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The addicted brain: differences between heroin and cocaine?
Masud Husain
doi : 10.1093/brain/awad065
Brain, Volume 146, Issue 4, April 2023, Page 1227
Engram and ecphory: the performing pianist and retrieval of memory
Geoffrey D Schott
doi : 10.1093/brain/awad030
Brain, Volume 146, Issue 4, April 2023, Pages 1228–1230
Cytotoxic T cells and plasma cells dominate early in temporal lobe epilepsy with GAD antibodies
Franziska S Thaler, Edgar Meinl
doi : 10.1093/brain/awad066
Brain, Volume 146, Issue 4, April 2023, Pages 1231–1233
Should concepts of brain functions be based on psychology or anatomy? An echo from Kurt Goldstein
Cornelius Weiller, Michel Rijntjes
doi : 10.1093/brain/awad081
Brain, Volume 146, Issue 4, April 2023, Pages 1234–1235
Targeting MCAM for next-generation modulation of leucocyte trafficking
Tilman Schneider-Hohendorf, Heinz Wiendl
doi : 10.1093/brain/awad079
Brain, Volume 146, Issue 4, April 2023, Pages 1236–1237
Localization of depressive symptoms based on focal brain lesions: adding ‘resilience’ to ‘risk’
Julian Klingbeil, Dorothee Saur
doi : 10.1093/brain/awad067
Brain, Volume 146, Issue 4, April 2023, Pages 1238–1239
An anti-amyloid therapy works for Alzheimer’s disease: why has it taken so long and what is next?
John Hardy, Catherine Mummery
doi : 10.1093/brain/awad049
Brain, Volume 146, Issue 4, April 2023, Pages 1240–1242
Quantitative myelin imaging with MRI and PET: an overview of techniques and their validation status
Chris W J van der Weijden, Emma Biondetti, Ingomar W Gutmann, Hildebrand Dijkstra, Rory McKerchar, Daniele de Paula Faria, Erik F J de Vries, Jan F Meilof, Rudi A J O Dierckx, Valentin H Prevost, Alexander Rauscher
doi : 10.1093/brain/awac436
Brain, Volume 146, Issue 4, April 2023, Pages 1243–1266
Myelin is the protective sheath wrapped around axons, consisting of a phospholipid bilayer with water between the wraps. The measurement of damage to the myelin sheaths, the evaluation of the efficacy of therapies aiming to promote remyelination and monitoring the degree of brain maturation in children all require non-invasive quantitative myelin imaging methods.
Cryptic mutations of PLC family members in brain disorders: recent discoveries and a deep-learning-based approach
Key-Hwan Lim, Sumin Yang, Sung-Hyun Kim, Euiseong Ko, Mingon Kang, Jae-Yeol Joo
doi : 10.1093/brain/awac451
Brain, Volume 146, Issue 4, April 2023, Pages 1267–1280
Phospholipase C (PLC) is an essential isozyme involved in the phosphoinositide signalling pathway, which maintains cellular homeostasis. Gain- and loss-of-function mutations in PLC affect enzymatic activity and are therefore associated with several disorders.
Assessment and prediction of glioblastoma therapy response: challenges and opportunities
Dan Qi, Jing Li, C Chad Quarles, Ekokobe Fonkem, Erxi Wu
doi : 10.1093/brain/awac450
Brain, Volume 146, Issue 4, April 2023, Pages 1281–1298
Glioblastoma is the most aggressive type of primary adult brain tumour. The median survival of patients with glioblastoma remains approximately 15 months, and the 5-year survival rate is <10%.
Vascular endothelial cells: a fundamental approach for brain waste clearance
Huimin Wei, Huimin Jiang, Yifan Zhou, Xuechun Xiao, Chen Zhou, Xunming Ji Author Notes
doi : 10.1093/brain/awac495
Brain, Volume 146, Issue 4, April 2023, Pages 1299–1315
Accumulation of neurotoxic protein aggregates is the pathological hallmark of neurodegenerative disease. Proper clearance of these waste metabolites is an essential process for maintaining brain microenvironment homeostasis and may delay or even halt the onset and progression of neurodegeneration
In silico versus functional characterization of genetic variants: lessons from muscle channelopathies
Vinojini Vivekanandam, Rebecca Ellmers, Dipa Jayaseelan, Henry Houlden, Roope Männikkö, Michael G Hanna
doi : 10.1093/brain/awac431
Brain, Volume 146, Issue 4, April 2023, Pages 1316–1321
Accurate determination of the pathogenicity of missense genetic variants of uncertain significance is a huge challenge for implementing genetic data in clinical practice. In silico predictive tools are used to score variants’ pathogenicity.
Mechanisms of imbalanced frontostriatal functional connectivity in obsessive-compulsive disorder
Sebastien Naze, Luke J Hearne, James A Roberts, Paula Sanz-Leon, Bjorn Burgher, Caitlin Hall, Saurabh Sonkusare, Zoie Nott, Leo Marcus, Emma Savage, Conor Robinson, Ye Ella Tian, Andrew Zalesky, Michael Breakspear, Luca Cocchi
doi : 10.1093/brain/awac425
Brain, Volume 146, Issue 4, April 2023, Pages 1322–1327
The diagnosis of obsessive-compulsive disorder (OCD) has been linked with changes in frontostriatal resting-state connectivity. However, replication of prior findings is lacking, and the mechanistic understanding of these effects is incomplete.
Randomized trial of bilateral gene therapy injection for m.11778G>A MT-ND4 Leber optic neuropathy
Nancy J Newman, Patrick Yu-Wai-Man, Prem S Subramanian, Mark L Moster, An-Guor Wang, Sean P Donahue, Bart P Leroy, Valerio Carelli, Valerie Biousse, Catherine Vignal-Clermont, Robert C Sergott, Alfredo A Sadun, Gema Rebolleda Fernández, Bart K Chwalisz, Rudrani Banik, Fabienne Bazin, Michel Roux, Eric D Cox, Magali Taiel, José-Alain Sahel, the LHON REFLECT Study Group
doi : 10.1093/brain/awac421
Brain, Volume 146, Issue 4, April 2023, Pages 1328–1341
Leber hereditary optic neuropathy (LHON) is an important example of mitochondrial blindness with the m.11778G>A mutation in the MT-ND4 gene being the most common disease-causing mtDNA variant worldwide.
The genomic landscape across 474 surgically accessible epileptogenic human brain lesions
Javier A López-Rivera, Costin Leu, Marie Macnee, Jean Khoury, Lucas Hoffmann, Roland Coras, Katja Kobow, Nisha Bhattarai, Eduardo Pérez-Palma, Hajo Hamer, Sebastian Brandner, Karl Rössler, Christian G Bien, Thilo Kalbhenn, Tom Pieper, Till Hartlieb, Elizabeth Butler, Giulio Genovese, Kerstin Becker, Janine Altmüller, Lisa-Marie Niestroj, Lisa Ferguson, Robyn M Busch, Peter Nürnberg, Imad Najm, Ingmar Blümcke, Dennis Lal
doi : 10.1093/brain/awac376
Brain, Volume 146, Issue 4, April 2023, Pages 1342–1356
Understanding the exact molecular mechanisms involved in the aetiology of epileptogenic pathologies with or without tumour activity is essential for improving treatment of drug-resistant focal epilepsy.
ATP6V0C variants impair V-ATPase function causing a neurodevelopmental disorder often associated with epilepsy
Kari A Mattison, Gilles Tossing, Fred Mulroe, Callum Simmons, Kameryn M Butler, Alison Schreiber, Adnan Alsadah, Derek E Neilson, Karin Naess, Anna Wedell, Anna Wredenberg, Arthur Sorlin, Emma McCann, George J Burghel, Beatriz Menendez, George E Hoganson, Lorenzo D Botto, Francis M Filloux, �ngel Aledo-Serrano, Antonio Gil-Nagel, Katrina Tatton-Brown, Nienke E Verbeek, Bert van der Zwaag, Kyrieckos A Aleck, Andrew C Fazenbaker, Jorune Balciuniene, Holly A Dubbs, Eric D Marsh, Kathryn Garber, Jakob Ek, Morten Duno, Christina E Hoei-Hansen, Matthew A Deardorff, Gordana Raca, Catherine Quindipan, Michele van Hirtum-Das, Jeroen Breckpot, Trine Bjørg Hammer, Rikke S Møller, Andrea Whitney, Andrew G L Douglas, Mira Kharbanda, Nicola Brunetti-Pierri, Manuela Morleo, Vincenzo Nigro, Halie J May, James X Tao, Emanuela Argilli, Elliot H Sherr, William B Dobyns, Genomics England Research Consortium, Richard A Baines, Jim Warwicker, J Alex Parker, Siddharth Banka, Philippe M Campeau, Andrew Escayg
doi : 10.1093/brain/awac330
Brain, Volume 146, Issue 4, April 2023, Pages 1357–1372
The vacuolar H+-ATPase is an enzymatic complex that functions in an ATP-dependent manner to pump protons across membranes and acidify organelles, thereby creating the proton/pH gradient required for membrane trafficking by several different types of transporters.
Loss-of-function variants in MYCBP2 cause neurobehavioural phenotypes and corpus callosum defects
Lama AlAbdi, Muriel Desbois, Domniţa-Valeria Rusnac, Raashda A Sulaiman, Jill A Rosenfeld, Seema Lalani, David R Murdock, Lindsay C Burrage, Undiagnosed Diseases Network, Ping Yee Billie Au, Shelley Towner, William G Wilson, Lawrence Wong, Theresa Brunet, Gertrud Strobl-Wildemann, Jennifer E Burton, George Hoganson, Kirsty McWalter, Amber Begtrup, Yuri A Zarate, Elyse L Christensen, Karla J Opperman, Andrew C Giles, Rana Helaby, Artur Kania, Ning Zheng, Brock Grill, Fowzan S Alkuraya
doi : 10.1093/brain/awac364
Brain, Volume 146, Issue 4, April 2023, Pages 1373–1387
The corpus callosum is a bundle of axon fibres that connects the two hemispheres of the brain. Neurodevelopmental disorders that feature dysgenesis of the corpus callosum as a core phenotype offer a valuable window into pathology derived from abnormal axon development.
Methylation of the 4q35 D4Z4 repeat defines disease status in facioscapulohumeral muscular dystrophy
Hannes Erdmann, Florentine Scharf, Stefanie Gehling, Anna Benet-Pagès, Sibylle Jakubiczka, Kerstin Becker, Maria Seipelt, Felix Kleefeld, Karl Christian Knop, Eva-Christina Prott, Miriam Hiebeler, Federica Montagnese, Dieter Gläser, Matthias Vorgerd, Tim Hagenacker, Maggie C Walter, Peter Reilich, Teresa Neuhann, Martin Zenker, Elke Holinski-Feder, Benedikt Schoser, Angela Abicht
doi : 10.1093/brain/awac336
Brain, Volume 146, Issue 4, April 2023, Pages 1388–1402
Genetic diagnosis of facioscapulohumeral muscular dystrophy (FSHD) remains a challenge in clinical practice as it cannot be detected by standard sequencing methods despite being the third most common muscular dystrophy.
Genetic regulatory and biological implications of the 10q24.32 schizophrenia risk locus
Junyang Wang, Jiewei Liu, Shiwu Li, Xiaoyan Li, Jinfeng Yang, Xinglun Dang, Changgai Mu, Yifan Li, Kaiqin Li, Jiao Li, Rui Chen, Yixing Liu, Di Huang, Zhijun Zhang, Xiong-Jian Luo
doi : 10.1093/brain/awac352
Brain, Volume 146, Issue 4, April 2023, Pages 1403–1419
Genome-wide association studies have identified 10q24.32 as a robust schizophrenia risk locus. Here we identify a regulatory variant (rs10786700) that disrupts binding of transcription factors at 10q24.32.
SPTSSA variants alter sphingolipid synthesis and cause a complex hereditary spastic paraplegia
Siddharth Srivastava, Hagar Mor Shaked, Kenneth Gable, Sita D Gupta, Xueyang Pan, Niranjanakumari Somashekarappa, Gongshe Han, Payam Mohassel, Marc Gotkine, Elizabeth Doney, Paula Goldenberg, Queenie K G Tan, Yi Gong, Benjamin Kleinstiver, Brian Wishart, Heidi Cope, Claudia Brito Pires, Hannah Stutzman, Rebecca C Spillmann, Undiagnosed Disease Network , Reza Sadjadi, Orly Elpeleg, Chia-Hsueh Lee, Hugo J Bellen, Simon Edvardson, Florian Eichler, Teresa M Dunn
doi : 10.1093/brain/awac460
Brain, Volume 146, Issue 4, April 2023, Pages 1420–1435
Sphingolipids are a diverse family of lipids with critical structural and signalling functions in the mammalian nervous system, where they are abundant in myelin membranes.
Temporal lobe epilepsy with GAD antibodies: neurons killed by T cells not by complement membrane attack complex
Anna R Tröscher, Katharina M Mair, Laia Verdú de Juan, Ulrike Köck, Anja Steinmaurer, Hartmut Baier, Albert Becker, Ingmar Blümcke, Martin Finzel, Christian Geis, Romana Höftberger, Christian Mawrin, Tim J von Oertzen, Julika Pitsch, Rainer Surges, Berthold Voges, Serge Weis, Michael Winklehner, Friedrich Woermann, Jan Bauer, Christian G Bien
doi : 10.1093/brain/awac404
Brain, Volume 146, Issue 4, April 2023, Pages 1436–1452
Temporal lobe epilepsy (TLE) is one of the syndromes linked to antibodies against glutamic acid decarboxylase (GAD). It has been questioned whether ‘limbic encephalitis with GAD antibodies’ is a meaningful diagnostic entity.
Tumour necrosis factor blockade after asphyxia in foetal sheep ameliorates cystic white matter injury
Christopher A Lear, Benjamin A Lear, Joanne O Davidson, Jialin Sae-Jiw, Johanna M Lloyd, Simerdeep K Dhillon, Alistair J Gunn, Laura Bennet
doi : 10.1093/brain/awac331
Brain, Volume 146, Issue 4, April 2023, Pages 1453–1466
Cystic white matter injury is highly associated with severe neurodevelopmental disability and cerebral palsy in preterm infants, yet its pathogenesis remains poorly understood and there is no established treatment.
Joint impact on attention, alertness and inhibition of lesions at a frontal white matter crossroad
Brigitte C Kaufmann, Dario Cazzoli, Manuela Pastore-Wapp, Tim Vanbellingen, Tobias Pflugshaupt, Daniel Bauer, René M Müri, Tobias Nef, Paolo Bartolomeo, Thomas Nyffeler
doi : 10.1093/brain/awac359
Brain, Volume 146, Issue 4, April 2023, Pages 1467–1482
In everyday life, information from different cognitive domains—such as visuospatial attention, alertness and inhibition—needs to be integrated between different brain regions.
MCAM+ brain endothelial cells contribute to neuroinflammation by recruiting pathogenic CD4+ T lymphocytes
Marc Charabati, Stephanie Zandee, Antoine P Fournier, Olivier Tastet, Karine Thai, Roxaneh Zaminpeyma, Marc-André Lécuyer, Lyne Bourbonnière, Sandra Larouche, Wendy Klement, Camille Grasmuck, Fiona Tea, Bettina Zierfuss, Ali Filali-Mouhim, Robert Moumdjian, Alain Bouthillier, Romain Cayrol, Evelyn Peelen, Nathalie Arbour, Catherine Larochelle, Alexandre Prat
doi : 10.1093/brain/awac389
Brain, Volume 146, Issue 4, April 2023, Pages 1483–1495
The trafficking of autoreactive leucocytes across the blood–brain barrier endothelium is a hallmark of multiple sclerosis pathogenesis. Although the blood–brain barrier endothelium represents one of the main CNS borders to interact with the infiltrating leucocytes, its exact contribution to neuroinflammation remains understudied.
PTPA variants and impaired PP2A activity in early-onset parkinsonism with intellectual disability
Christina Fevga, Christelle Tesson, Ana Carreras Mascaro, Thomas Courtin, Riaan van Coller, Salma Sakka, Federico Ferraro, Nouha Farhat, Soraya Bardien, Mariem Damak, Jonathan Carr, Mélanie Ferrien, Valerie Boumeester, Jasmijn Hundscheid, Nicola Grillenzoni, Irini A Kessissoglou, Demy J S Kuipers, Marialuisa Quadri, French and Mediterranean Parkinson disease Genetics Study Group , International Parkinsonism Genetics Network , Jean-Christophe Corvol, Chokri Mhiri, Bassem A Hassan, Guido J Breedveld, Suzanne Lesage, Wim Mandemakers, Alexis Brice, Vincenzo Bonifati
doi : 10.1093/brain/awac326
Brain, Volume 146, Issue 4, April 2023, Pages 1496–1510
The protein phosphatase 2A complex (PP2A), the major Ser/Thr phosphatase in the brain, is involved in a number of signalling pathways and functions, including the regulation of crucial proteins for neurodegeneration, such as alpha-synuclein, tau and LRRK2. Here, we report the identification of variants in the PTPA/PPP2R4 gene, encoding a major PP2A activator, in two families with early-onset parkinsonism and intellectual disability.
Intact finger representation within primary sensorimotor cortex of musician’s dystonia
Anna Sadnicka, Tobias Wiestler, Katherine Butler, Eckart Altenmüller, Mark J Edwards, Naveed Ejaz, Jörn Diedrichsen
doi : 10.1093/brain/awac356
Brain, Volume 146, Issue 4, April 2023, Pages 1511–1522
Musician’s dystonia presents with a persistent deterioration of motor control during musical performance. A predominant hypothesis has been that this is underpinned by maladaptive neural changes to the somatotopic organization of finger representations within primary somatosensory cortex.
Cortical neuronal hyperexcitability and synaptic changes in SGCE mutation-positive myoclonus dystonia
Alessandra Sperandeo, Claudia Tamburini, Zoe Noakes, Daniel Cabezas de la Fuente, Francesca Keefe, Olena Petter, William Plumbly, Nicholas E Clifton, Meng Li, Kathryn J Peall
doi : 10.1093/brain/awac365
Brain, Volume 146, Issue 4, April 2023, Pages 1523–1541
Myoclonus dystonia is a childhood-onset hyperkinetic movement disorder with a combined motor and psychiatric phenotype. It represents one of the few autosomal dominant inherited dystonic disorders and is caused by mutations in the ε-sarcoglycan (SGCE) gene.
Supplementary motor area driving changes of structural brain network in blepharospasm
Jinping Xu, Yuhan Luo, Kangqiang Peng, Yaomin Guo, Linchang Zhong, Ying Liu, Ai Weng, Zilin Ou, Zhicong Yan, Ying Wang, Jinsheng Zeng, Weixi Zhang, Qingmao Hu, Gang Liu
doi : 10.1093/brain/awac341
Brain, Volume 146, Issue 4, April 2023, Pages 1542–1553
Blepharospasm is traditionally thought to be a movement disorder that results from basal ganglia dysfunction. Recently, accumulating morphometric studies have revealed structural alterations outside the basal ganglia, such as in the brainstem, cerebellum and sensorimotor cortex, suggesting that blepharospasm may result from network disorders.
Retigabine suppresses loss of force in mouse models of hypokalaemic periodic paralysis
Marbella Quiñonez, Marino DiFranco, Fenfen Wu, Stephen C Cannon
doi : 10.1093/brain/awac441
Brain, Volume 146, Issue 4, April 2023, Pages 1554–1560
Recurrent episodes of weakness in periodic paralysis are caused by intermittent loss of muscle fibre excitability, as a consequence of sustained depolarization of the resting potential. Repolarization is favoured by increasing the fibre permeability to potassium.
Loss of forebrain BIN1 attenuates hippocampal pathology and neuroinflammation in a tauopathy model
Moorthi Ponnusamy, Shuai Wang, Melike Yuksel, Mitchell T Hansen, Danielle M Blazier, Joseph D McMillan, Xiaolin Zhang, Eric B Dammer, Lisa Collier, Gopal Thinakaran
doi : 10.1093/brain/awac318
Brain, Volume 146, Issue 4, April 2023, Pages 1561–1579
Bridging integrator 1 (BIN1) is the second most prevalent genetic risk factor identified by genome-wide association studies (GWAS) for late-onset Alzheimer’s disease.
Phospho-tau with subthreshold tau-PET predicts increased tau accumulation rates in amyloid-positive individuals
Colin Groot, Ruben Smith, Erik Stomrud, Alexa Pichet Binette, Antoine Leuzy, Anika Wuestefeld, Laura E M Wisse, Sebastian Palmqvist, Niklas Mattsson-Carlgren, Shorena Janelidze, Olof Strandberg, Rik Ossenkoppele, Oskar Hansson
doi : 10.1093/brain/awac329
Brain, Volume 146, Issue 4, April 2023, Pages 1580–1591
Different tau biomarkers become abnormal at different stages of Alzheimer’s disease, with CSF phospho-tau typically becoming elevated at subthreshold levels of tau-PET binding.
Head-to-head comparison of 10 plasma phospho-tau assays in prodromal Alzheimer’s disease
Shorena Janelidze, Divya Bali, Nicholas J Ashton, Nicolas R Barthélemy, Jeroen Vanbrabant, Erik Stoops, Eugeen Vanmechelen, Yingxin He, Anna Orduña Dolado, Gallen Triana-Baltzer, Michael J Pontecorvo, Henrik Zetterberg, Hartmuth Kolb, Manu Vandijck, Kaj Blennow, Randall J Bateman, Oskar Hansson
doi : 10.1093/brain/awac333
Brain, Volume 146, Issue 4, April 2023, Pages 1592–1601
Plasma phospho-tau (p-tau) species have emerged as the most promising blood-based biomarkers of Alzheimer's disease. Here, we performed a head-to-head comparison of p-tau181, p-tau217 and p-tau231 measured using 10 assays to detect abnormal brain amyloid-β (Aβ) status and predict future progression to Alzheimer's dementia.
Measures of cortical microstructure are linked to amyloid pathology in Alzheimer’s disease
Nicola Spotorno, Olof Strandberg, Geraline Vis, Erik Stomrud, Markus Nilsson, Oskar Hansson
doi : 10.1093/brain/awac343
Brain, Volume 146, Issue 4, April 2023, Pages 1602–1614
Markers of downstream events are a key component of clinical trials of disease-modifying therapies for Alzheimer’s disease. Morphological metrics like cortical thickness are established measures of atrophy but are not sensitive enough to detect amyloid-beta (Aβ)- related changes that occur before overt atrophy become visible.
Functional cognitive disorder affects reaction time, subjective mental effort and global metacognition
Tiago Teodoro, Akihiro Koreki, Jiaying Chen, Jan Coebergh, Norman Poole, Joaquim J Ferreira, Mark J Edwards, Jeremy D Isaacs
doi : 10.1093/brain/awac363
Brain, Volume 146, Issue 4, April 2023, Pages 1615–1623
We previously hypothesized that functional cognitive disorder is characterized by heightened subjective mental effort, exhausted attentional reserve and metacognitive failure.
Patients carrying the mutation p.R406W in MAPT present with non-conforming phenotypic spectrum
Helena Gossye, Sara Van Mossevelde, Anne Sieben, Maria Bjerke, Elisabeth Hendrickx Van de Craen, Julie van der Zee, Peter P De Deyn, Jan De Bleecker, Jan Versijpt, Jenneke van den Ende, Olivier Deryck, Paul Bourgeois, Jean-Christophe Bier, Maarten Goethals, Rik Vandenberghe, Sebastiaan Engelborghs, Christine Van Broeckhoven
doi : 10.1093/brain/awac362
Brain, Volume 146, Issue 4, April 2023, Pages 1624–1636
The missense mutation p.R406W in microtubule-associated protein tau leads to frontotemporal lobar degeneration with an amnestic, Alzheimer’s disease-like phenotype with an autosomal dominant pattern of inheritance.
Clinical features and prognostic factors in adults with brain abscess
Jacob Bodilsen, Lærke Storgaard Duerlund, Theis Mariager, Christian Thomas Brandt, Pelle Trier Petersen, Lykke Larsen, Birgitte Rønde Hansen, Lars Haukali Omland, Malte Mose Tetens, Lothar Wiese, Rasmus Langelund Jørgensen, Steffen Leth, Henrik Nielsen, the DASGIB study group
doi : 10.1093/brain/awac312
Brain, Volume 146, Issue 4, April 2023, Pages 1637–1647
Studies on brain abscess are hampered by single-centre design with limited sample size and incomplete follow-up. Thus, robust analyses on clinical prognostic factors remain scarce.
Neurological manifestations of COVID-19 in adults and children
Sung-Min Cho, Nicole White, Lavienraj Premraj, Denise Battaglini, Jonathon Fanning, Jacky Suen, Gianluigi Li Bassi, John Fraser, Chiara Robba, Matthew Griffee, Bhagteshwar Singh, ;?>Barbara Wanjiru Citarella, Laura Merson, Tom Solomon, David Thomson, ISARIC Clinical Characterisation Group
doi : 10.1093/brain/awac332
Brain, Volume 146, Issue 4, April 2023, Pages 1648–1661
Different neurological manifestations of coronavirus disease 2019 (COVID-19) in adults and children and their impact have not been well characterized. We aimed to determine the prevalence of neurological manifestations and in-hospital complications among hospitalized COVID-19 patients and ascertain differences between adults and children.
Common and distinct fronto-striatal volumetric changes in heroin and cocaine use disorders
Ahmet O Ceceli, Yuefeng Huang, Greg Kronberg, Pias Malaker, Pazia Miller, Sarah G King, Pierre-Olivier Gaudreault, Natalie McClain, Lily Gabay, Devarshi Vasa, Jeffrey H Newcorn, Defne Ekin, Nelly Alia-Klein, Rita Z Goldstein
doi : 10.1093/brain/awac366
Brain, Volume 146, Issue 4, April 2023, Pages 1662–1671
Different drugs of abuse impact the morphology of fronto-striatal dopaminergic targets in both common and unique ways. While dorsal striatal volume tracks with addiction severity across drug classes, opiates impact ventromedial prefrontal cortex (vmPFC) and nucleus accumbens (NAcc) neuroplasticity in preclinical models, and psychostimulants alter inhibitory control, rooted in cortical regions such as the inferior frontal gyrus (IFG).
Large-scale lesion symptom mapping of depression identifies brain regions for risk and resilience
Nicholas T Trapp, Joel E Bruss, Kenneth Manzel, Jordan Grafman, Daniel Tranel, Aaron D Boes
doi : 10.1093/brain/awac361
Brain, Volume 146, Issue 4, April 2023, Pages 1672–1685
Understanding neural circuits that support mood is a central goal of affective neuroscience, and improved understanding of the anatomy could inform more targeted interventions in mood disorders.
Brain functional connectivity mirrors genetic pleiotropy in psychiatric conditions
Clara A Moreau, Kuldeep Kumar, Annabelle Harvey, Guillaume Huguet, Sebastian G W Urchs, Laura M Schultz, Hanad Sharmarke, Khadije Jizi, Charles-Olivier Martin, Nadine Younis, Petra Tamer, Jean-Louis Martineau, Pierre Orban, Ana Isabel Silva, Jeremy Hall, Marianne B M van den Bree, Michael J Owen, David E J Linden, Sarah Lippé, Carrie E Bearden, Laura Almasy, David C Glahn, Paul M Thompson, Thomas Bourgeron, Pierre Bellec, Sebastien Jacquemont
doi : 10.1093/brain/awac315
Brain, Volume 146, Issue 4, April 2023, Pages 1686–1696
Pleiotropy occurs when a genetic variant influences more than one trait. This is a key property of the genomic architecture of psychiatric disorders and has been observed for rare and common genomic variants. It is reasonable to hypothesize that the microscale genetic overlap (pleiotropy) across psychiatric conditions and cognitive traits may lead to similar overlaps at the macroscale brain level such as large-scale brain functional networks.
Inhibition of YAP/TAZ-driven TEAD activity prevents growth of NF2-null schwannoma and meningioma
Liyam Laraba, Lily Hillson, Julio Grimm de Guibert, Amy Hewitt, Maisie R Jaques, Tracy T Tang, Leonard Post, Emanuela Ercolano, Ganesha Rai, Shyh-Ming Yang, Daniel J Jagger, Waldemar Woznica, Philip Edwards, Aditya G Shivane, C Oliver Hanemann, David B Parkinson
doi : 10.1093/brain/awac342
Brain, Volume 146, Issue 4, April 2023, Pages 1697–1713
Schwannoma tumours typically arise on the eighth cranial nerve and are mostly caused by loss of the tumour suppressor Merlin (NF2). There are no approved chemotherapies for these tumours and the surgical removal of the tumour carries a high risk of damage to the eighth or other close cranial nerve tissue. New treatments for schwannoma and other NF2-null tumours such as meningioma are urgently required.
Structural connectome quantifies tumour invasion and predicts survival in glioblastoma patients
Yiran Wei, Chao Li, Zaixu Cui, Roxanne Claudeve Mayrand, Jingjing Zou, Adrianna Leanne Kok Chi Wong, Rohitashwa Sinha, Tomasz Matys, Carola-Bibiane Schönlieb, Stephen John Price
doi : 10.1093/brain/awac360
Brain, Volume 146, Issue 4, April 2023, Pages 1714–1727
Glioblastoma is characterized by diffuse infiltration into the surrounding tissue along white matter tracts. Identifying the invisible tumour invasion beyond focal lesion promises more effective treatment, which remains a significant challenge.
The Wernicke conundrum is misinterpreted
Marsel Mesulam, Cynthia Thompson, Sandra Weintraub, Emily Rogalski
doi : 10.1093/brain/awac482
Brain, Volume 146, Issue 4, April 2023, Pages e21–e22
Reply: The Wernicke conundrum is misinterpreted
William Matchin, Dirk-Bart den Ouden, Gregory Hickok, Argye E Hillis, Leonardo Bonilha, Julius Fridriksson
doi : 10.1093/brain/awac483
Brain, Volume 146, Issue 4, April 2023, Pages e23–e24
Correction to: Store-operated calcium entry is reduced in spastin-linked hereditary spastic paraplegia
doi : 10.1093/brain/awac491
Brain, Volume 146, Issue 4, April 2023, Page e25
Correction to: SLC12A2 variants cause a neurodevelopmental disorder or cochleovestibular defect
doi : 10.1093/brain/awad012
Brain, Volume 146, Issue 4, April 2023, Page e26
