scholarly journals Awarded abstracts from 20th annual Julius Marmur Symposium

2017 ◽  
Vol 31 (1&2) ◽  
pp. 40
Author(s):  
Philip D. Campbell ◽  
Florence L. Marlow ◽  
Fanny Cazettes ◽  
Jose L. Pena ◽  
Veronika Miskolci ◽  
...  

VITAL ROLES OF KINESINS IN DEVELOPMENT AND DISEASE IN ZEBRAFISH Philip D. Campbell. Mentor: Dr. Florence L. Marlow HOW THE BRAIN HANDLES SENSORY UNCERTAINTY Fanny Cazettes. Mentor: Dr. Jose L. Pena OPTICAL TOOLS TO STUDY THE ISOFORM-SPECIFIC ROLES OF SMALL GTPASES IN IMMUNE CELLS Veronika Miskolci. Mentor: Dr. Dianne Cox & Dr. Louis Hodgson NEUTROPHIL AGING IS REGULATED BY THE MICROBIOME Dachuan Zhang. Mentor: Dr. Paul S. Frenette

2016 ◽  
Vol 196 (8) ◽  
pp. 3479-3493 ◽  
Author(s):  
Veronika Miskolci ◽  
Bin Wu ◽  
Yasmin Moshfegh ◽  
Dianne Cox ◽  
Louis Hodgson

2021 ◽  
Vol 22 (11) ◽  
pp. 6141
Author(s):  
Teodora Larisa Timis ◽  
Ioan Alexandru Florian ◽  
Sergiu Susman ◽  
Ioan Stefan Florian

Aneurysms and vascular malformations of the brain represent an important source of intracranial hemorrhage and subsequent mortality and morbidity. We are only beginning to discern the involvement of microglia, the resident immune cell of the central nervous system, in these pathologies and their outcomes. Recent evidence suggests that activated proinflammatory microglia are implicated in the expansion of brain injury following subarachnoid hemorrhage (SAH) in both the acute and chronic phases, being also a main actor in vasospasm, considerably the most severe complication of SAH. On the other hand, anti-inflammatory microglia may be involved in the resolution of cerebral injury and hemorrhage. These immune cells have also been observed in high numbers in brain arteriovenous malformations (bAVM) and cerebral cavernomas (CCM), although their roles in these lesions are currently incompletely ascertained. The following review aims to shed a light on the most significant findings related to microglia and their roles in intracranial aneurysms and vascular malformations, as well as possibly establish the course for future research.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 957
Author(s):  
Brad T. Casali ◽  
Erin G. Reed-Geaghan

Microglia are the resident immune cells of the brain, deriving from yolk sac progenitors that populate the brain parenchyma during development. During development and homeostasis, microglia play critical roles in synaptogenesis and synaptic plasticity, in addition to their primary role as immune sentinels. In aging and neurodegenerative diseases generally, and Alzheimer’s disease (AD) specifically, microglial function is altered in ways that significantly diverge from their homeostatic state, inducing a more detrimental inflammatory environment. In this review, we discuss the receptors, signaling, regulation and gene expression patterns of microglia that mediate their phenotype and function contributing to the inflammatory milieu of the AD brain, as well as strategies that target microglia to ameliorate the onset, progression and symptoms of AD.


2014 ◽  
Vol 24 (6) ◽  
pp. 623-630 ◽  
Author(s):  
Myka L. Estes ◽  
A. Kimberley McAllister
Keyword(s):  

Author(s):  
Taïssia Lelekov-Boissard ◽  
Guillemette Chapuisat ◽  
Jean-Pierre Boissel ◽  
Emmanuel Grenier ◽  
Marie-Aimée Dronne

The inflammatory process during stroke consists of activation of resident brain microglia and recruitment of leucocytes, namely neutrophils and monocytes/macrophages. During inflammation, microglial cells, neutrophils and macrophages secrete inflammatory cytokines and chemokines, and phagocytize dead cells. The recruitment of blood cells (neutrophils and macrophages) is mediated by the leucocyte–endothelium interactions and more specifically by cell adhesion molecules. A mathematical model is proposed to represent the dynamics of various brain cells and of immune cells (neutrophils and macrophages). This model is based on a set of six ordinary differential equations and explores the beneficial and deleterious effects of inflammation, respectively phagocytosis by immune cells and the release of pro-inflammatory mediators and nitric oxide (NO). The results of our simulations are qualitatively consistent with those observed in experiments in vivo and would suggest that the increase of phagocytosis could contribute to the increase of the percentage of living cells. The inhibition of the production of cytokines and NO and the blocking of neutrophil and macrophage infiltration into the brain parenchyma led also to the improvement of brain cell survival. This approach may help to explore the respective contributions of the beneficial and deleterious roles of the inflammatory process in stroke, and to study various therapeutic strategies in order to reduce stroke damage.


2018 ◽  
Vol 215 (11) ◽  
pp. 2702-2704 ◽  
Author(s):  
Aleksandra Deczkowska ◽  
Michal Schwartz

Immune cells patrol the brain and can support its function, but can we modulate brain–immune communication to fight neurological diseases? Here, we briefly discuss the mechanisms orchestrating the cross-talk between the brain and the immune system and describe how targeting this interaction in a well-controlled manner could be developed as a universal therapeutic approach to treat neurodegeneration.


2022 ◽  
Author(s):  
Zhen-Ge Luo ◽  
Xin-Yao Sun ◽  
Xiang-Chun Ju ◽  
Yang Li ◽  
Peng-Ming Zeng ◽  
...  

The recently developed brain organoids have been used to recapitulate the processes of brain development and related diseases. However, the lack of vasculatures, which regulate neurogenesis, brain disorders, and aging process, limits the utility of brain organoids. In this study, we induced vessel and brain organoids respectively, and then fused two types of organoids together to obtain vascularized brain organoids. The fused brain organoids were engrafted with robust vascular network-like structures, and exhibited increased number of neural progenitors, in line with the possibility that vessels regulate neural development. Fusion organoids also contained functional blood-brain-barrier (BBB)-like structures, as well as microglial cells, a specific population of immune cells in the brain. The incorporated microglia responded actively to immune stimuli to the fused brain organoids. Thus, the fusion organoids established in this study allow modeling interactions between the neuronal and non-neuronal components in vitro, in particular the vasculature and microglia niche.


2021 ◽  
Vol 12 ◽  
Author(s):  
Austin Ferro ◽  
Yohan S. S. Auguste ◽  
Lucas Cheadle

Intercellular signaling molecules such as cytokines and their receptors enable immune cells to communicate with one another and their surrounding microenvironments. Emerging evidence suggests that the same signaling pathways that regulate inflammatory responses to injury and disease outside of the brain also play powerful roles in brain development, plasticity, and function. These observations raise the question of how the same signaling molecules can play such distinct roles in peripheral tissues compared to the central nervous system, a system previously thought to be largely protected from inflammatory signaling. Here, we review evidence that the specialized roles of immune signaling molecules such as cytokines in the brain are to a large extent shaped by neural activity, a key feature of the brain that reflects active communication between neurons at synapses. We discuss the known mechanisms through which microglia, the resident immune cells of the brain, respond to increases and decreases in activity by engaging classical inflammatory signaling cascades to assemble, remodel, and eliminate synapses across the lifespan. We integrate evidence from (1) in vivo imaging studies of microglia-neuron interactions, (2) developmental studies across multiple neural circuits, and (3) molecular studies of activity-dependent gene expression in microglia and neurons to highlight the specific roles of activity in defining immune pathway function in the brain. Given that the repurposing of signaling pathways across different tissues may be an important evolutionary strategy to overcome the limited size of the genome, understanding how cytokine function is established and maintained in the brain could lead to key insights into neurological health and disease.


2019 ◽  
Author(s):  
Ulrik Beierholm ◽  
Tim Rohe ◽  
Ambra Ferrari ◽  
Oliver Stegle ◽  
Uta Noppeney

AbstractTo form the most reliable percept of the environment, the brain needs to represent sensory uncertainty. Current theories of perceptual inference assume that the brain computes sensory uncertainty instantaneously and independently for each stimulus.In a series of psychophysics experiments human observers localized auditory signals that were presented in synchrony with spatially disparate visual signals. Critically, the visual noise changed dynamically over time with or without intermittent jumps. Our results show that observers integrate audiovisual inputs weighted by sensory reliability estimates that combine information from past and current signals as predicted by an optimal Bayesian learner or approximate strategies of exponential discountingOur results challenge classical models of perceptual inference where sensory uncertainty estimates depend only on the current stimulus. They demonstrate that the brain capitalizes on the temporal dynamics of the external world and estimates sensory uncertainty by combining past experiences with new incoming sensory signals.


Sign in / Sign up

Export Citation Format

Share Document