Exploration of Neuroscience

Open Access

Editorial

Cutting edges in neuroscience to exceed borders

Dirk M. Hermann

Published: September 01, 2022 Explor Neurosci. 2022;1:1–3
DOI: https://doi.org/10.37349/en.2022.00001

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Review

Impact of circadian clock dysfunction on human health

All living organisms exhibit circadian rhythms. Humans show circadian rhythm of the different physiological functions such as sleep-wake cycle, core body temperature, feeding behavior, metabolic act [...] Read more.

Saptadip Samanta, Sk Asif Ali

Published: September 29, 2022 Explor Neurosci. 2022;1:4–30
DOI: https://doi.org/10.37349/en.2022.00002
This article belongs to the special issue Circadian Rhythm and Melatonin

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Review

Neuregulins: subcellular localization, signaling pathways and their relationship with neuroplasticity and neurological diseases

Neuregulins (NRGs) and their cognate ErbB receptors (ErbB2–ErbB4) constitute a vast group of proteins encoded by six different genes (NRG1–6) and many isoforms with critical [...] Read more.

Neuregulins (NRGs) and their cognate ErbB receptors (ErbB2–ErbB4) constitute a vast group of proteins encoded by six different genes (NRG1–6) and many isoforms with critical roles in the development and functioning of the nervous system. NRGs are known to regulate important processes in the nervous system like neural development, neuronal differentiation, neurite outgrowth, and specification. These factors are involved in the regulation of neurotransmission pathways and the modulation of several forms of synaptic plasticity. Due to NRGs’ role in synaptic plasticity, defects in their normal functioning are translated into altered signaling networks, which have been linked to susceptibility to developing psychiatric disorders like schizophrenia (SZ), autism, depression, and bipolar disorders. Additionally, deviation of the NRG normal functioning is involved in neurological diseases like Alzheimer’s and Parkinson’s disease. Contrastingly, NRG/ErbB signaling is also involved in the recovery after traumatic brain injuries (e.g., ischemic stroke). The NRG/ErbB signaling complex is highly unusual because the ligands (mainly NRG1–NRG3, with their multiple isoforms) and receptors (ErbB2–ErbB4) can orchestrate vast signaling complexes, with a wide reach within the processes that govern the development and appropriate function of the nervous system. This may explain why NRGs and ErbB receptor genes have been linked to complex brain disorders, like SZ. This review, are discussed important aspects of NRG and their relevance for nervous system functioning, including 1) subcellular localization, 2) signaling pathways involved in neuronal functions, 3) effect on neurite development and synapse formation, 4) modulation of some mechanisms of synaptic plasticity [long-term potentiation (LTP), depotentiation, long-term depression (LTD)] and 5) roles of NRGs in some neurological diseases. This review intends to present a summary of the main findings about this family of proteins, which might position them as one of the master regulators of brain functioning.

Marines Longart ... Juan Carlos Martínez

Published: September 29, 2022 Explor Neurosci. 2022;1:31–53
DOI: https://doi.org/10.37349/en.2022.00003

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Neuregulins (NRGs) and their cognate ErbB receptors (ErbB2–ErbB4) constitute a vast group of proteins encoded by six different genes (NRG1–6) and many isoforms with critical roles in the development and functioning of the nervous system. NRGs are known to regulate important processes in the nervous system like neural development, neuronal differentiation, neurite outgrowth, and specification. These factors are involved in the regulation of neurotransmission pathways and the modulation of several forms of synaptic plasticity. Due to NRGs’ role in synaptic plasticity, defects in their normal functioning are translated into altered signaling networks, which have been linked to susceptibility to developing psychiatric disorders like schizophrenia (SZ), autism, depression, and bipolar disorders. Additionally, deviation of the NRG normal functioning is involved in neurological diseases like Alzheimer’s and Parkinson’s disease. Contrastingly, NRG/ErbB signaling is also involved in the recovery after traumatic brain injuries (e.g., ischemic stroke). The NRG/ErbB signaling complex is highly unusual because the ligands (mainly NRG1–NRG3, with their multiple isoforms) and receptors (ErbB2–ErbB4) can orchestrate vast signaling complexes, with a wide reach within the processes that govern the development and appropriate function of the nervous system. This may explain why NRGs and ErbB receptor genes have been linked to complex brain disorders, like SZ. This review, are discussed important aspects of NRG and their relevance for nervous system functioning, including 1) subcellular localization, 2) signaling pathways involved in neuronal functions, 3) effect on neurite development and synapse formation, 4) modulation of some mechanisms of synaptic plasticity [long-term potentiation (LTP), depotentiation, long-term depression (LTD)] and 5) roles of NRGs in some neurological diseases. This review intends to present a summary of the main findings about this family of proteins, which might position them as one of the master regulators of brain functioning.

Open Access

Perspective

Recent developments and future perspectives of neuropathology

This brief statement describes some recent achievements of neuropathological research, with the focus on Alzheimer’s and other age-related diseases, neurodegenerative disorders (tauopathies, synucleinopathies), multimorbidity of [...] Read more.

Kurt A. Jellinger

Published: September 30, 2022 Explor Neurosci. 2022;1:54–60
DOI: https://doi.org/10.37349/en.2022.00004

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Review

Neuroprotective and neurorestorative actions of mesenchymal stromal cell-derived small extracellular vesicles in the ischemic brain

Ischemic stroke is a highly prevalent condition that frequently results in life-long disability and death. Considerable efforts have been made to establish treatments that prevent secondary ischemic [...] Read more.

Chen Wang ... Dirk M. Hermann

Published: October 09, 2022 Explor Neurosci. 2022;1:61–74
DOI: https://doi.org/10.37349/en.2022.00005
This article belongs to the special issue Extracellular Vesicles as Cell-based Therapeutics

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Perspective

Should we rethink neurodegeneration?

The therapy of many neurological disorders has advanced markedly during recent decades. Not so for neurodegenerative disorders. Early detection, deep individual genotyping and phenotyping, and perso [...] Read more.

Jussi O. T. Sipilä

Published: December 26, 2022 Explor Neurosci. 2022;1:75–82
DOI: https://doi.org/10.37349/en.2022.00006

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Review

Updates in mechanical thrombectomy

Stroke is a leading cause of morbidity and mortality. The advent of mechanical thrombectomy has largely improved patient outcomes. This article reviews the features and outcomes associated with aspi [...] Read more.

Kevin Pierre ... Brandon Lucke-Wold

Published: December 30, 2022 Explor Neurosci. 2022;1:83–99
DOI: https://doi.org/10.37349/en.2022.00007

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Review

Cellular and molecular mechanisms of stress-induced memory impairment

Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and t [...] Read more.

Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain.

Ameneh Rezayof ... Shiva Hashemizadeh

Published: December 30, 2022 Explor Neurosci. 2022;1:100–119
DOI: https://doi.org/10.37349/en.2022.00008
This article belongs to the special issue Neuroinflammation in the Ageing and the Injured Brain

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Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain.

Open Access

Review

Modify gut microbiome in autism: a promising strategy?

The gut microbiota and dysbiosis have been implicated in various metabolic diseases and gastrointestinal disorders. Recently, there has been growing evidence suggesting the influence of gut microbio [...] Read more.

Jean Demarquoy ... Caroline Demarquoy

Published: August 31, 2023 Explor Neurosci. 2023;2:140–152
DOI: https://doi.org/10.37349/en.2023.00018

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Case Report

Covered stent graft for treatment of carotid artery stenosis with post-stenotic aneurysm

Several bare metals, self-expanding stents have been approved by the Food and Drug Administration (FDA) to treat carotid stenosis, but no covered stents have been particularly examined or approved f [...] Read more.

Mosaad Soliman ... Reem Soliman

Published: August 31, 2023 Explor Neurosci. 2023;2:153–159
DOI: https://doi.org/10.37349/en.2023.00019

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Review

Multiple sclerosis with comorbidity depression and its association with vitamin D deficiency in a narrative review of the current literature

Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseas [...] Read more.

Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseases are characterized by an imbalance of proinflammatory and antiinflammatory cytokines, increased serum neurofilament light chains (sNfLs), disruption of the blood-brain barrier (BBB), abolition of the physiological function of the various types of microglia (MG), decreased calcidiol-serum levels, and disorders of the gut microbiome in combination with hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis/microbiome-gut-brain-axis characterized. In depression, stress initiates cellular and molecular changes in the brain via increased cortisol release in the HPA-axis. Microglial activation and neuronal damage as well as dysregulation of neuroplastic and neurotrophic factors complete the spectrum of pathological damage. It is shown that gut dysbiosis leads to increased gut permeability, which favors endotoxemia and ultimately paves the way to systemic inflammation. A VitD supplementation could restore the balance of microorganisms in the intestine and reduce the inflammatory processes at various levels. VitD promotes regulatory T cell (Treg) proliferation, inhibits the expression of T helper 1 (Th1) cells and Th17 immune cells, and inhibits proinflammatory interleukin-17 (IL-17). 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] reduces also the secretion of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Increased calcitriol levels lead to a reduction in MG activation, oxidative stress, and lower BBB permeability. An early, permanent, daily sufficient VitD supplementation as an add-on therapy under control of the serum 25-hydroxyvitamin D [s25(OH)D] levels is an essential therapeutic tool to slow down the disability caused by MS and thereby primarily prevent or reduce the stress and subsequently the manifestation of depression. Through the future continuous measurement of the biomarkers serum neurofilament ligth chains and glial fibrillary acidic proteins as well as the s25(OH)D level in MS and comorbidity depression, future therapy successes or failures can be avoided.

Hans-Klaus Goischke

Published: August 31, 2023 Explor Neurosci. 2023;2:160–192
DOI: https://doi.org/10.37349/en.2023.00020
This article belongs to the special issue Novel Therapeutic Approaches for the Treatment of Depression

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Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseases are characterized by an imbalance of proinflammatory and antiinflammatory cytokines, increased serum neurofilament light chains (sNfLs), disruption of the blood-brain barrier (BBB), abolition of the physiological function of the various types of microglia (MG), decreased calcidiol-serum levels, and disorders of the gut microbiome in combination with hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis/microbiome-gut-brain-axis characterized. In depression, stress initiates cellular and molecular changes in the brain via increased cortisol release in the HPA-axis. Microglial activation and neuronal damage as well as dysregulation of neuroplastic and neurotrophic factors complete the spectrum of pathological damage. It is shown that gut dysbiosis leads to increased gut permeability, which favors endotoxemia and ultimately paves the way to systemic inflammation. A VitD supplementation could restore the balance of microorganisms in the intestine and reduce the inflammatory processes at various levels. VitD promotes regulatory T cell (Treg) proliferation, inhibits the expression of T helper 1 (Th1) cells and Th17 immune cells, and inhibits proinflammatory interleukin-17 (IL-17). 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] reduces also the secretion of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Increased calcitriol levels lead to a reduction in MG activation, oxidative stress, and lower BBB permeability. An early, permanent, daily sufficient VitD supplementation as an add-on therapy under control of the serum 25-hydroxyvitamin D [s25(OH)D] levels is an essential therapeutic tool to slow down the disability caused by MS and thereby primarily prevent or reduce the stress and subsequently the manifestation of depression. Through the future continuous measurement of the biomarkers serum neurofilament ligth chains and glial fibrillary acidic proteins as well as the s25(OH)D level in MS and comorbidity depression, future therapy successes or failures can be avoided.

Open Access

Review

Negative environmental influences on the developing brain mediated by epigenetic modifications

Brain development, a complex process, consisting of several phases, starting as early as two weeks after conception, and continuing through childhood till early adolescence, is crucial for the devel [...] Read more.

Maya Komar-Fletcher ... Joanna Michalina Jurek

Published: September 28, 2023 Explor Neurosci. 2023;2:193–211
DOI: https://doi.org/10.37349/en.2023.00021

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Review

Sleep disorders contribute to the development of dementia and Alzheimer’s disease

Life is the highest form of adaptation to the environment which is based on energy metabolism. To maintain life, the neuromuscular system must constantly interact with the environment. The striatal [...] Read more.

Janusz Wiesław Błaszczyk

Published: October 08, 2023 Explor Neurosci. 2023;2:212–223
DOI: https://doi.org/10.37349/en.2023.00022
This article belongs to the special issue Alzheimer’s Disease

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Review

Investigation into the vascular contributors to dementia and the associated treatments

As the average lifespan has increased, memory disorders have become a more pressing public health concern. However, dementia in the elderly population is often neglected in light of other health pri [...] Read more.

Caroline Grace Davidson ... Brandon Lucke-Wold

Published: October 15, 2023 Explor Neurosci. 2023;2:224–237
DOI: https://doi.org/10.37349/en.2023.00023

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Original Article

Estimation of the allelic status of apolipoprotein E4 isoforms with fully automated LUMIPULSE^® assays

Aim: Apolipoprotein E (ApoE) isoforms, especially the ApoE4 isoform, are genetic risk factors for Alzheimer’s disease (AD). Moreover, the APOE ε4 haplotype has a dose-dependent association wit [...] Read more.

Tatsushi Yuri ... Hisashi Nojima

Published: October 16, 2023 Explor Neurosci. 2023;2:238–244
DOI: https://doi.org/10.37349/en.2023.00024
This article belongs to the special issue Alzheimer’s Disease

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Mini Review

Nutritional treatment with the ketogenic diet in children with refractory epilepsy: a narrative review

The two mainstays of therapy for refractory epilepsy are medication and surgery. Child behavioral and cognitive aspects of epilepsy can be improved by using a specialized dietary regimen such as the [...] Read more.

Srilaxmi Vityala ... Swathi Nenavath

Published: October 30, 2023 Explor Neurosci. 2023;2:245–250
DOI: https://doi.org/10.37349/en.2023.00025
This article belongs to the special issue Epilepsy

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Review

Metabolic correction of neurodegenerative pathologies: the role of macronutrients and timing

Despite decades of intensive research, effective treatment and prevention strategies for neurodegenerative diseases (NDDs) remain elusive. This review focuses on Alzheimer’s and Parkinson’s dise [...] Read more.

Yuri Zilberter, Tanya Zilberter

Published: April 21, 2023 Explor Neurosci. 2023;2:67–81
DOI: https://doi.org/10.37349/en.2023.00013

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Review

Inflammatory responses involved in post-cardiac arrest brain injury: mechanisms, regulation, and therapeutic potential

Neuroinflammation plays a key role in the pathogenesis of post-cardiac arrest (CA) brain injury. Innate immune cells sense a variety of danger signals through pattern-recognition receptors and evoke [...] Read more.

Yuzhen Zhang ... Kaibin Huang

Published: April 26, 2023 Explor Neurosci. 2023;2:82–97
DOI: https://doi.org/10.37349/en.2023.00014

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Perspective

Mesenchymal stem cell stroke therapy: current limitations in its clinical translation

For more than a decade now, research studies, proof of concept work, and clinical trials have endeavored to understand how mesenchymal stem cells might be used to help protect, repair, and/or regene [...] Read more.

Ylenia Pastorello, Mark Slevin

Published: June 28, 2023 Explor Neurosci. 2023;2:98–105
DOI: https://doi.org/10.37349/en.2023.00015
This article belongs to the special issue Neuroinflammation in the Ageing and the Injured Brain

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Review

Therapeutic potential of extracellular vesicles in Parkinson’s disease

Globally, the incidence of Parkinson’s disease (PD) is increasing faster than other neurodegenerative disorders. Neuropathologically, PD is characterized by the loss of dopaminergic neurons in the [...] Read more.

Michelli Ramires Teixeira ... Rodrigo Pinheiro Araldi

Published: June 29, 2023 Explor Neurosci. 2023;2:106–122
DOI: https://doi.org/10.37349/en.2023.00016
This article belongs to the special issue Extracellular Vesicles as Cell-based Therapeutics

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