women pioneers in tissue culture influenced Hogue and her research.
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http://dx.doi.org/10.1080/0964704X.2018.1468967 | DOI Listing |
Trends Immunol
December 2024
Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland. Electronic address:
Diverse macrophage populations inhabit the rodent and human central nervous system (CNS), including microglia in the parenchyma and border-associated macrophages (BAMs) in the meninges, choroid plexus, and perivascular spaces. These innate immune phagocytes are essential in brain development and maintaining homeostasis, but they also play diverse roles in neurological diseases. In this review, we highlight the emerging roles of CNS macrophages in regulating vascular function in health and disease.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois, USA.
Introduction: Type 2 diabetes increases the risk of Alzheimer's disease (AD) dementia. Insulin signaling dysfunction exacerbates tau protein phosphorylation, a hallmark of AD pathology. However, the comprehensive impact of diabetes on patterns of AD-related phosphoprotein in the human brain remains underexplored.
View Article and Find Full Text PDFBMJ Ment Health
December 2024
Research Center for Child Mental Development, University of Fukui, Fukui, Japan.
Question: Cognitive-behavioural therapy (CBT) is frequently implemented for individuals with attention-deficit hyperactivity disorder (ADHD). It is still unknown which specific components are effective, because CBT is a complex intervention with several components. The objective of this review was to assess the efficacy of CBT components for ADHD.
View Article and Find Full Text PDFMol Cell Neurosci
December 2024
Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Türkiye; Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir, Türkiye; Department of Neuroscience, Institute of Health Sciences, Dokuz Eylul University, Izmir, Türkiye. Electronic address:
Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the accumulation of amyloid plaques, phosphorylated tau tangles and microglia toxicity, resulting in neuronal death and cognitive decline. Since microglia are recognized as one of the key players in the disease, it is crucial to understand how microglia operate in disease conditions and incorporate them into models. The studies on human microglia functions are thought to reflect the post-symptomatic stage of the disease.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
December 2024
Department of Psychiatry, University of Cambridge, Cambridge, UK; Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany. Electronic address:
Background: A preference for sooner-smaller over later-larger rewards, known as delay discounting, is a candidate transdiagnostic marker of waiting impulsivity and a research domain criterion. While abnormal discounting rates have been associated with many psychiatric diagnoses and abnormal brain structure, the underlying neuropsychological processes remain largely unknown. Here, we deconstruct delay discounting into choice and rate processes by testing different computational models and investigate their associations with white matter tracts.
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