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Book ; Online ; E-Book: Inflammation and epilepsy

Janigro, Damir / Nehlig, Astrid / Marchi, Nicola

new vistas

(Progress in Inflammation Research ; 88)

2021

Abstract: This book provides comprehensive information, both for clinicians and scientists, on the basic mechanisms, clinical features, and therapeutic approaches to epilepsy as an inflammatory disease. Inflammation has been for many years considered as an ... ...

Author's details	Damir Janigro, Astrid Nehlig, Nicola Marchi, editors
Series title	Progress in Inflammation Research ; 88
Abstract	This book provides comprehensive information, both for clinicians and scientists, on the basic mechanisms, clinical features, and therapeutic approaches to epilepsy as an inflammatory disease. Inflammation has been for many years considered as an etiologic player (and a therapeutic target) for a specific group of epilepsies. However, it turns out that this concept underestimated the impact of inflammation in seizure disorders. Many accepted therapies for non-inflammatory epilepsies act in part as an inflammatory drug. The CNS actively responds to acute immune challenges by altering body temperature, stimulating the HPA axis, as well as up- and down-regulating specific sympathetic pathways.
Keywords	Epilepsy ; Inflamació ; Epilèpsia
Subject code	616.853
Language	English
Size	1 online resource (VII, 237 p. 19 illus., 17 illus. in color.)
Edition	1st ed. 2021.
Publisher	Springer
Publishing place	Cham, Switzerland
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
ISBN	3-030-67403-7 ; 3-030-67402-9 ; 978-3-030-67403-8 ; 978-3-030-67402-1
DOI	10.1007/978-3-030-67403-8
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Diagnostic biomarker kinetics: how brain-derived biomarkers distribute through the human body, and how this affects their diagnostic significance: the case of S100B.

Murcko, Robert / Marchi, Nicola / Bailey, Damian / Janigro, Damir

Fluids and barriers of the CNS

2022 Volume 19, Issue 1, Page(s) 32

Abstract: Blood biomarkers of neurological diseases are often employed to rule out or confirm the presence of significant intracranial or cerebrovascular pathology or for the differential diagnosis of conditions with similar presentations (e.g., hemorrhagic vs. ... ...

Abstract	Blood biomarkers of neurological diseases are often employed to rule out or confirm the presence of significant intracranial or cerebrovascular pathology or for the differential diagnosis of conditions with similar presentations (e.g., hemorrhagic vs. embolic stroke). More widespread utilization of biomarkers related to brain health is hampered by our incomplete understanding of the kinetic properties, release patterns, and excretion of molecules derived from the brain. This is, in particular, true for S100B, an astrocyte-derived protein released across the blood-brain barrier (BBB). We developed an open-source pharmacokinetic computer model that allows investigations of biomarker's movement across the body, the sources of biomarker's release, and its elimination. This model was derived from a general in silico model of drug pharmacokinetics adapted for protein biomarkers. We improved the model's predictive value by adding realistic blood flow values, organ levels of S100B, lymphatic and glymphatic circulation, and glomerular filtration for excretion in urine. Three key variables control biomarker levels in blood or saliva: blood-brain barrier permeability, the S100B partition into peripheral organs, and the cellular levels of S100B in astrocytes. A small contribution to steady-state levels of glymphatic drainage was also observed; this mechanism also contributed to the uptake of organs of circulating S100B. This open-source model can also mimic the kinetic behavior of other markers, such as GFAP or NF-L. Our results show that S100B, after uptake by various organs from the systemic circulation, can be released back into systemic fluids at levels that do not significantly affect the clinical significance of venous blood or salivary levels after an episode of BBB disruption.
MeSH term(s)	Biomarkers ; Brain/metabolism ; Human Body ; Humans ; Kinetics ; S100 Calcium Binding Protein beta Subunit
Chemical Substances	Biomarkers ; S100 Calcium Binding Protein beta Subunit ; S100B protein, human
Language	English
Publishing date	2022-05-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-022-00329-9
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Article ; Online: Neurovascular unit dysfunction as a mechanism of seizures and epilepsy during aging.

van Vliet, Erwin A / Marchi, Nicola

Epilepsia

2022 Volume 63, Issue 6, Page(s) 1297–1313

Abstract: The term neurovascular unit (NVU) describes the structural and functional liaison between specialized brain endothelium, glial and mural cells, and neurons. Within the NVU, the blood-brain barrier (BBB) is the microvascular structure regulating neuronal ... ...

Abstract	The term neurovascular unit (NVU) describes the structural and functional liaison between specialized brain endothelium, glial and mural cells, and neurons. Within the NVU, the blood-brain barrier (BBB) is the microvascular structure regulating neuronal physiology and immune cross-talk, and its properties adapt to brain aging. Here, we analyze a research framework where NVU dysfunction, caused by acute insults or disease progression in the aging brain, represents a converging mechanism underlying late-onset seizures or epilepsy and neurological or neurodegenerative sequelae. Furthermore, seizure activity may accelerate brain aging by sustaining regional NVU dysfunction, and a cerebrovascular pathology may link seizures to comorbidities. Next, we focus on NVU diagnostic approaches that could be tailored to seizure conditions in the elderly. We also examine the impending disease-modifying strategies based on the restoration of the NVU and, more in general, the homeostatic control of anti- and pro-inflammatory players. We conclude with an outlook on current pre-clinical knowledge gaps and clinical challenges pertinent to seizure onset and conditions in an aging population.
MeSH term(s)	Aged ; Aging ; Blood-Brain Barrier ; Brain ; Epilepsy ; Humans ; Seizures
Language	English
Publishing date	2022-04-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/epi.17210
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Zs.A 517: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Central nervous system lymphatic unit, immunity, and epilepsy: Is there a link?

Noé, Francesco M / Marchi, Nicola

Epilepsia open

2019 Volume 4, Issue 1, Page(s) 30–39

Abstract: The recent definition of a network of lymphatic vessels in the meninges surrounding the brain and the spinal cord has advanced our knowledge on the functional anatomy of fluid movement within the central nervous system (CNS). Meningeal lymphatic vessels ... ...

Abstract	The recent definition of a network of lymphatic vessels in the meninges surrounding the brain and the spinal cord has advanced our knowledge on the functional anatomy of fluid movement within the central nervous system (CNS). Meningeal lymphatic vessels along dural sinuses and main nerves contribute to cerebrospinal fluid (CSF) drainage, integrating the cerebrovascular and periventricular routes, and forming a circuit that we here define as the CNS-lymphatic unit. The latter unit is important for parenchymal waste clearance, brain homeostasis, and the regulation of immune or inflammatory processes within the brain. Disruption of fluid drain mechanisms may promote or sustain CNS disease, conceivably applicable to epilepsy where extracellular accumulation of macromolecules and metabolic by-products occur in the interstitial and perivascular spaces. Herein we address an emerging concept and propose a theoretical framework on: (a) how a defect of brain clearance of macromolecules could favor neuronal hyperexcitability and seizures, and (b) whether meningeal lymphatic vessel dysfunction contributes to the neuroimmune cross-talk in epileptic pathophysiology. We propose possible molecular interventions targeting meningeal lymphatic dysfunctions, a potential target for immune-mediated epilepsy.
Language	English
Publishing date	2019-02-14
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2470-9239
ISSN	2470-9239
DOI	10.1002/epi4.12302
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Article: Peripheral Routes to Neurodegeneration: Passing Through the Blood-Brain Barrier.

Giannoni, Patrizia / Claeysen, Sylvie / Noe, Francesco / Marchi, Nicola

Frontiers in aging neuroscience

2020 Volume 12, Page(s) 3

Abstract: A bidirectional crosstalk between peripheral players of immunity and the central nervous system (CNS) exists. Hence, blood-brain barrier (BBB) breakdown is emerging as a participant mechanism of dysregulated peripheral-CNS interplay, promoting diseases. ... ...

Abstract	A bidirectional crosstalk between peripheral players of immunity and the central nervous system (CNS) exists. Hence, blood-brain barrier (BBB) breakdown is emerging as a participant mechanism of dysregulated peripheral-CNS interplay, promoting diseases. Here, we examine the implication of BBB damage in neurodegeneration, linking it to peripheral brain-directed autoantibodies and gut-brain axis mechanisms. As BBB breakdown is a factor contributing to, or even anticipating, neuronal dysfunction(s), we here identify contemporary pharmacological strategies that could be exploited to repair the BBB in disease conditions. Developing neurovascular, add on, therapeutic strategies may lead to a more efficacious pre-clinical to clinical transition with the goal of curbing the progression of neurodegeneration.
Language	English
Publishing date	2020-02-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2020.00003
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Article ; Online: Abnormal timing of slow wave synchronization processes in non-rapid eye movement sleep parasomnias.

Cataldi, Jacinthe / Stephan, Aurélie M / Marchi, Nicola A / Haba-Rubio, José / Siclari, Francesca

Sleep

2022 Volume 45, Issue 7

Abstract: Study objectives: Sleepwalking, confusional arousals, and sleep terrors are parasomnias occurring out of non-rapid eye movement (NREM) sleep. Several previous studies have described EEG changes associated with NREM parasomnia episodes, but it remains ... ...

Abstract	Study objectives: Sleepwalking, confusional arousals, and sleep terrors are parasomnias occurring out of non-rapid eye movement (NREM) sleep. Several previous studies have described EEG changes associated with NREM parasomnia episodes, but it remains unclear whether these changes are specific to parasomnia episodes or whether they are part of the normal awakening process. Here we directly compared regional brain activity, measured with high-density (hd-) EEG, between parasomnia episodes and normal awakenings (without behavioral manifestations of parasomnia). Methods: Twenty adult patients with non-rapid eye movement parasomnias underwent a baseline hd-EEG recording (256 electrodes) followed by a recovery sleep recording after 25 h of total sleep deprivation, during which auditory stimuli were administered to provoke parasomnia episodes. Results: Both normal awakenings (n = 25) and parasomnia episodes (n = 96) were preceded by large, steep, and "K-complex-like" slow waves in frontal and central brain regions, and by a concomitant increase in high-frequency EEG (beta) activity. Compared to normal awakenings, parasomnia episodes occurred on a less activated EEG background and displayed higher slow wave activity (SWA) and lower beta activity in frontal and central brain regions after movement onset. Conclusions: Our results suggest that non-rapid eye movement awakenings, irrespective of behavioral manifestations of parasomnia episodes, involve an arousal-related slow wave synchronization process that predominantly recruits frontal and central brain areas. In parasomnia episodes, this synchronization process comes into play abnormally during periods of high SWA and is associated with higher SWA after movement onset. Thus, an abnormal timing of arousal-related slow wave synchronization processes could underlie the occurrence of NREM parasomnias.
MeSH term(s)	Adult ; Eye Movements ; Humans ; Parasomnias ; Polysomnography/methods ; Sleep ; Sleep Stages ; Somnambulism
Language	English
Publishing date	2022-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsac111
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Article ; Online: CAR Protects Females from Diet-Induced Steatosis and Associated Metabolic Disorders.

Oliviero, Fabiana / Klement, Wendy / Mary, Lucile / Dauwe, Yannick / Lippi, Yannick / Naylies, Claire / Gayrard, Véronique / Marchi, Nicola / Mselli-Lakhal, Laila

Cells

2023 Volume 12, Issue 18

Abstract: Non-Alcoholic Fatty Liver Disease (NAFLD) is the most common cause of chronic liver disease worldwide, affecting 70-90% of obese individuals. In humans, a lower NAFLD incidence is reported in pre-menopausal women, although the mechanisms affording this ... ...

Abstract	Non-Alcoholic Fatty Liver Disease (NAFLD) is the most common cause of chronic liver disease worldwide, affecting 70-90% of obese individuals. In humans, a lower NAFLD incidence is reported in pre-menopausal women, although the mechanisms affording this protection remain under-investigated. Here, we tested the hypothesis that the constitutive androstane nuclear receptor (CAR) plays a role in the pathogenesis of experimental NAFLD. Male and female wild-type (WT) and CAR knock-out (CAR-/-) mice were subjected to a high-fat diet (HFD) for 16 weeks. We examined the metabolic phenotype of mice through body weight follow-up, glucose tolerance tests, analysis of plasmatic metabolic markers, hepatic lipid accumulation, and hepatic transcriptome. Finally, we examined the potential impact of HFD and CAR deletion on specific brain regions, focusing on glial cells. HFD-induced weight gain and hepatic steatosis are more pronounced in WT males than females. CAR-/- females present a NASH-like hepatic transcriptomic signature suggesting a potential NAFLD to NASH transition. Transcriptomic correlation analysis highlighted a possible cross-talk between CAR and ERα receptors. The peripheral effects of CAR deletion in female mice were associated with astrogliosis in the hypothalamus. These findings prove that nuclear receptor CAR may be a potential mechanism entry-point and a therapeutic target for treating NAFLD/NASH.
MeSH term(s)	Female ; Male ; Humans ; Animals ; Mice ; Non-alcoholic Fatty Liver Disease/etiology ; Metabolic Diseases ; Diet, High-Fat/adverse effects ; Obesity ; Body Weight
Language	English
Publishing date	2023-09-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12182218
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Article ; Online: Pesticides at brain borders: Impact on the blood-brain barrier, neuroinflammation, and neurological risk trajectories.

Cresto, Noemie / Forner-Piquer, Isabel / Baig, Asma / Chatterjee, Mousumi / Perroy, Julie / Goracci, Jacopo / Marchi, Nicola

Chemosphere

2023 Volume 324, Page(s) 138251

Abstract: Pesticides are omnipresent, and they pose significant environmental and health risks. Translational studies indicate that acute exposure to high pesticide levels is detrimental, and prolonged contact with low concentrations of pesticides, as single and ... ...

Abstract	Pesticides are omnipresent, and they pose significant environmental and health risks. Translational studies indicate that acute exposure to high pesticide levels is detrimental, and prolonged contact with low concentrations of pesticides, as single and cocktail, could represent a risk factor for multi-organ pathophysiology, including the brain. Within this research template, we focus on pesticides' impact on the blood-brain barrier (BBB) and neuroinflammation, physical and immunological borders for the homeostatic control of the central nervous system (CNS) neuronal networks. We examine the evidence supporting a link between pre- and postnatal pesticide exposure, neuroinflammatory responses, and time-depend vulnerability footprints in the brain. Because of the pathological influence of BBB damage and inflammation on neuronal transmission from early development, varying exposures to pesticides could represent a danger, perhaps accelerating adverse neurological trajectories during aging. Refining our understanding of how pesticides influence brain barriers and borders could enable the implementation of pesticide-specific regulatory measures directly relevant to environmental neuroethics, the exposome, and one-health frameworks.
MeSH term(s)	Humans ; Blood-Brain Barrier ; Pesticides/toxicity ; Neuroinflammatory Diseases ; Brain/pathology ; Central Nervous System ; Inflammation/chemically induced
Chemical Substances	Pesticides
Language	English
Publishing date	2023-03-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2023.138251
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Article ; Online: Continuous low-level dietary exposure to glyphosate elicits dose and sex-dependent synaptic and microglial adaptations in the rodent brain.

Cresto, Noemie / Courret, Margot / Génin, Athénaïs / Martin, Céline Marie Pauline / Bourret, Julie / Sakkaki, Sophie / de Bock, Frederic / Janvier, Alicia / Polizzi, Arnaud / Payrastre, Laurence / Ellero-Simatos, Sandrine / Audinat, Etienne / Perroy, Julie / Marchi, Nicola

Environmental pollution (Barking, Essex : 1987)

2024 Volume 345, Page(s) 123477

Abstract: Prolonged exposure to low levels of dietary contaminants is a context in modern life that could alter organ physiology gradually. Here, we aimed to investigate the impact of continuous exposure to acceptable daily intake (ADI) and non-observable adverse ... ...

Abstract	Prolonged exposure to low levels of dietary contaminants is a context in modern life that could alter organ physiology gradually. Here, we aimed to investigate the impact of continuous exposure to acceptable daily intake (ADI) and non-observable adverse effect level (NOAEL) of glyphosate from gestation to adulthood using C57BL/6J mice and incorporating these levels into their food pellets. From adulthood, we analyzed neurophysiological and neuro-glia cellular adaptations in male and female animals. Using ex-vivo hippocampal slice electrophysiology, we found a reduced efficacy of Schaffer collateral-to-CA1 excitatory synapses in glyphosate-exposed dietary conditions, with ADI and NOAEL dose-dependent effects. Short-term facilitation of excitatory synaptic transmission was specifically increased in NOAEL conditions, with a predominant influence in males, suggesting a reduced probability of neurotransmitter release. Long-term synaptic potentiation (LTP) was decreased in NOAEL-exposed mice. Next, we explore whether these neurophysiological modifications are associated with neuro-glia changes in the somatosensory cortex and hippocampus. High-resolution confocal microscopy analyses unveil a dose-dependent increased density of excitatory Vglut1
MeSH term(s)	Mice ; Male ; Female ; Animals ; Microglia ; Glyphosate ; Rodentia ; Dietary Exposure ; Mice, Inbred C57BL ; Brain
Chemical Substances	Glyphosate (4632WW1X5A)
Language	English
Publishing date	2024-01-31
Publishing country	England
Document type	Journal Article
ZDB-ID	280652-6
ISSN	1873-6424 ; 0013-9327 ; 0269-7491
ISSN (online)	1873-6424
ISSN	0013-9327 ; 0269-7491
DOI	10.1016/j.envpol.2024.123477
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Article ; Online: REM sleep is reduced in late middle-aged and older APOE4 allele carriers.

André, Claire / Martineau-Dussault, Marie-Ève / Baril, Andrée-Ann / Marchi, Nicola Andrea / Daneault, Véronique / Lorrain, Dominique / Hudon, Carol / Bastien, Célyne H / Petit, Dominique / Thompson, Cynthia / Poirier, Judes / Montplaisir, Jacques / Gosselin, Nadia / Carrier, Julie

Sleep

2024

Abstract: Study objectives: Apolipoprotein E ɛ4 (APOE4) is the strongest genetic risk factor for Alzheimer's disease (AD). In addition, APOE4 carriers may exhibit sleep disturbances, but conflicting results have been reported, such that there is no clear ... ...

Abstract	Study objectives: Apolipoprotein E ɛ4 (APOE4) is the strongest genetic risk factor for Alzheimer's disease (AD). In addition, APOE4 carriers may exhibit sleep disturbances, but conflicting results have been reported, such that there is no clear consensus regarding which aspects of sleep are impacted. Our objective was to compare objective sleep architecture between APOE4 carriers and non-carriers, and to investigate the modulating impact of age, sex, cognitive status and obstructive sleep apnea. Methods: 198 dementia-free participants aged >55 years old (mean age: 68.7 ± 8.08 years old, 40.91% women, 41 APOE4 carriers) were recruited in this cross-sectional study. They underwent polysomnography, APOE4 genotyping and a neuropsychological evaluation. ANCOVAs assessed the effect of APOE4 status on sleep architecture, controlling for age, sex, cognitive status and the apnea-hypopnea index. Interaction terms were added between APOE4 status and covariates. Results: REM sleep percentage (F=9.95, p=0.002, ηp2=0.049) and duration (F=9.23, p=0.003, ηp2=0.047) were lower in APOE4 carriers. The results were replicated in a subsample of 112 participants without moderate-to-severe obstructive sleep apnea. There were no significant interactions between APOE4 status and age, sex, cognitive status and obstructive sleep apnea in the whole sample. Conclusions: Our results show that APOE4 carriers exhibit lower REM sleep duration, including in cognitively unimpaired individuals, possibly resulting from early neurodegenerative processes in regions involved in REM sleep generation and maintenance.
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsae094
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