scholarly journals Astrocytic Ca2+ Signaling in Epilepsy

2021 ◽  
Vol 15 ◽  
Author(s):  
Kjell Heuser ◽  
Rune Enger
Keyword(s):  
Brain Function ◽  
Current Knowledge ◽  
Symptomatic Treatment ◽  
Pharmacological Therapy ◽  
Signaling Mechanism ◽  
Network Function ◽  
Central Tenet ◽  
Intracellular Ca ◽  
The Brain ◽  
Synaptic Mechanisms

Epilepsy is one of the most common neurological disorders – estimated to affect at least 65 million worldwide. Most of the epilepsy research has so far focused on how to dampen neuronal discharges and to explain how changes in intrinsic neuronal activity or network function cause seizures. As a result, pharmacological therapy has largely been limited to symptomatic treatment targeted at neurons. Given the expanding spectrum of functions ascribed to the non-neuronal constituents of the brain, in both physiological brain function and in brain disorders, it is natural to closely consider the roles of astrocytes in epilepsy. It is now widely accepted that astrocytes are key controllers of the composition of the extracellular fluids, and may directly interact with neurons by releasing gliotransmitters. A central tenet is that astrocytic intracellular Ca2+ signals promote release of such signaling substances, either through synaptic or non-synaptic mechanisms. Accruing evidence suggests that astrocytic Ca2+ signals play important roles in both seizures and epilepsy, and this review aims to highlight the current knowledge of the roles of this central astrocytic signaling mechanism in ictogenesis and epileptogenesis.

Implications of neural networks for how we think about brain function

1992 ◽  
Vol 15 (4) ◽  
pp. 644-655
Author(s):  
David A. Robinson
Keyword(s):  
Neural Networks ◽  
Control Systems ◽  
Brain Function ◽  
Single Unit ◽  
Task Complexity ◽  
The Other ◽  
Network Function ◽  
A Cell ◽  
Single Unit Recordings ◽  
The Brain

Abstract Engineers use neural networks to control systems too complex for conventional engineering solutions. To examine the behavior of individual hidden units would defeat the purpose of this approach because it would be largely uninterpretable. Yet neurophysiologists spend their careers doing just that! Hidden units contain bits and scraps of signals that yield only arcane hints about network function and no information about how its individual units process signals. Most literature on single-unit recordings attests to this grim fact. On the other hand, knowing a system's function and describing it with elegant mathematics tell one very little about what to expect of interneuronal behavior. Examples of simple networks based on neurophysiology are taken from the oculomotor literature to suggest how single-unit interpretability might decrease with increasing task complexity. It is argued that trying to explain how any real neural network works on a cell-by-cell, reductionist basis is futile and we may have to be content with trying to understand the brain at higher levels of organization.

Frontier concept of rabi chip for intelligent humanoid

2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Preecha Yupapin ◽  
Amiri I. S. ◽  
Ali J. ◽  
Ponsuwancharoen N. ◽  
Youplao P.
Keyword(s):  
Human Brain ◽  
Brain Function ◽  
Rabi Oscillation ◽  
Liquid Core ◽  
Brain Surface ◽  
Dipole Oscillation ◽  
On Chip ◽  
The Brain ◽  
Robotic Applications ◽  
Atom System

The sequence of the human brain can be configured by the originated strongly coupling fields to a pair of the ionic substances(bio-cells) within the microtubules. From which the dipole oscillation begins and transports by the strong trapped force, which is known as a tweezer. The tweezers are the trapped polaritons, which are the electrical charges with information. They will be collected on the brain surface and transport via the liquid core guide wave, which is the mixture of blood content and water. The oscillation frequency is called the Rabi frequency, is formed by the two-level atom system. Our aim will manipulate the Rabi oscillation by an on-chip device, where the quantum outputs may help to form the realistic human brain function for humanoid robotic applications.

Neurotoxic and Neuroprotective Role of Exosomes in Parkinson’s Disease

2020 ◽  
Vol 25 (42) ◽  
pp. 4510-4522 ◽  
Author(s):  
Biancamaria Longoni ◽  
Irene Fasciani ◽  
Shivakumar Kolachalam ◽  
Ilaria Pietrantoni ◽  
Francesco Marampon ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Potential Role ◽  
Current Knowledge ◽  
Biological Fluids ◽  
Cell Communication ◽  
Target Cells ◽  
Cellular Debris ◽  
The Brain

: Exosomes are extracellular vesicles produced by eukaryotic cells that are also found in most biological fluids and tissues. While they were initially thought to act as compartments for removal of cellular debris, they are now recognized as important tools for cell-to-cell communication and for the transfer of pathogens between the cells. They have attracted particular interest in neurodegenerative diseases for their potential role in transferring prion-like proteins between neurons, and in Parkinson’s disease (PD), they have been shown to spread oligomers of α-synuclein in the brain accelerating the progression of this pathology. A potential neuroprotective role of exosomes has also been equally proposed in PD as they could limit the toxicity of α-synuclein by clearing them out of the cells. Exosomes have also attracted considerable attention for use as drug vehicles. Being nonimmunogenic in nature, they provide an unprecedented opportunity to enhance the delivery of incorporated drugs to target cells. In this review, we discuss current knowledge about the potential neurotoxic and neuroprotective role of exosomes and their potential application as drug delivery systems in PD.

Finding Community of Brain Networks Based on Neighbor Index and DPSO with Dynamic Crossover

2020 ◽  
Vol 15 (4) ◽  
pp. 287-299
Author(s):  
Jie Zhang ◽  
Junhong Feng ◽  
Fang-Xiang Wu
Keyword(s):  
Brain Function ◽  
Brain Networks ◽  
Discrete Particle Swarm Optimization ◽  
Mri Brain ◽  
Mutation Operators ◽  
Neural Unit ◽  
Crossover And Mutation ◽  
The Brain ◽  
Index Table ◽  
Dynamic Crossover

Background: : The brain networks can provide us an effective way to analyze brain function and brain disease detection. In brain networks, there exist some import neural unit modules, which contain meaningful biological insights. Objective:: Therefore, we need to find the optimal neural unit modules effectively and efficiently. Method:: In this study, we propose a novel algorithm to find community modules of brain networks by combining Neighbor Index and Discrete Particle Swarm Optimization (DPSO) with dynamic crossover, abbreviated as NIDPSO. The differences between this study and the existing ones lie in that NIDPSO is proposed first to find community modules of brain networks, and dose not need to predefine and preestimate the number of communities in advance. Results: : We generate a neighbor index table to alleviate and eliminate ineffective searches and design a novel coding by which we can determine the community without computing the distances amongst vertices in brain networks. Furthermore, dynamic crossover and mutation operators are designed to modify NIDPSO so as to alleviate the drawback of premature convergence in DPSO. Conclusion: The numerical results performing on several resting-state functional MRI brain networks demonstrate that NIDPSO outperforms or is comparable with other competing methods in terms of modularity, coverage and conductance metrics.

Experimental Rodent Models of Vascular Dementia: A Systematic Review

2021 ◽  
Vol 19 ◽  
Author(s):  
Nidhi Tiwari ◽  
Jyoti Upadhyay ◽  
Mohd Nazam Ansari ◽  
Syed Shadab Raza ◽  
Wasim Ahmad ◽  
...  
Keyword(s):  
Vascular Dementia ◽  
Small Vessel Disease ◽  
Current Knowledge ◽  
Vascular Cognitive Impairment ◽  
Experimental Models ◽  
New Drugs ◽  
Amyloid Angiopathy ◽  
Vessel Disease ◽  
The Brain ◽  
Large Vessel Disease

: Vascular dementia (VaD) occurs due to cerebrovascular insufficiency, which leads to decreased blood circulation to the brain, thereby resulting in mental disabilities. The main causes of vascular cognitive impairment (VCI) are severe hypoperfusion, stroke, hypertension, large vessel disease (cortical), small vessel disease (subcortical VaD), strategic infarct, hemorrhage (microbleed), cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and cerebral amyloid angiopathy (CAA),which leads to decreased cerebrovascular perfusion. Many metabolic disorders such as diabetes mellitus (DM), dyslipidemia, and hyperhomocysteinemia are also related to VaD. The rodent experimental models provide a better prospective for the investigation of the molecular mechanism of new drugs. A plethora of experimental models are available that mimic the pathological conditions and lead to VaD. This review article updates the current knowledge on the basis of VaD, risk factors, pathophysiology, mechanism, advantages, limitations, and the modification of various available rodent experimental models.

Neuroethics

2017 ◽  
Keyword(s):  
Brain Function ◽  
Ethical Issues ◽  
Wearable Technologies ◽  
Definition Of Death ◽  
Populations At Risk ◽  
The Future ◽  
Aging Adults ◽  
Definition Of ◽  
The Brain ◽  
New Criteria

We have new answers to how the brain works and tools which can now monitor and manipulate brain function. Rapid advances in neuroscience raise critical questions with which society must grapple. What new balances must be struck between diagnosis and prediction, and invasive and noninvasive interventions? Are new criteria needed for the clinical definition of death in cases where individuals are eligible for organ donation? How will new mobile and wearable technologies affect the future of growing children and aging adults? To what extent is society responsible for protecting populations at risk from environmental neurotoxins? As data from emerging technologies converge and are made available on public databases, what frameworks and policies will maximize benefits while ensuring privacy of health information? And how can people and communities with different values and perspectives be maximally engaged in these important questions? Neuroethics: Anticipating the Future is written by scholars from diverse disciplines—neurology and neuroscience, ethics and law, public health, sociology, and philosophy. With its forward-looking insights and considerations for the future, the book examines the most pressing current ethical issues.

Implantable neural interfaces

2018 ◽  
Author(s):  
Stefano Vassanelli
Keyword(s):  
Brain Function ◽  
Large Scale ◽  
Ionic Channels ◽  
Patch Clamp Technique ◽  
Advantages And Disadvantages ◽  
Optogenetic Stimulation ◽  
Physical Interfaces ◽  
The Brain

Establishing direct communication with the brain through physical interfaces is a fundamental strategy to investigate brain function. Starting with the patch-clamp technique in the seventies, neuroscience has moved from detailed characterization of ionic channels to the analysis of single neurons and, more recently, microcircuits in brain neuronal networks. Development of new biohybrid probes with electrodes for recording and stimulating neurons in the living animal is a natural consequence of this trend. The recent introduction of optogenetic stimulation and advanced high-resolution large-scale electrical recording approaches demonstrates this need. Brain implants for real-time neurophysiology are also opening new avenues for neuroprosthetics to restore brain function after injury or in neurological disorders. This chapter provides an overview on existing and emergent neurophysiology technologies with particular focus on those intended to interface neuronal microcircuits in vivo. Chemical, electrical, and optogenetic-based interfaces are presented, with an analysis of advantages and disadvantages of the different technical approaches.

scholarly journals L2HGDH Missense Variant in a Cat with L-2-Hydroxyglutaric Aciduria

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 682
Author(s):  
Matthias Christen ◽  
Nils Janzen ◽  
Anne Fraser ◽  
Adrian C. Sewell ◽  
Vidhya Jagannathan ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Genetic Defect ◽  
Clinical Signs ◽  
Missense Variant ◽  
Microcytic Anemia ◽  
Abnormal Behavior ◽  
Functional Candidate Gene ◽  
History Of ◽  
The Brain ◽  
Hydroxyglutaric Acid

A 7-month-old, spayed female, domestic longhair cat with L-2-hydroxyglutaric aciduria (L-2-HGA) was investigated. The aim of this study was to investigate the clinical signs, metabolic changes and underlying genetic defect. The owner of the cat reported a 4-month history of multiple paroxysmal seizure-like episodes, characterized by running around the house, often in circles, with abnormal behavior, bumping into obstacles, salivating and often urinating. The episodes were followed by a period of disorientation and inappetence. Neurological examination revealed an absent bilateral menace response. Routine blood work revealed mild microcytic anemia but biochemistry, ammonia, lactate and pre- and post-prandial bile acids were unremarkable. MRI of the brain identified multifocal, bilaterally symmetrical and T2-weighted hyperintensities within the prosencephalon, mesencephalon and metencephalon, primarily affecting the grey matter. Urinary organic acids identified highly increased levels of L-2-hydroxyglutaric acid. The cat was treated with the anticonvulsants levetiracetam and phenobarbitone and has been seizure-free for 16 months. We sequenced the genome of the affected cat and compared the data to 48 control genomes. L2HGDH, coding for L-2-hydroxyglutarate dehydrogenase, was investigated as the top functional candidate gene. This search revealed a single private protein-changing variant in the affected cat. The identified homozygous variant, XM_023255678.1:c.1301A>G, is predicted to result in an amino acid change in the L2HGDH protein, XP_023111446.1:p.His434Arg. The available clinical and biochemical data together with current knowledge about L2HGDH variants and their functional impact in humans and dogs allow us to classify the p.His434Arg variant as a causative variant for the observed neurological signs in this cat.

scholarly journals Aquaporin-1 and aquaporin-9 gene variations in sudden infant death syndrome

2021 ◽  
Author(s):  
Siri Hauge Opdal ◽  
Linda Ferrante ◽  
Torleiv Ole Rognum ◽  
Arne Stray-Pedersen
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Brain Function ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Unexpected Death ◽  
Aquaporin 9 ◽  
Genes Encoding ◽  
External Risk ◽  
The Brain

AbstractSeveral studies have indicated that a vulnerability in the development and regulation of brain function is involved in sudden infant death syndrome (SIDS). The aim of this study was to investigate the genes encoding the brain aquaporins (AQPs) AQP1 and AQP9 in SIDS. The hypothesis was that specific variants of these genes are part of the genetic vulnerability predisposing infants to sudden unexpected death. The study included 168 SIDS cases with a median age of 15.5 (range 2–52) weeks and 372 adolescent/adult deceased controls with a median age of 44 (range 11–91) years. In the AQP1 gene, the rs17159702 CC/CT genotypes were found to be associated with SIDS (p = 0.02). In the AQP9 gene, the combination of a TT genotype of rs8042354, rs2292711 and rs13329178 was more frequent in SIDS cases than in controls (p = 0.03). In the SIDS group, an association was found between genetic variations in the AQP1 gene and maternal smoking and between the 3xTT combination in the AQP9 gene and being found lifeless in a prone position. In conclusion, this study adds further evidence to the involvement of brain aquaporins in SIDS, suggesting that specific variants of AQP genes constitute a genetic predisposition, making the infant vulnerable to sudden death together with external risk factors and probably other genetic factors.

scholarly journals The L1-dependant and Pol III transcribed Alu retrotransposon, from its discovery to innate immunity

2021 ◽  
Vol 48 (3) ◽  
pp. 2775-2789
Author(s):  
Ludwig Stenz
Keyword(s):  
Human Genome ◽  
Viral Infections ◽  
De Novo ◽  
Current Knowledge ◽  
Innate Immune ◽  
De Novo Mutation ◽  
Neuronal Diversity ◽  
Alu Sequences ◽  
Pol Iii ◽  
The Brain

AbstractThe 300 bp dimeric repeats digestible by AluI were discovered in 1979. Since then, Alu were involved in the most fundamental epigenetic mechanisms, namely reprogramming, pluripotency, imprinting and mosaicism. These Alu encode a family of retrotransposons transcribed by the RNA Pol III machinery, notably when the cytosines that constitute their sequences are de-methylated. Then, Alu hijack the functions of ORF2 encoded by another transposons named L1 during reverse transcription and integration into new sites. That mechanism functions as a complex genetic parasite able to copy-paste Alu sequences. Doing that, Alu have modified even the size of the human genome, as well as of other primate genomes, during 65 million years of co-evolution. Actually, one germline retro-transposition still occurs each 20 births. Thus, Alu continue to modify our human genome nowadays and were implicated in de novo mutation causing diseases including deletions, duplications and rearrangements. Most recently, retrotransposons were found to trigger neuronal diversity by inducing mosaicism in the brain. Finally, boosted during viral infections, Alu clearly interact with the innate immune system. The purpose of that review is to give a condensed overview of all these major findings that concern the fascinating physiology of Alu from their discovery up to the current knowledge.

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