10,008 results match your criteria Brain[Journal]


Increased perception-action binding in Tourette syndrome.

Brain 2020 May 28. Epub 2020 May 28.

Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Dresden, Germany.

Gilles de la Tourette syndrome is a multifaceted neurodevelopmental disorder characterized by multiple motor and vocal tics. Research in Tourette syndrome has traditionally focused on the motor system. However, there is increasing evidence that perceptual and cognitive processes play a crucial role as well. Read More

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http://dx.doi.org/10.1093/brain/awaa111DOI Listing

Slow blood-to-brain transport underlies enduring barrier dysfunction in American football players.

Brain 2020 May 28. Epub 2020 May 28.

Departments of Physiology and Cell Biology, Brain and Cognitive Sciences, The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Repetitive mild traumatic brain injury in American football players has garnered increasing public attention following reports of chronic traumatic encephalopathy, a progressive tauopathy. While the mechanisms underlying repetitive mild traumatic brain injury-induced neurodegeneration are unknown and antemortem diagnostic tests are not available, neuropathology studies suggest a pathogenic role for microvascular injury, specifically blood-brain barrier dysfunction. Thus, our main objective was to demonstrate the effectiveness of a modified dynamic contrast-enhanced MRI approach we have developed to detect impairments in brain microvascular function. Read More

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http://dx.doi.org/10.1093/brain/awaa140DOI Listing

NAD(P)HX dehydratase protein-truncating mutations are associated with neurodevelopmental disorder exacerbated by acute illness.

Brain 2020 May 27. Epub 2020 May 27.

Diagnostics and Therapeutics of Intractable Diseases, Intractable Disease Research Center, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo 113-8421, Japan.

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http://dx.doi.org/10.1093/brain/awaa130DOI Listing

Reply: NAD(P)HX dehydratase protein-truncating mutations are associated with neurodevelopmental disorder exacerbated by acute illness.

Brain 2020 May 27. Epub 2020 May 27.

Brain and Mitochondrial Research Group, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, Australia.

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http://dx.doi.org/10.1093/brain/awaa131DOI Listing

Essential tremor as the early symptom of NOTCH2NLC gene-related repeat expansion disorder.

Brain 2020 May 25. Epub 2020 May 25.

Department of Neurology, the First Affiliated Hospital of Soochow University, Suzhou, 215000, China.

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http://dx.doi.org/10.1093/brain/awaa142DOI Listing

Encephalitis lethargica: a dying fall.

Authors:
Michael S Zandi

Brain 2019 Sep;142(9):2888-2891

National Hospital for Neurology and Neurosurgery, and UCL Queen Square Institute of Neurology, London, UK.

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http://dx.doi.org/10.1093/brain/awz228DOI Listing
September 2019

Neurology and what?

Authors:
Neil Scolding

Brain 2020 May;143(5):1613-1615

Bristol, UK and Gulu, Uganda.

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http://dx.doi.org/10.1093/brain/awaa132DOI Listing

Redefining the multidimensional clinical phenotypes of frontotemporal lobar degeneration syndromes.

Brain 2020 May;143(5):1555-1571

Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.

The syndromes caused by frontotemporal lobar degeneration have highly heterogeneous and overlapping clinical features. There has been great progress in the refinement of clinical diagnostic criteria in the past decade, but we propose that a better understanding of aetiology, pathophysiology and symptomatic treatments can arise from a transdiagnostic approach to clinical phenotype and brain morphometry. In a cross-sectional epidemiological study, we examined 310 patients with a syndrome likely to be caused by frontotemporal lobar degeneration, including behavioural variant frontotemporal dementia, non-fluent, and semantic variants of primary progressive aphasia (PPA), progressive supranuclear palsy and corticobasal syndrome. Read More

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http://dx.doi.org/10.1093/brain/awaa097DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241953PMC

Editorial.

Brain 2020 May;143(5):1285

London, UK.

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http://dx.doi.org/10.1093/brain/awaa118DOI Listing

Neither white nor black: embracing clinical variability in dementia diagnosis.

Authors:
Olivier Piguet

Brain 2020 May;143(5):1291-1293

The University of Sydney, School of Psychology and Brain & Mind Centre, Sydney NSW 2005, Australia.

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http://dx.doi.org/10.1093/brain/awaa119DOI Listing

Shaking with fear: the role of noradrenaline in modulating resting tremor.

Brain 2020 May;143(5):1288-1291

Brain and Mind Center, The University of Sydney, Sydney, Australia.

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http://dx.doi.org/10.1093/brain/awaa109DOI Listing

The NLRP3 inflammasome in progressive multiple sclerosis.

Brain 2020 May;143(5):1286-1288

Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

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http://dx.doi.org/10.1093/brain/awaa135DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241945PMC

Elucidating neural network changes induced by deep brain stimulation for OCD.

Brain 2020 May;143(5):1293-1296

Department of Psychiatry and Psychotherapy, University Hospital Cologne, University of Cologne, Cologne, Germany.

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http://dx.doi.org/10.1093/brain/awaa108DOI Listing

Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.

Brain 2020 May 21. Epub 2020 May 21.

Cerebral dynamics, learning and plasticity, Integrative Neuroscience and Cognition Center - UMR 8002, Paris, France.

Absence seizures in children and teenagers are generally considered relatively benign because of their non-convulsive nature and the large incidence of remittance in early adulthood. Recent studies, however, show that 30% of children with absence seizures are pharmaco-resistant and 60% are affected by severe neuropsychiatric comorbid conditions, including impairments in attention, cognition, memory and mood. In particular, attention deficits can be detected before the epilepsy diagnosis, may persist even when seizures are pharmacologically controlled and are aggravated by valproic acid monotherapy. Read More

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http://dx.doi.org/10.1093/brain/awaa072DOI Listing

Reply: ARSA gene variants and Parkinson's disease.

Brain 2020 May 21. Epub 2020 May 21.

Department of Neurology, Juntendo University, School of Medicine, Tokyo 113-8421, Japan.

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http://dx.doi.org/10.1093/brain/awaa136DOI Listing

Distinctive binding properties of human monoclonal LGI1 autoantibodies determine pathogenic mechanisms.

Brain 2020 May 21. Epub 2020 May 21.

Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.

Autoantibodies against leucine-rich glioma inactivated 1 (LGI1) are found in patients with limbic encephalitis and focal seizures. Here, we generate patient-derived monoclonal antibodies (mAbs) against LGI1. We explore their sequences and binding characteristics, plus their pathogenic potential using transfected HEK293T cells, rodent neuronal preparations, and behavioural and electrophysiological assessments in vivo after mAb injections into the rodent hippocampus. Read More

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http://dx.doi.org/10.1093/brain/awaa104DOI Listing

ARSA gene variants and Parkinson's disease.

Brain 2020 May 21. Epub 2020 May 21.

Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450000, Henan, China.

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http://dx.doi.org/10.1093/brain/awaa134DOI Listing

Novel GDAP2 pathogenic variants cause autosomal recessive spinocerebellar ataxia-27 (SCAR27) in a Chinese family.

Brain 2020 May 21. Epub 2020 May 21.

Department of Neurology and Research Center of Neurology in Second Affiliated Hospital, and Key Laboratory of Medical Neurobiology of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou, China.

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http://dx.doi.org/10.1093/brain/awaa121DOI Listing

Arginine is a disease modifier for polyQ disease models that stabilizes polyQ protein conformation.

Brain 2020 May 21. Epub 2020 May 21.

Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.

The polyglutamine (polyQ) diseases are a group of inherited neurodegenerative diseases that include Huntington's disease, various spinocerebellar ataxias, spinal and bulbar muscular atrophy, and dentatorubral pallidoluysian atrophy. They are caused by the abnormal expansion of a CAG repeat coding for the polyQ stretch in the causative gene of each disease. The expanded polyQ stretches trigger abnormal β-sheet conformational transition and oligomerization followed by aggregation of the polyQ proteins in the affected neurons, leading to neuronal toxicity and neurodegeneration. Read More

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http://dx.doi.org/10.1093/brain/awaa115DOI Listing

The role of the inferior parietal lobule in writer's cramp.

Brain 2020 May 18. Epub 2020 May 18.

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.

Humans have a distinguishing ability for fine motor control that is subserved by a highly evolved cortico-motor neuronal network. The acquisition of a particular motor skill involves a long series of practice movements, trial and error, adjustment and refinement. At the cortical level, this acquisition begins in the parieto-temporal sensory regions and is subsequently consolidated and stratified in the premotor-motor cortex. Read More

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http://dx.doi.org/10.1093/brain/awaa138DOI Listing

Reduced oligodendrocyte exosome secretion in multiple system atrophy involves SNARE dysfunction.

Brain 2020 May 18. Epub 2020 May 18.

Department of Pathology, University of Washington School of Medicine, 325 9th Ave, HMC Box 359635, Seattle, WA 98104, USA.

Transportation of key proteins via extracellular vesicles has been recently implicated in various neurodegenerative disorders, including Parkinson's disease, as a new mechanism of disease spreading and a new source of biomarkers. Extracellular vesicles likely to be derived from the brain can be isolated from peripheral blood and have been reported to contain higher levels of α-synuclein (α-syn) in Parkinson's disease patients. However, very little is known about extracellular vesicles in multiple system atrophy, a disease that, like Parkinson's disease, involves pathological α-syn aggregation, though the process is centred around oligodendrocytes in multiple system atrophy. Read More

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http://dx.doi.org/10.1093/brain/awaa110DOI Listing

Functional preservation and enhanced capacity for visual restoration in subacute occipital stroke.

Brain 2020 May 18. Epub 2020 May 18.

Flaum Eye Institute, University of Rochester, Rochester, NY, USA.

Stroke damage to the primary visual cortex (V1) causes a loss of vision known as hemianopia or cortically-induced blindness. While perimetric visual field improvements can occur spontaneously in the first few months post-stroke, by 6 months post-stroke, the deficit is considered chronic and permanent. Despite evidence from sensorimotor stroke showing that early injury responses heighten neuroplastic potential, to date, visual rehabilitation research has focused on patients with chronic cortically-induced blindness. Read More

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http://dx.doi.org/10.1093/brain/awaa128DOI Listing

Reply: Novel GDAP2 pathogenic variants cause autosomal recessive spinocerebellar ataxia-27 (SCAR27) in a Chinese family.

Brain 2020 May 18. Epub 2020 May 18.

Department of Neurology, Donders Institute for Brain, Cognition, and Behavior, Radboud University Medical Centre, 6525 GC Nijmegen, The Netherlands.

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http://dx.doi.org/10.1093/brain/awaa122DOI Listing

Neural stem cells restore myelin in a demyelinating model of Pelizaeus-Merzbacher disease.

Brain 2020 May;143(5):1383-1399

School of Veterinary Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8TA, UK.

Pelizaeus-Merzbacher disease is a fatal X-linked leukodystrophy caused by mutations in the PLP1 gene, which is expressed in the CNS by oligodendrocytes. Disease onset, symptoms and mortality span a broad spectrum depending on the nature of the mutation and thus the degree of CNS hypomyelination. In the absence of an effective treatment, direct cell transplantation into the CNS to restore myelin has been tested in animal models of severe forms of the disease with failure of developmental myelination, and more recently, in severely affected patients with early disease onset due to point mutations in the PLP1 gene, and absence of myelin by MRI. Read More

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http://dx.doi.org/10.1093/brain/awaa080DOI Listing

Book Review Migraine: back in the brain and beyond ….

Authors:
R Allan Purdy

Brain 2019 Dec;142(12):4003-4005

Division of Neurology, Dalhousie University, Halifax, Nova Scotia, Canada.

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http://dx.doi.org/10.1093/brain/awz336DOI Listing
December 2019

Unravelling the enigma of cortical tremor and other forms of cortical myoclonus.

Brain 2020 May 17. Epub 2020 May 17.

Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, London, UK.

Cortical tremor is a fine rhythmic oscillation involving distal upper limbs, linked to increased sensorimotor cortex excitability, as seen in cortical myoclonus. Cortical tremor is the hallmark feature of autosomal dominant familial cortical myoclonic tremor and epilepsy (FCMTE), a syndrome not yet officially recognized and characterized by clinical and genetic heterogeneity. Non-coding repeat expansions in different genes have been recently recognized to play an essential role in its pathogenesis. Read More

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http://dx.doi.org/10.1093/brain/awaa129DOI Listing

Book ReviewTales of the expected.

Authors:
Jason Warren

Brain 2019 Nov;142(11):3655-3659

UCL Queen Square Institute of Neurology, London, UK.

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http://dx.doi.org/10.1093/brain/awz304DOI Listing
November 2019

Inhibition between human brain areas or methodological artefact?

Brain 2020 May;143(5):e38

Center of Neurology, Division of Neuropsychology, Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.

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http://dx.doi.org/10.1093/brain/awaa092DOI Listing

Reply: Inhibition between human brain areas or methodological artefact?

Brain 2020 May;143(5):e39

Institute of Computational Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

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http://dx.doi.org/10.1093/brain/awaa093DOI Listing

Gene replacement therapy provides benefit in an adult mouse model of Leigh syndrome.

Brain 2020 May 15. Epub 2020 May 15.

Université Grenoble Alpes, Inserm, U1216, Grenoble Institut des Neurosciences, 38000 Grenoble, France.

Mutations in nuclear-encoded mitochondrial genes are responsible for a broad spectrum of disorders among which Leigh syndrome is the most common in infancy. No effective therapies are available for this severe disease mainly because of the limited capabilities of the standard adeno-associated viral (AAV) vectors to transduce both peripheral organs and the CNS when injected systemically in adults. Here, we used the brain-penetrating AAV-PHP. Read More

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http://dx.doi.org/10.1093/brain/awaa105DOI Listing

Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study.

Brain 2020 May;143(5):1431-1446

Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.

Conformation-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG) are detectable in patients with optic neuritis, myelitis, opticomyelitis, acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM) and brainstem/cerebral cortical encephalitis, but are rarely detected in patients with prototypic multiple sclerosis. So far, there has been no systematic study on the pathological relationship between demyelinating lesions and cellular/humoral immunity in MOG antibody-associated disease. Furthermore, it is unclear whether the pathomechanisms of MOG antibody-mediated demyelination are similar to the demyelination patterns of multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) with AQP4 antibody, or ADEM. Read More

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http://dx.doi.org/10.1093/brain/awaa102DOI Listing

Neurofilaments: neurobiological foundations for biomarker applications.

Brain 2020 May 14. Epub 2020 May 14.

Department of Brain Sciences, Imperial College, London, UK.

Interest in neurofilaments has risen sharply in recent years with recognition of their potential as biomarkers of brain injury or neurodegeneration in CSF and blood. This is in the context of a growing appreciation for the complexity of the neurobiology of neurofilaments, new recognition of specialized roles for neurofilaments in synapses and a developing understanding of mechanisms responsible for their turnover. Here we will review the neurobiology of neurofilament proteins, describing current understanding of their structure and function, including recently discovered evidence for their roles in synapses. Read More

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http://dx.doi.org/10.1093/brain/awaa098DOI Listing

Tissue-resident memory T cells invade the brain parenchyma in multiple sclerosis white matter lesions.

Brain 2020 May 13. Epub 2020 May 13.

Department of Neuroimmunology, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands.

Multiple sclerosis is a chronic inflammatory, demyelinating disease, although it has been suggested that in the progressive late phase, inflammatory lesion activity declines. We recently showed in the Netherlands Brain Bank multiple sclerosis-autopsy cohort considerable ongoing inflammatory lesion activity also at the end stage of the disease, based on microglia/macrophage activity. We have now studied the role of T cells in this ongoing inflammatory lesion activity in chronic multiple sclerosis autopsy cases. Read More

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http://dx.doi.org/10.1093/brain/awaa117DOI Listing

Tau immunophenotypes in chronic traumatic encephalopathy recapitulate those of ageing and Alzheimer's disease.

Brain 2020 May;143(5):1572-1587

Department of Neurosurgery, Penn Center for Brain Injury and Repair, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Traumatic brain injury (TBI) is a risk factor for neurodegenerative disease, including chronic traumatic encephalopathy (CTE). Preliminary consensus criteria define the pathognomonic lesion of CTE as patchy tau pathology within neurons and astrocytes at the depths of cortical sulci. However, the specific tau isoform composition and post-translational modifications in CTE remain largely unexplored. Read More

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http://dx.doi.org/10.1093/brain/awaa071DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241956PMC
May 2020
9.196 Impact Factor

Early clinical markers of aggressive multiple sclerosis.

Brain 2020 May;143(5):1400-1413

CORe Unit, Department of Medicine, University of Melbourne, Melbourne, Australia.

Patients with the 'aggressive' form of multiple sclerosis accrue disability at an accelerated rate, typically reaching Expanded Disability Status Score (EDSS) ≥ 6 within 10 years of symptom onset. Several clinicodemographic factors have been associated with aggressive multiple sclerosis, but less research has focused on clinical markers that are present in the first year of disease. The development of early predictive models of aggressive multiple sclerosis is essential to optimize treatment in this multiple sclerosis subtype. Read More

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http://dx.doi.org/10.1093/brain/awaa081DOI Listing
May 2020
9.196 Impact Factor

Blunted medial prefrontal cortico-limbic reward-related effective connectivity and depression.

Brain 2020 May 8. Epub 2020 May 8.

Division of Imaging Science and Technology, Medical School, University of Dundee, Dundee, UK.

Major depressive disorder is a leading cause of disability and significant mortality, yet mechanistic understanding remains limited. Over the past decade evidence has accumulated from case-control studies that depressive illness is associated with blunted reward activation in the basal ganglia and other regions such as the medial prefrontal cortex. However it is unclear whether this finding can be replicated in a large number of subjects. Read More

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http://dx.doi.org/10.1093/brain/awaa106DOI Listing

Hippocampal α-synuclein pathology correlates with memory impairment in multiple system atrophy.

Brain 2020 May 8. Epub 2020 May 8.

Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK.

Recent post-mortem studies reported 22-37% of patients with multiple system atrophy can develop cognitive impairment. With the aim of identifying associations between cognitive impairment including memory impairment and α-synuclein pathology, 148 consecutive patients with pathologically proven multiple system atrophy were reviewed. Among them, 118 (79. Read More

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http://dx.doi.org/10.1093/brain/awaa126DOI Listing

Bidirectional gut-to-brain and brain-to-gut propagation of synucleinopathy in non-human primates.

Brain 2020 May;143(5):1462-1475

University of Bordeaux, Neurodegenerative Diseases Institute, UMR 5293, F-33000 Bordeaux, France.

In Parkinson's disease, synucleinopathy is hypothesized to spread from the enteric nervous system, via the vagus nerve, to the CNS. Here, we compare, in baboon monkeys, the pathological consequences of either intrastriatal or enteric injection of α-synuclein-containing Lewy body extracts from patients with Parkinson's disease. This study shows that patient-derived α-synuclein aggregates are able to induce nigrostriatal lesions and enteric nervous system pathology after either enteric or striatal injection in a non-human primate model. Read More

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http://dx.doi.org/10.1093/brain/awaa096DOI Listing

Microglial activation and tau burden predict cognitive decline in Alzheimer's disease.

Brain 2020 May;143(5):1588-1602

Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.

Tau pathology, neuroinflammation, and neurodegeneration are key aspects of Alzheimer's disease. Understanding whether these features predict cognitive decline, alone or in combination, is crucial to develop new prognostic measures and enhanced stratification for clinical trials. Here, we studied how baseline assessments of in vivo tau pathology (measured by 18F-AV-1451 PET), neuroinflammation (measured by 11C-PK11195 PET) and brain atrophy (derived from structural MRI) predicted longitudinal cognitive changes in patients with Alzheimer's disease pathology. Read More

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http://dx.doi.org/10.1093/brain/awaa088DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241955PMC

Onset of hippocampal network aberration and memory deficits in P301S tau mice are associated with an early gene signature.

Brain 2020 May 6. Epub 2020 May 6.

Dementia Research Centre and Department of Biomedical Sciences, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, 2109, NSW, Australia.

Hyperphosphorylation and deposition of tau in the brain characterizes frontotemporal dementia and Alzheimer's disease. Disease-associated mutations in the tau-encoding MAPT gene have enabled the generation of transgenic mouse models that recapitulate aspects of human neurodegenerative diseases, including tau hyperphosphorylation and neurofibrillary tangle formation. Here, we characterized the effects of transgenic P301S mutant human tau expression on neuronal network function in the murine hippocampus. Read More

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http://dx.doi.org/10.1093/brain/awaa133DOI Listing

Brain responsivity provides an individual readout for motor recovery after stroke.

Brain 2020 May 6. Epub 2020 May 6.

Medical Faculty, University of Cologne, and Department of Neurology, University Hospital Cologne, Cologne, Germany.

Promoting the recovery of motor function and optimizing rehabilitation strategies for stroke patients is closely associated with the challenge of individual prediction. To date, stroke research has identified critical pathophysiological neural underpinnings at the cellular level as well as with regard to network reorganization. However, in order to generate reliable readouts at the level of individual patients and thereby realize translation from bench to bedside, we are still in a need for innovative methods. Read More

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http://dx.doi.org/10.1093/brain/awaa127DOI Listing

Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury.

Brain 2020 May 6. Epub 2020 May 6.

Cellular Neuroscience, Neurodegeneration and Repair Program, Yale University School of Medicine, New Haven, CT, USA.

After CNS trauma such as spinal cord injury, the ability of surviving neural elements to sprout axons, reorganize neural networks and support recovery of function is severely restricted, contributing to chronic neurological deficits. Among limitations on neural recovery are myelin-associated inhibitors functioning as ligands for neuronal Nogo receptor 1 (NgR1). A soluble decoy (NgR1-Fc, AXER-204) blocks these ligands and provides a means to promote recovery of function in multiple preclinical rodent models of spinal cord injury. Read More

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http://dx.doi.org/10.1093/brain/awaa116DOI Listing

A venous mechanism of ventriculomegaly shared between traumatic brain injury and normal ageing.

Brain 2020 May 6. Epub 2020 May 6.

Department of Psychiatry, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Recently, age-related timing dissociation between the superficial and deep venous systems has been observed; this was particularly pronounced in patients with normal pressure hydrocephalus, suggesting a common mechanism of ventriculomegaly. Establishing the relationship between venous drainage and ventricular enlargement would be clinically relevant and could provide insight into the mechanisms underlying brain ageing. To investigate a possible link between venous drainage and ventriculomegaly in both normal ageing and pathological conditions, we compared 225 healthy subjects (137 males and 88 females) and 71 traumatic brain injury patients of varying ages (53 males and 18 females) using MRI-based volumetry and a novel perfusion-timing analysis. Read More

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http://dx.doi.org/10.1093/brain/awaa125DOI Listing

Reply: The influence of sample size and arbitrary statistical thresholds in lesion-network mapping.

Brain 2020 May;143(5):e41

Berenson-Allen Center for Non-Invasive Brain Stimulation and Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

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http://dx.doi.org/10.1093/brain/awaa095DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241951PMC

The influence of sample size and arbitrary statistical thresholds in lesion-network mapping.

Brain 2020 May;143(5):e40

Centre of Neurology, Division of Neuropsychology, Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.

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http://dx.doi.org/10.1093/brain/awaa094DOI Listing

A lack of consistent brain grey matter alterations in migraine.

Brain 2020 May 3. Epub 2020 May 3.

Department of Central Laboratory, Affiliated Yancheng Hospital, School of Medicine, Southeast University, Yancheng, China.

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http://dx.doi.org/10.1093/brain/awaa123DOI Listing

Reply: A lack of consistent brain grey matter alterations in migraine.

Brain 2020 May 3. Epub 2020 May 3.

Berenson-Allen Center for Noninvasive Brain Stimulation, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

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http://dx.doi.org/10.1093/brain/awaa124DOI Listing

In vivo stress granule misprocessing evidenced in a FUS knock-in ALS mouse model.

Brain 2020 May;143(5):1350-1367

Tsinghua-Peking Joint Center for Life Science, Beijing, China.

Many RNA-binding proteins, including TDP-43, FUS, and TIA1, are stress granule components, dysfunction of which causes amyotrophic lateral sclerosis (ALS). However, whether a mutant RNA-binding protein disrupts stress granule processing in vivo in pathogenesis is unknown. Here we establish a FUS ALS mutation, p. Read More

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http://dx.doi.org/10.1093/brain/awaa076DOI Listing

Corrigendum.

Authors:

Brain 2020 May 1. Epub 2020 May 1.

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http://dx.doi.org/10.1093/brain/awaa103DOI Listing