Brain

دسترسی یکساله به بیش از ۵۰۰ ژورنال روز جهان موجود در سامانه

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سفارش

Why the next generation of UK clinician scientists is under threat

Masud Husain

doi : 10.1093/brain/awab381

Brain, Volume 144, Issue 11, November 2021, Pages 3277–3278

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Functional neurological disorder: lighting the way to a new paradigm for medicine

Mark J Edwards

doi : 10.1093/brain/awab358

Brain, Volume 144, Issue 11, November 2021, Pages 3279–3282

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Plasma sTREM2: a potential marker of cerebrovascular injury in neurodegenerative disorders

Elena Rodriguez-Vieitez, Nicholas J Ashton

doi : 10.1093/brain/awab399

Brain, Volume 144, Issue 11, November 2021, Pages 3283–3285

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Hitching a ride on exosomes: a new approach for the delivery of siRNA-mediated therapies

Allison Snyder, Christopher Grunseich

doi : 10.1093/brain/awab398

Brain, Volume 144, Issue 11, November 2021, Pages 3286–3287

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Random forest: random results or meaningful insights for patients with facioscapulohumeral muscular dystrophy?

Lindsay N Alfano, Tahseen Mozaffar

doi : 10.1093/brain/awab389

Brain, Volume 144, Issue 11, November 2021, Pages 3288–3290

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The neuroethics of disorders of consciousness: a brief history of evolving ideas

Michael J Young, Yelena G Bodien, Joseph T Giacino, Joseph J Fins, Robert D Truog, Leigh R Hochberg, Brian L Edlow

doi : 10.1093/brain/awab290

Brain, Volume 144, Issue 11, November 2021, Pages 3291–3310

Neuroethical questions raised by recent advances in the diagnosis and treatment of disorders of consciousness are rapidly expanding, increasingly relevant and yet underexplored. The aim of this thematic review is to provide a clinically applicable framework for understanding the current taxonomy of disorders of consciousness and to propose an approach to identifying and critically evaluating actionable neuroethical issues that are frequently encountered in research and clinical care for this vulnerable population. Increased awareness of these issues and clarity about opportunities for optimizing ethically responsible care in this domain are especially timely given recent surges in critically ill patients with prolonged disorders of consciousness associated with coronavirus disease 2019 around the world. We begin with an overview of the field of neuroethics: what it is, its history and evolution in the context of biomedical ethics at large. We then explore nomenclature used in disorders of consciousness, covering categories proposed by the American Academy of Neurology, the American Congress of Rehabilitation Medicine and the National Institute on Disability, Independent Living and Rehabilitation Research, including definitions of terms such as coma, the vegetative state, unresponsive wakefulness syndrome, minimally conscious state, covert consciousness and the confusional state. We discuss why these definitions matter, and why there has been such evolution in this nosology over the years, from Jennett and Plum in 1972 to the Multi-Society Task Force in 1994, the Aspen Working Group in 2002 and the 2018 American and 2020 European Disorders of Consciousness guidelines. We then move to a discussion of clinical aspects of disorders of consciousness, the natural history of recovery and ethical issues that arise within the context of caring for people with disorders of consciousness. We conclude with a discussion of key challenges associated with assessing residual consciousness in disorders of consciousness, potential solutions and future directions, including integration of crucial disability rights perspectives.

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Evidence and implications of abnormal predictive coding in dementia

Ece Kocagoncu, Anastasia Klimovich-Gray, Laura E Hughes, James B Rowe

doi : 10.1093/brain/awab254

Brain, Volume 144, Issue 11, November 2021, Pages 3311–3321

The diversity of cognitive deficits and neuropathological processes associated with dementias has encouraged divergence in pathophysiological explanations of disease. Here, we review an alternative framework that emphasizes convergent critical features of cognitive pathophysiology. Rather than the loss of ‘memory centres’ or ‘language centres’, or singular neurotransmitter systems, cognitive deficits are interpreted in terms of aberrant predictive coding in hierarchical neural networks. This builds on advances in normative accounts of brain function, specifically the Bayesian integration of beliefs and sensory evidence in which hierarchical predictions and prediction errors underlie memory, perception, speech and behaviour. We describe how analogous impairments in predictive coding in parallel neurocognitive systems can generate diverse clinical phenomena, including the characteristics of dementias. The review presents evidence from behavioural and neurophysiological studies of perception, language, memory and decision-making. The reformulation of cognitive deficits in terms of predictive coding has several advantages. It brings diverse clinical phenomena into a common framework; it aligns cognitive and movement disorders; and it makes specific predictions on cognitive physiology that support translational and experimental medicine studies. The insights into complex human cognitive disorders from the predictive coding framework may therefore also inform future therapeutic strategies.

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Survival of brain tumour patients with epilepsy

Maximilian Mastall, Fabian Wolpert, Dorothee Gramatzki, Lukas Imbach, Denise Becker, Anton Schmick, Caroline Hertler, Patrick Roth, Michael Weller, Hans-Georg Wirsching

doi : 10.1093/brain/awab188

Brain, Volume 144, Issue 11, November 2021, Pages 3322–3327

Pro-tumorigenic electrochemical synapses between neurons and brain tumour cells in preclinical studies suggest unfavourable effects of epilepsy on patient survival. We investigated associations of epilepsy and survival in three cohorts of brain tumour patients (meningioma, glioblastoma and brain metastases). Cohorts were segregated into three groups for comparative analyses: (i) no epilepsy; (ii) epilepsy without status epilepticus; and (iii) status epilepticus. Status epilepticus was considered a surrogate of extensive neuronal hyperexcitability. The main outcome was progression-free survival (meningioma) and overall survival (glioblastoma and brain metastases), adjusted for established prognostic factors and onset of epilepsy by time-dependent multivariate Cox modelling. The primary analysis population comprised 1792 patients (742 meningioma, 249 glioblastoma, 801 brain metastases). Epilepsy was associated with favourable prognostic factors. However, on multivariate analyses, status epilepticus was associated with inferior overall survival of patients with glioblastoma [status epilepticus versus no epilepsy multivariate hazard ratio (HR) 3.72, confidence interval (CI) 1.78–7.76, P < 0.001] and brain metastases (status epilepticus versus no epilepsy HR 2.30, CI 1.10–4.79, P = 0.026). Among brain metastases patients, but not among patients with meningioma or glioblastoma, epilepsy was similarly associated with inferior overall survival (epilepsy versus no epilepsy HR 2.16, CI 1.60–2.93, P < 0.001). We conclude that epilepsy may convey inferior survival of patients with malignant brain tumours.

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Repetitive transcranial magnetic stimulation for neuropathic pain: a randomized multicentre sham-controlled trial

Nadine Attal, Frédérique Poindessous-Jazat, Edwige De Chauvigny, Charles Quesada, Alaa Mhalla, Samar S Ayache, Christophe Fermanian, Julien Nizard, Roland Peyron, Jean-Pascal Lefaucheur, Didier Bouhassira

doi : 10.1093/brain/awab208

Brain, Volume 144, Issue 11, November 2021, Pages 3328–3339

Repetitive transcranial magnetic stimulation (rTMS) has been proposed to treat neuropathic pain but the quality of evidence remains low. We aimed to assess the efficacy and safety of neuronavigated rTMS to the primary motor cortex (M1) or dorsolateral prefrontal cortex (DLPFC) in neuropathic pain over 25?weeks.

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Six-dimensional dynamic tractography atlas of language connectivity in the developing brain

Masaki Sonoda, Brian H Silverstein, Jeong-Won Jeong, Ayaka Sugiura, Yasuo Nakai, Takumi Mitsuhashi, Robert Rothermel, Aimee F Luat, Sandeep Sood, Eishi Asano

doi : 10.1093/brain/awab225

Brain, Volume 144, Issue 11, November 2021, Pages 3340–3354

During a verbal conversation, our brain moves through a series of complex linguistic processing stages: sound decoding, semantic comprehension, retrieval of semantically coherent words, and overt production of speech outputs. Each process is thought to be supported by a network consisting of local and long-range connections bridging between major cortical areas. Both temporal and extratemporal lobe regions have functional compartments responsible for distinct language domains, including the perception and production of phonological and semantic components.

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Activation of ?7 nicotinic acetylcholine receptor ameliorates HIV-associated neurology and neuropathology

Xiaojie Zhao, Kelly Wilson, Victor Uteshev, Johnny J He

doi : 10.1093/brain/awab251

Brain, Volume 144, Issue 11, November 2021, Pages 3355–3370

HIV-associated neurocognitive disorders (HAND) in the era of combination antiretroviral therapy are primarily manifested as impaired behaviours, glial activation/neuroinflammation and compromised neuronal integrity, for which there are no effective treatments currently available.

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Plasma soluble TREM2 is associated with white matter lesions independent of amyloid and tau

Hsin-Hsi Tsai, Ya-Fang Chen, Ruoh-Fang Yen, Yen-Ling Lo, Kai-Chien Yang, Jiann-Shing Jeng, Li-Kai Tsai, Che-Feng Chang

doi : 10.1093/brain/awab332

Brain, Volume 144, Issue 11, November 2021, Pages 3371–3380

Cerebral small vessel disease is one of the most common causes of cognitive decline and stroke. While several lines of evidence have established a relationship between inflammation and cerebrovascular pathology, the mechanistic link has not yet been elucidated. Recent studies suggest activation of immune mediators, including the soluble form of triggering receptor expressed on myeloid cells 2 (TREM2), may be critical regulators.

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The efficacy and deficiency of contemporary treatment for spinal cord arteriovenous shunts

Jia-Xing Yu, Chuan He, Ming Ye, Gui-Lin Li, Li-Song Bian, Fan Yang, Xiao-Dong Zhai, Feng Ling, Hong-Qi Zhang, Tao Hong

doi : 10.1093/brain/awab237

Brain, Volume 144, Issue 11, November 2021, Pages 3381–3391

Contemporary treatments for spinal cord arteriovenous shunts are only based on clinicians’ treatment experiences and expertise due to its rarity. We reviewed the clinical course of the largest multicentred cohort to evaluate the efficacy and deficiency of contemporary interventional treatments for spinal cord arteriovenous shunts.

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Guillain-Barré syndrome after SARS-CoV-2 infection in an international prospective cohort study

Linda W G Luijten, Sonja E Leonhard, Annemiek A van der Eijk, Alex Y Doets, Luise Appeltshauser, Samuel Arends, Shahram Attarian, Luana Benedetti, Chiara Briani, Carlos Casasnovas, Francesca Castellani, Efthimios Dardiotis, Andoni Echaniz-Laguna, Marcel P J Garssen, Thomas Harbo, Ruth Huizinga, Andrea M Humm, Korné Jellema, Anneke J van der Kooi, Krista Kuitwaard, Thierry Kuntzer, Susumu Kusunoki, Agustina M Lascano, Eugenia Martinez-Hernandez, Simon Rinaldi, Johnny P A Samijn, Olivier Scheidegger, Pinelopi Tsouni, Alex Vicino, Leo H Visser, Christa Walgaard, Yuzhong Wang, Paul W Wirtz, Paolo Ripellino, Bart C Jacobs, the IGOS consortium

doi : 10.1093/brain/awab279

Brain, Volume 144, Issue 11, November 2021, Pages 3392–3404

In the wake of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, an increasing number of patients with neurological disorders, including Guillain-Barré syndrome (GBS), have been reported following this infection. It remains unclear, however, if these cases are coincidental or not, as most publications were case reports or small regional retrospective cohort studies. The International GBS Outcome Study is an ongoing prospective observational cohort study enrolling patients with GBS within 2?weeks from onset of weakness. Data from patients included in this study, between 30 January 2020 and 30 May 2020, were used to investigate clinical and laboratory signs of a preceding or concurrent SARS-CoV-2 infection and to describe the associated clinical phenotype and disease course. Patients were classified according to the SARS-CoV-2 case definitions of the European Centre for Disease Prevention and Control and laboratory recommendations of the World Health Organization. Forty-nine patients with GBS were included, of whom eight (16%) had a confirmed and three (6%) a probable SARS-CoV-2 infection. Nine of these 11 patients had no serological evidence of other recent preceding infections associated with GBS, whereas two had serological evidence of a recent Campylobacter jejuni infection. Patients with a confirmed or probable SARS-CoV-2 infection frequently had a sensorimotor variant 8/11 (73%) and facial palsy 7/11 (64%). The eight patients who underwent electrophysiological examination all had a demyelinating subtype, which was more prevalent than the other patients included in the same time window [14/30 (47%), P?=?0.012] as well as historical region and age-matched control subjects included in the International GBS Outcome Study before the pandemic [23/44 (52%), P?=?0.016]. The median time from the onset of infection to neurological symptoms was 16?days (interquartile range 12–22). Patients with SARS-CoV-2 infection shared uniform neurological features, similar to those previously described in other post-viral GBS patients. The frequency (22%) of a preceding SARS-CoV-2 infection in our study population was higher than estimates of the contemporaneous background prevalence of SARS-CoV-2, which may be a result of recruitment bias during the pandemic, but could also indicate that GBS may rarely follow a recent SARS-CoV-2 infection. Consistent with previous studies, we found no increase in patient recruitment during the pandemic for our ongoing International GBS Outcome Study compared to previous years, making a strong relationship of GBS with SARS-CoV-2 unlikely. A case-control study is required to determine if there is a causative link or not.

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GPR151 in nociceptors modulates neuropathic pain via regulating P2X3 function and microglial activation

Li-Ping Xia, Hao Luo, Qiang Ma, Ya-Kai Xie, Wei Li, Hailan Hu, Zhen-Zhong Xu

doi : 10.1093/brain/awab245

Brain, Volume 144, Issue 11, November 2021, Pages 3405–3420

Neuropathic pain is a major health problem that affects up to 7–10% of the population worldwide. Currently, neuropathic pain is difficult to treat because of its elusive mechanisms.

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Therapeutic reversal of Huntington’s disease by in vivo self-assembled siRNAs

Li Zhang, Tengteng Wu, Yangyang Shan, Ge Li, Xue Ni, Xiaorui Chen, Xiuting Hu, Lishan Lin, Yongchao Li, Yalun Guan, Jinfeng Gao, Dingbang Chen, Yu Zhang, Zhong Pei, Xi Chen

doi : 10.1093/brain/awab354

Brain, Volume 144, Issue 11, November 2021, Pages 3421–3435

Huntington’s disease is an autosomal-dominant neurodegenerative disease caused by CAG expansion in exon 1 of the huntingtin (HTT) gene. Since mutant huntingtin (mHTT) protein is the root cause of Huntington’s disease, oligonucleotide-based therapeutic approaches using small interfering RNAs (siRNAs) and antisense oligonucleotides designed to specifically silence mHTT may be novel therapeutic strategies for Huntington’s disease. Unfortunately, the lack of an effective in vivo delivery system remains a major obstacle to realizing the full potential of oligonucleotide therapeutics, especially regarding the delivery of oligonucleotides to the cortex and striatum, the most severely affected brain regions in Huntington’s disease.

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Misdirected attentional focus in functional tremor

Anne-Catherine M L Huys, Patrick Haggard, Kailash P Bhatia, Mark J Edwards

doi : 10.1093/brain/awab230

Brain, Volume 144, Issue 11, November 2021, Pages 3436–3450

A characteristic and intriguing feature of functional neurological disorder is that symptoms typically manifest with attention and improve or disappear with distraction. Attentional phenomena are therefore likely to be important in functional neurological disorder, but exactly how this manifests is unknown. The aim of the study was to establish whether in functional tremor the attentional focus is misdirected, and whether this misdirection is detrimental to the movement, or rather reflects a beneficial compensatory strategy.

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Predictors of functional outcomes in patients with facioscapulohumeral muscular dystrophy

Natalie K Katz, John Hogan, Ryan Delbango, Colin Cernik, Rabi Tawil, Jeffrey M Statland

doi : 10.1093/brain/awab326

Brain, Volume 144, Issue 11, November 2021, Pages 3451–3460

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most prevalent muscular dystrophies characterized by considerable variability in severity, rates of progression and functional outcomes. Few studies follow FSHD cohorts long enough to understand predictors of disease progression and functional outcomes, creating gaps in our understanding, which impacts clinical care and the design of clinical trials. Efforts to identify molecularly targeted therapies create a need to better understand disease characteristics with predictive value to help refine clinical trial strategies and understand trial outcomes.

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TDP-43 stabilizes G3BP1 mRNA: relevance to amyotrophic lateral sclerosis/frontotemporal dementia

Hadjara Sidibé, Yousra Khalfallah, Shangxi Xiao, Nicolás B Gómez, Hana Fakim, Elizabeth M H Tank, Geneviève Di Tomasso, Eric Bareke, Anaïs Aulas, Paul M McKeever, Ze’ev Melamed, Laurie Destroimaisons, Jade-Emmanuelle Deshaies, Lorne Zinman, J Alex Parker, Pascale Legault, Martine Tétreault, Sami J Barmada, Janice Robertson, Christine Vande Velde

doi : 10.1093/brain/awab217

Brain, Volume 144, Issue 11, November 2021, Pages 3461–3476

TDP-43 nuclear depletion and concurrent cytoplasmic accumulation in vulnerable neurons is a hallmark feature of progressive neurodegenerative proteinopathies such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cellular stress signalling and stress granule dynamics are now recognized to play a role in ALS/FTD pathogenesis. Defective stress granule assembly is associated with increased cellular vulnerability and death. Ras-GAP SH3-domain-binding protein 1 (G3BP1) is a critical stress granule assembly factor.

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Dopamine-dependent early synaptic and motor dysfunctions induced by ?-synuclein in the nigrostriatal circuit

Alessandro Tozzi, Miriam Sciaccaluga, Vittorio Loffredo, Alfredo Megaro, Ada Ledonne, Antonella Cardinale, Mauro Federici, Laura Bellingacci, Silvia Paciotti, Elena Ferrari, Antonino La Rocca, Alessandro Martini, Nicola B Mercuri, Fabrizio Gardoni, Barbara Picconi, Veronica Ghiglieri, Elvira De Leonibus, Paolo Calabresi

doi : 10.1093/brain/awab242

Brain, Volume 144, Issue 11, November 2021, Pages 3477–3491

Misfolding and aggregation of ?-synuclein are specific features of Parkinson’s disease and other neurodegenerative diseases defined as synucleinopathies. Parkinson’s disease progression has been correlated with the formation and extracellular release of ?-synuclein aggregates, as well as with their spread from neuron to neuron. Therapeutic interventions in the initial stages of Parkinson’s disease require a clear understanding of the mechanisms by which ?-synuclein disrupts the physiological synaptic and plastic activity of the basal ganglia. For this reason, we identified two early time points to clarify how the intrastriatal injection of ?-synuclein-preformed fibrils in rodents via retrograde transmission induces time-dependent electrophysiological and behavioural alterations. We found that intrastriatal ?-synuclein-preformed fibrils perturb the firing rate of dopaminergic neurons in the substantia nigra pars compacta, while the discharge of putative GABAergic cells of the substantia nigra pars reticulata is unchanged. The ?-synuclein-induced dysregulation of nigrostriatal function also impairs, in a time-dependent manner, the two main forms of striatal synaptic plasticity, long-term potentiation and long-term depression. We also observed an increased glutamatergic transmission measured as an augmented frequency of spontaneous excitatory synaptic currents. These changes in neuronal function in the substantia nigra pars compacta and striatum were observed before overt neuronal death occurred. In an additional set of experiments, we were able to rescue ?-synuclein-induced alterations of motor function, striatal synaptic plasticity and increased spontaneous excitatory synaptic currents by subchronic treatment with L-DOPA, a precursor of dopamine widely used in the therapy of Parkinson’s disease, clearly demonstrating that a dysfunctional dopamine system plays a critical role in the early phases of the disease.

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Metabolic derangements are associated with impaired glucose delivery following traumatic brain injury

Jeroen Hermanides, Young T Hong, Monica Trivedi, Joanne Outtrim, Franklin Aigbirhio, Peter J Nestor, Matthew Guilfoyle, Stefan Winzeck, Virginia F J Newcombe, Tilak Das, Marta M Correia, Keri L H Carpenter, Peter J A Hutchinson, Arun K Gupta, Tim D Fryer, John D Pickard, David K Menon, Jonathan P Coles

doi : 10.1093/brain/awab255

Brain, Volume 144, Issue 11, November 2021, Pages 3492–3504

Metabolic derangements following traumatic brain injury are poorly characterized. In this single-centre observational cohort study we combined 18F-FDG and multi-tracer oxygen-15 PET to comprehensively characterize the extent and spatial pattern of metabolic derangements.

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Plasma GFAP is an early marker of amyloid-? but not tau pathology in Alzheimer’s disease

Joana B Pereira, Shorena Janelidze, Ruben Smith, Niklas Mattsson-Carlgren, Sebastian Palmqvist, Charlotte E Teunissen, Henrik Zetterberg, Erik Stomrud, Nicholas J Ashton, Kaj Blennow, Oskar Hansson

doi : 10.1093/brain/awab223

Brain, Volume 144, Issue 11, November 2021, Pages 3505–3516

Although recent clinical trials targeting amyloid-? in Alzheimer’s disease have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with amyloid-? metabolism and amyloid pathology might be important to halt the clinical deterioration. In particular, there is evidence supporting a critical role of astroglial activation and astrocytosis in Alzheimer’s disease. However, so far, no studies have assessed whether astrocytosis is independently related to either amyloid-? or tau pathology in vivo.

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Longitudinal 18F-MK-6240 tau tangles accumulation follows Braak stages

Tharick A Pascoal, Andrea L Benedet, Dana L Tudorascu, Joseph Therriault, Sulantha Mathotaarachchi, Melissa Savard, Firoza Z Lussier, Cécile Tissot, Mira Chamoun, Min Su Kang, Jenna Stevenson, Gassan Massarweh, Marie-Christine Guiot, Jean-Paul Soucy, Serge Gauthier, Pedro Rosa-Neto

doi : 10.1093/brain/awab248

Brain, Volume 144, Issue 11, November 2021, Pages 3517–3528

Tracking longitudinal tau tangles accumulation across the Alzheimer’s disease continuum is crucial to better understand the natural history of tau pathology and for clinical trials. Although the available first-generation tau PET tracers detect tau accumulation in symptomatic individuals, their nanomolar affinity offers limited sensitivity to detect early tau accumulation in asymptomatic subjects.

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Potential optimization of focused ultrasound capsulotomy for obsessive compulsive disorder

Jürgen Germann, Gavin J B Elias, Clemens Neudorfer, Alexandre Boutet, Clement T Chow, Emily H Y Wong, Roohie Parmar, Flavia Venetucci Gouveia, Aaron Loh, Peter Giacobbe, Se Joo Kim, Hyun Ho Jung, Venkat Bhat, Walter Kucharczyk, Jin Woo Chang, Andres M Lozano

doi : 10.1093/brain/awab232

Brain, Volume 144, Issue 11, November 2021, Pages 3529–3540

Obsessive-compulsive disorder is a debilitating and often refractory psychiatric disorder. Magnetic resonance-guided focused ultrasound is a novel, minimally invasive neuromodulatory technique that has shown promise in treating this condition.

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