An impairment in brain function

2021 ◽  
pp. 89-102
Author(s):  
Mark Selikowitz

ADHD is usually due to a depletion of certain chemical messengers in the front part of the brain. The major cause of this depletion relates to a number of defective genes. ADHD shares some of its causative genes with certain other conditions, so having ADHD makes also having these other conditions more likely. To help many children with learning and behavioural difficulties, we need to treat an impairment in their brain function. This chapter discusses impairment in brain function as a cause of ADHD, including executive function deficits, frontal lobe underactivity, neurotransmitter depletion, gene defects, and non-genetic factors. It also describes the mechanism of comorbidity.

2021 ◽  
Author(s):  
J. S. Jones ◽  
D. E. Astle ◽  

AbstractBehavioural difficulties are seen as hallmarks of many neurodevelopmental conditions. Differences in functional brain organisation have been observed in these conditions, but little is known about how they are related to a child’s profile of behavioural difficulties. We investigated whether behavioural difficulties are associated with how the brain is functionally organised in an intentionally heterogeneous and transdiagnostic sample of 957 children aged 5-15. We used consensus community detection to derive data-driven profiles of behavioural difficulties and constructed functional connectomes from a subset of 238 children with resting-state functional Magnetic Resonance Imaging (fMRI) data. We identified three distinct profiles of behaviour that were characterised by principal difficulties with hot executive function, cool executive function, and learning. Global organisation of the functional connectome did not differ between the groups, but multivariate patterns of connectivity at the level of Intrinsic Connectivity Networks (ICNs), nodes, and hubs significantly predicted group membership in held-out data. Fronto-parietal connector hubs were under-connected in all groups relative to a comparison sample, and children with hot vs cool executive function difficulties were distinguished by connectivity in ICNs associated with cognitive control, emotion processing, and social cognition. This demonstrates both general and specific neurodevelopmental risk factors in the functional connectome.


2021 ◽  
Author(s):  
Victor Oliveira Araújo ◽  
Isadora Mônica Ponte de Oliveira ◽  
Lara Maria de Oliveira Paiva Freitas ◽  
Júlio César Claudino dos Santos

Introduction: Covid-19 infection can affect not only the airways but also other organs such as the brain. Individuals that tested positive for SARSCoV-2 may be asymptomatic, but can also have symptoms - such as “brain fog” - during the acute phase and/or the post-acute phase (being the last ones defined as long haulers). “Brain fog” is a set of symptoms characterized by cognitive dysfunction that includes the inability to concentrate, executive function deficits, anterograde and retrograde amnesia. Objective: Review the pathophysiology of individuals with Covid-19 post-acute phase brain fog. Design and setting: A literature review was conducted on the topic. Methods: 12 original selected articles in English and Portuguese from PubMed and Google Academic databases dated from 2017 to 2021. Results: Research evidenced that 18-36% of the patients hospitalized for Covid-19 that had neurological symptoms also experienced brain fog in the post-acute phase. Although not completely elucidated, there are hypothesized mechanisms to clarify the neurological symptoms in the “long haulers’’ patients, such as the release of pro-inflammatory substances that reduce synaptic fidelity due to dysregulation in the levels of neurotransmitters which are fundamental for brain function. In addition, SARS-CoV-2 provides microthrombus formation and possible small cerebral ischemia. Conclusion: The pathophysiology of brain fog is not yet fully proven, since the literature on the subject is limited. Therefore, more robust research in patients who developed neurological symptoms after infection by the new coronavirus is needed to clarify the pathophysiology, clinical management and most appropriate treatment for individuals with brain fog.


2012 ◽  
Author(s):  
Kaley Mirabal ◽  
Lisa J. Kasper ◽  
R. Matt Alderson ◽  
Kristen L. Hudec

Author(s):  
Preecha Yupapin ◽  
Amiri I. S. ◽  
Ali J. ◽  
Ponsuwancharoen N. ◽  
Youplao P.

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.


2020 ◽  
Vol 15 (4) ◽  
pp. 287-299
Author(s):  
Jie Zhang ◽  
Junhong Feng ◽  
Fang-Xiang Wu

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.


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.


Author(s):  
Stefano Vassanelli

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.


Author(s):  
Siri Hauge Opdal ◽  
Linda Ferrante ◽  
Torleiv Ole Rognum ◽  
Arne Stray-Pedersen

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.


2021 ◽  
Vol 22 (9) ◽  
pp. 4511
Author(s):  
Chiara A. De Benedictis ◽  
Claudia Haffke ◽  
Simone Hagmeyer ◽  
Ann Katrin Sauer ◽  
Andreas M. Grabrucker

In the last years, research has shown that zinc ions play an essential role in the physiology of brain function. Zinc acts as a potent neuromodulatory agent and signaling ions, regulating healthy brain development and the function of both neurons and glial cells. Therefore, the concentration of zinc within the brain and its cells is tightly controlled. Zinc transporters are key regulators of (extra-) cellular zinc levels, and deregulation of zinc homeostasis and zinc transporters has been associated with neurodegenerative and neuropsychiatric disorders. However, to date, the presence of specific family members and their subcellular localization within brain cells have not been investigated in detail. Here, we analyzed the expression of all zinc transporters (ZnTs) and Irt-like proteins (ZIPs) in the rat brain. We further used primary rat neurons and rat astrocyte cell lines to differentiate between the expression found in neurons or astrocytes or both. We identified ZIP4 expressed in astrocytes but significantly more so in neurons, a finding that has not been reported previously. In neurons, ZIP4 is localized to synapses and found in a complex with major postsynaptic scaffold proteins of excitatory synapses. Synaptic ZIP4 reacts to short-term fluctuations in local zinc levels. We conclude that ZIP4 may have a so-far undescribed functional role at excitatory postsynapses.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Juan Kou ◽  
Chunmei Lan ◽  
Yingying Zhang ◽  
Qianqian Wang ◽  
Feng Zhou ◽  
...  

AbstractIntranasal oxytocin exerts wide-ranging effects on socioemotional behavior and is proposed as a potential therapeutic intervention in psychiatric disorders. However, following intranasal administration, oxytocin could penetrate directly into the brain or influence its activity via increased peripheral concentrations crossing the blood–brain barrier or influencing vagal projections. In the current randomized, placebo-controlled, pharmaco-imaging clinical trial we investigated effects of 24IU oral (lingual) oxytocin spray, restricting it to peripherally mediated blood-borne and vagal effects, on responses to face emotions in 80 male subjects and compared them with 138 subjects treated intranasally with 24IU. Oral, but not intranasal oxytocin administration increased both arousal ratings for faces and associated brain reward responses, the latter being partially mediated by blood concentration changes. Furthermore, while oral oxytocin increased amygdala and arousal responses to face emotions, after intranasal administration they were decreased. Thus, oxytocin can produce markedly contrasting motivational effects in relation to socioemotional cues when it influences brain function via different routes. These findings have important implications for future therapeutic use since administering oxytocin orally may be both easier and have potentially stronger beneficial effects by enhancing responses to emotional cues and increasing their associated reward.


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