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Predicting behavioural outcomes after stroke: from computational challenge towards individualized rehabilitation?
Dorothee Saur
doi : 10.1093/brain/awad119
Brain, Volume 146, Issue 5, May 2023, Pages 1729–1730
Climate change and the brain
Sanjay M Sisodiya
doi : 10.1093/brain/awad076
Brain, Volume 146, Issue 5, May 2023, Pages 1731–1733
Demystifying interictal discharges and seizure initiation in focal epilepsy
Catherine Schevon, Andrew Michalak
doi : 10.1093/brain/awad108
Brain, Volume 146, Issue 5, May 2023, Pages 1734–1736
A distinctive IgG-mediated pathogenesis for primary progressive multiple sclerosis?
Yong Guo, Vanda A Lennon
doi : 10.1093/brain/awad107
Brain, Volume 146, Issue 5, May 2023, Pages 1737–1739
The emerging era of staging Alzheimer’s disease pathology using plasma biomarkers
Niklas Mattsson-Carlgren, Sebastian Palmqvist
doi : 10.1093/brain/awad112
Brain, Volume 146, Issue 5, May 2023, Pages 1740–1742
The U-shaped curve predicting cognitive vulnerability to delirium severity
Richard C Lennertz, Robert D Sanders
doi : 10.1093/brain/awad115
Brain, Volume 146, Issue 5, May 2023, Pages 1743–1744
Physical activity as an exogenous risk factor for amyotrophic lateral sclerosis: a review of the evidence
Laura Chapman, Johnathan Cooper-Knock, Pamela J Shaw
doi : 10.1093/brain/awac470
Brain, Volume 146, Issue 5, May 2023, Pages 1745–1757
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal neurodegenerative disorder. The only established epidemiological risk factors for ALS are male sex and increasing age.
Cell-free DNA-based liquid biopsies in neurology
Hallie Gaitsch, Robin J M Franklin, Daniel S Reich
doi : 10.1093/brain/awac438
Brain, Volume 146, Issue 5, May 2023, Pages 1758–1774
This article reviews recent developments in the application of cell-free DNA-based liquid biopsies to neurological diseases.
Beyond Broca: neural architecture and evolution of a dual motor speech coordination system
Gregory Hickok, Jonathan Venezia, Alex Teghipco
doi : 10.1093/brain/awac454
Brain, Volume 146, Issue 5, May 2023, Pages 1775–1790
Classical neural architecture models of speech production propose a single system centred on Broca’s area coordinating all the vocal articulators from lips to larynx.
The evidence against somatotopic organization of function in the primate corticospinal tract
Roger N Lemon, Robert J Morecraft
doi : 10.1093/brain/awac496
Brain, Volume 146, Issue 5, May 2023, Pages 1791–1803
We review the spatial organization of corticospinal outputs from different cortical areas and how this reflects the varied functions mediated by the corticospinal tract.
Neuropathological hallmarks of antenatal mitochondrial diseases with a corpus callosum defect
Lucile Boutaud, Benedetta Ruzzenente, Aude Tessier, Olivia Anselem, Emmanuelle Pannier, Sarah Grotto, Naïma Talhi, Daniel Amram, Marjolaine Willems, Constance Wells, Patricia Blanchet, Yuri Musizzano, Clémence Jauny, Patrick Nitschke, Christine Bole-Feysot, Bettina Bessières, Houria Salhi, Amale Achaiaa, Metodi D Metodiev, Ferechte Razavi, Agnès Rötig, Laurence Loeuilllet, Tania Attié-Bitach
doi : 10.1093/brain/awac417
Brain, Volume 146, Issue 5, May 2023, Pages 1804–1811
Corpus callosum defects are frequent congenital cerebral disorders caused by mutations in more than 300 genes. These include genes implicated in corpus callosum development or function, as well as genes essential for mitochondrial physiology.
NMDA-receptor-Fc-fusion constructs neutralize anti-NMDA receptor antibodies
Stephan Steinke, Toni Kirmann, Eleonora A Loi, Jana Nerlich, Iron Weichard, Philipp Kuhn, Torsten Bullmann, Andreas Ritzau-Jost, Filiz Sila Rizalar, Harald Prüss, Volker Haucke, Christian Geis, Michael Hust, Stefan Hallermann
doi : 10.1093/brain/awac497
Brain, Volume 146, Issue 5, May 2023, Pages 1812–1820
N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most common subtype of autoimmune encephalitis characterized by a complex neuropsychiatric syndrome usually including memory impairment. Patients develop an intrathecal immune response against NMDARs with antibodies that presumably bind to the amino-terminal domain of the GluN1 subunit.
The effect of GLP-1RA exenatide on idiopathic intracranial hypertension: a randomized clinical trial
James L Mitchell, Hannah S Lyons, Jessica K Walker, Andreas Yiangou, Olivia Grech, Zerin Alimajstorovic, Nigel H Greig, Yazhou Li, Georgios Tsermoulas, Kristian Brock, Susan P Mollan, Alexandra J Sinclair
doi : 10.1093/brain/awad003
Brain, Volume 146, Issue 5, May 2023, Pages 1821–1830
Therapeutics to reduce intracranial pressure are an unmet need. Preclinical data have demonstrated a novel strategy to lower intracranial pressure using glucagon-like peptide-1 (GLP-1) receptor signalling.
Parallel in-depth analysis of repeat expansions in ataxia patients by long-read sequencing
Hannes Erdmann, Florian Schöberl, Mădălina Giurgiu, Rafaela Magalhaes Leal Silva, Veronika Scholz, Florentine Scharf, Martin Wendlandt, Stephanie Kleinle, Marcus Deschauer, Georg Nübling, Wolfgang Heide, Sait Seymen Babacan, Christine Schneider, Teresa Neuhann, Katrin Hahn, Benedikt Schoser, Elke Holinski-Feder, Dieter A Wolf, Angela Abicht
doi : 10.1093/brain/awac377
Brain, Volume 146, Issue 5, May 2023, Pages 1831–1843
Instability of simple DNA repeats has been known as a common cause of hereditary ataxias for over 20 years. Routine genetic diagnostics of these phenotypically similar diseases still rely on an iterative workflow for quantification of repeat units by PCR-based methods of limited precision.
Imbalance of NRG1-ERBB2/3 signalling underlies altered myelination in Charcot–Marie–Tooth disease 4H
Lara El-Bazzal, Adeline Ghata, Clothilde Estève, Jihane Gadacha, Patrice Quintana, Christel Castro, Nathalie Roeckel-Trévisiol, Frédérique Lembo, Nicolas Lenfant, André Mégarbané, Jean-Paul Borg, Nicolas Lévy, Marc Bartoli, Yannick Poitelon, Pierre L Roubertoux, Valérie Delague, Nathalie Bernard-Marissal
doi : 10.1093/brain/awac402
Brain, Volume 146, Issue 5, May 2023, Pages 1844–1858
Charcot–Marie–Tooth (CMT) disease is one of the most common inherited neurological disorders, affecting either axons from the motor and/or sensory neurons or Schwann cells of the peripheral nervous system (PNS) and caused by more than 100 genes.
GALC variants affect galactosylceramidase enzymatic activity and risk of Parkinson’s disease
Konstantin Senkevich, Cornelia E Zorca, Aliza Dworkind, Uladzislau Rudakou, Emma Somerville, Eric Yu, Alexey Ermolaev, Daria Nikanorova, Jamil Ahmad, Jennifer A Ruskey, Farnaz Asayesh, Dan Spiegelman, Stanley Fahn, Cheryl Waters, Oury Monchi, Yves Dauvilliers, Nicolas Dupré, Lior Greenbaum, Sharon Hassin-Baer, Francis P Grenn, Ming Sum Ruby Chiang, S Pablo Sardi, Benoît Vanderperre, Cornelis Blauwendraat, Jean-François Trempe, Edward A Fon, Thomas M Durcan, Roy N Alcalay, Ziv Gan-Or
doi : 10.1093/brain/awac413
Brain, Volume 146, Issue 5, May 2023, Pages 1859–1872
The association between glucocerebrosidase, encoded by GBA, and Parkinson’s disease (PD) highlights the role of the lysosome in PD pathogenesis. Genome-wide association studies in PD have revealed multiple associated loci, including the GALC locus on chromosome 14.
Association between the LRP1B and APOE loci and the development of Parkinson’s disease dementia
Raquel Real, Alejandro Martinez-Carrasco, Regina H Reynolds, Michael A Lawton, Manuela M X Tan, Maryam Shoai, Jean-Christophe Corvol, Mina Ryten, Catherine Bresner, Leon Hubbard, Alexis Brice, Suzanne Lesage, Johann Faouzi, Alexis Elbaz, Fanny Artaud, Nigel Williams, Michele T M Hu, Yoav Ben-Shlomo, Donald G Grosset, John Hardy, Huw R Morris
doi : 10.1093/brain/awac414
Brain, Volume 146, Issue 5, May 2023, Pages 1873–1887
Parkinson’s disease is one of the most common age-related neurodegenerative disorders. Although predominantly a motor disorder, cognitive impairment and dementia are important features of Parkinson’s disease, particularly in the later stages of the disease.
Glycolysis regulates neuronal excitability via lactate receptor, HCA1R
Daria Skwarzynska, Huayu Sun, John Williamson, Izabela Kasprzak, Jaideep Kapur
doi : 10.1093/brain/awac419
Brain, Volume 146, Issue 5, May 2023, Pages 1888–1902
Repetitively firing neurons during seizures accelerate glycolysis to meet energy demand, which leads to the accumulation of extracellular glycolytic by-product lactate. Here, we demonstrate that lactate rapidly modulates neuronal excitability in times of metabolic stress via the hydroxycarboxylic acid receptor type 1 (HCA1R) to modify seizure activity.
Interictal discharges in the human brain are travelling waves arising from an epileptogenic source
Joshua M Diamond, C Price Withers, Julio I Chapeton, Shareena Rahman, Sara K Inati, Kareem A Zaghloul
doi : 10.1093/brain/awad015
Brain, Volume 146, Issue 5, May 2023, Pages 1903–1915
While seizure activity may be electrographically widespread, increasing evidence has suggested that ictal discharges may in fact represent travelling waves propagated from a focal seizure source.
Non-invasive mapping of epileptogenic networks predicts surgical outcome
Ludovica Corona, Eleonora Tamilia, M Scott Perry, Joseph R Madsen, Jeffrey Bolton, Scellig S D Stone, Steve M Stufflebeam, Phillip L Pearl, Christos Papadelis
doi : 10.1093/brain/awac477
Brain, Volume 146, Issue 5, May 2023, Pages 1916–1931
Epilepsy is increasingly considered a disorder of brain networks. Studying these networks with functional connectivity can help identify hubs that facilitate the spread of epileptiform activity.
Anti-pan-neurofascin antibodies induce subclass-related complement activation and nodo-paranodal damage
Luise Appeltshauser, Helena Junghof, Julia Messinger, Janis Linke, Axel Haarmann, Ilya Ayzenberg, Panoraia Baka, Johannes Dorst, Anna L Fisse, Thomas Grüter, Valerie Hauschildt, Alexander Jörk, Frank Leypoldt, Mathias Mäurer, Edgar Meinl, Sebastian Michels, Jeremias Motte, Kalliopi Pitarokoili, Mark Stettner, Carmen Villmann, Marc Weihrauch, Gabriel S Welte, Inga Zerr, Katrin G Heinze, Claudia Sommer, Kathrin Doppler
doi : 10.1093/brain/awac418
Brain, Volume 146, Issue 5, May 2023, Pages 1932–1949
Autoimmune neuropathy associated with antibodies against pan-neurofascin is a new subtype of nodo-paranodopathy. It is relevant because it is associated with high morbidity and mortality.
Using in vivo functional and structural connectivity to predict chronic stroke aphasia deficits
Ying Zhao, Christopher R Cox, Matthew A Lambon Ralph, Ajay D Halai
doi : 10.1093/brain/awac388
Brain, Volume 146, Issue 5, May 2023, Pages 1950–1962
Focal brain damage caused by stroke can result in aphasia and advances in cognitive neuroscience suggest that impairment may be associated with network-level disorder rather than just circumscribed cortical damage.
Latent disconnectome prediction of long-term cognitive-behavioural symptoms in stroke
Lia Talozzi, Stephanie J Forkel, Valentina Pacella, Victor Nozais, Etienne Allart, Céline Piscicelli, Dominic Pérennou, Daniel Tranel, Aaron Boes, Maurizio Corbetta, Parashkev Nachev, Michel Thiebaut de Schotten
doi : 10.1093/brain/awad013
Brain, Volume 146, Issue 5, May 2023, Pages 1963–1978
Stroke significantly impacts the quality of life. However, the long-term cognitive evolution in stroke is poorly predictable at the individual level. There is an urgent need to better predict long-term symptoms based on acute clinical neuroimaging data.
Cerebrospinal fluid immunoglobulins in primary progressive multiple sclerosis are pathogenic
Jamie K Wong, Jerry Lin, Nathan J Kung, Alexandra L Tse, Serena J E Shimshak, Anna K Roselle, Francesca M Cali, Jessie Huang, Joseph M Beaty, Taylor M Shue, Saud A Sadiq
doi : 10.1093/brain/awad031
Brain, Volume 146, Issue 5, May 2023, Pages 1979–1992
Multiple sclerosis is clinically characterized by relapses and remissions (relapsing-remitting multiple sclerosis) that over time may evolve to a progressive course (secondary progressive multiple sclerosis) or as having a progressive course from disease onset (primary progressive multiple sclerosis).
Siblings reduce multiple sclerosis risk by preventing delayed primary Epstein–Barr virus infection
Klaus Rostgaard, Nete Munk Nielsen, Mads Melbye, Morten Frisch, Henrik Hjalgrim
doi : 10.1093/brain/awac401
Brain, Volume 146, Issue 5, May 2023, Pages 1993–2002
Epstein–Barr virus infection, and perhaps almost exclusively delayed Epstein–Barr virus infection, seems to be a prerequisite for the development of multiple sclerosis. Siblings provide protection against infectious mononucleosis by occasionally preventing delayed primary Epstein–Barr virus infection, with its associated high risk of infectious mononucleosis.
The clinical and molecular spectrum of ZFYVE26-associated hereditary spastic paraplegia: SPG15
Afshin Saffari, 1,2 Melanie Kellner, 3,4 Catherine Jordan, 1 Helena Rosengarten, 1 Alisa Mo, 1 Bo Zhang,1,5 Oleksandr Strelko, 1,6 Sonja Neuser, 7 Marie Y. Davis, 8,9 Nobuaki Yoshikura, 10 Naonobu Futamura, 11 Tomoya Takeuchi,12 Shin Nabatame, 13 Hiroyuki Ishiura, 14 Shoji Tsuji, 15,16 Huda Shujaa Aldeen, 17 Elisa Cali, 17 Clarissa Rocca,17 Henry Houlden, 17 Stephanie Efthymiou, 17 Birgit Assmann,2 Grace Yoon, 18 Bianca A. Trombetta, 19 Pia Kivisäkk,19 Florian Eichler, 20 Haitian Nan, 21 Yoshihisa Takiyama,21,22 Alessandra Tessa,23 Filippo M. Santorelli, 23 Mustafa Sahin,1,6 Craig Blackstone, 24 Edward Yang, 25 Rebecca Schüle 3,4 and Darius Ebrahimi-Fakhari1,26
doi : 10.1093/brain/awac391
Brain, Volume 146, Issue 5, May 2023, Pages 2003–2015
In the field of hereditary spastic paraplegia (HSP), progress in molecular diagnostics needs to be translated into robust phenotyping studies to understand genetic and phenotypic heterogeneity and to support interventional trials.
Promoting regeneration while blocking cell death preserves motor neuron function in a model of ALS
Josette J Wlaschin, Caroline Donahue, Jacob Gluski, Jennifer F Osborne, Leana M Ramos, Hanna Silberberg, Claire E Le Pichon
doi : 10.1093/brain/awac415
Brain, Volume 146, Issue 5, May 2023, Pages 2016–2028
Amyotrophic lateral sclerosis (ALS) is a devastating and fatal neurodegenerative disease of motor neurons with very few treatment options. We had previously found that motor neuron degeneration in a mouse model of ALS can be delayed by deleting the axon damage sensor MAP3K12 or dual leucine zipper kinase (DLK).
Predicting amyloid PET and tau PET stages with plasma biomarkers
Clifford R Jack, Jr, Heather J Wiste, Alicia Algeciras-Schimnich, Dan J Figdore, Christopher G Schwarz, Val J Lowe, Vijay K Ramanan, Prashanthi Vemuri, Michelle M Mielke, David S Knopman, Jonathan Graff-Radford, Bradley F Boeve, Kejal Kantarci, Petrice M Cogswell, Matthew L Senjem, Jeffrey L Gunter, Terry M Therneau, Ronald C Petersen
doi : 10.1093/brain/awad042
Brain, Volume 146, Issue 5, May 2023, Pages 2029–2044
Staging the severity of Alzheimer’s disease pathology using biomarkers is useful for therapeutic trials and clinical prognosis. Disease staging with amyloid and tau PET has face validity; however, this would be more practical with plasma biomarkers. Our objectives were, first, to examine approaches for staging amyloid and tau PET and, second, to examine prediction of amyloid and tau PET stages using plasma biomarkers.
Predicting progression to Alzheimer’s disease with human hippocampal progenitors exposed to serum
Aleksandra Maruszak, Edina Silajdžić, Hyunah Lee, Tytus Murphy, Benjamine Liu, Liu Shi, Chiara de Lucia, Abdel Douiri, Evgenia Salta, Alejo J Nevado, Charlotte E Teunissen, Pieter J Visser, Jack Price, Henrik Zetterberg, Simon Lovestone, Sandrine Thuret
doi : 10.1093/brain/awac472
Brain, Volume 146, Issue 5, May 2023, Pages 2045–2058
Adult hippocampal neurogenesis is important for learning and memory and is altered early in Alzheimer’s disease. As hippocampal neurogenesis is modulated by the circulatory systemic environment, evaluating a proxy of how hippocampal neurogenesis is affected by the systemic milieu could serve as an early biomarker for Alzheimer’s disease progression.
Educational attainment, structural brain reserve and Alzheimer’s disease: a Mendelian randomization analysis
Aida Seyedsalehi, Varun Warrier, Richard A I Bethlehem, Benjamin I Perry, Stephen Burgess, Graham K Murray
doi : 10.1093/brain/awac392
Brain, Volume 146, Issue 5, May 2023, Pages 2059–2074
Higher educational attainment is observationally associated with lower risk of Alzheimer’s disease. However, the biological mechanisms underpinning this association remain unclear.
Cholinergic white matter pathways along the Alzheimer's disease continuum
Milan Nemy, Martin Dyrba, Frederic Brosseron, Katharina Buerger, Peter Dechent, Laura Dobisch, Michael Ewers, Klaus Fliessbach, Wenzel Glanz, Doreen Goerss, Michael T Heneka, Stefan Hetzer, Enise I Incesoy, Daniel Janowitz, Ingo Kilimann, Christoph Laske, Franziska Maier, Matthias H Munk, Robert Perneczky, Oliver Peters, Lukas Preis, Josef Priller, Boris-Stephan Rauchmann, Sandra Röske, Nina Roy, Klaus Scheffler, Anja Schneider, Björn H Schott, Annika Spottke, Eike J Spruth, Michael Wagner, Jens Wiltfang, Renat Yakupov, Maria Eriksdotter, Eric Westman, Olga Stepankova, Lenka Vyslouzilova, Emrah Düzel, Frank Jessen, Stefan J Teipel, Daniel Ferreira
doi : 10.1093/brain/awac385
Brain, Volume 146, Issue 5, May 2023, Pages 2075–2088
Previous studies have shown that the cholinergic nucleus basalis of Meynert and its white matter projections are affected in Alzheimer’s disease dementia and mild cognitive impairment.
Transthyretin attenuates TDP-43 proteinopathy by autophagy activation via ATF4 in FTLD-TDP
Yuan-Ping Chu, Lee-Way Jin, Liang-Chao Wang, Pei-Chuan Ho, Wei-Yen Wei, Kuen-Jer Tsai
doi : 10.1093/brain/awac412
Brain, Volume 146, Issue 5, May 2023, Pages 2089–2106
TAR DNA-binding protein-43 (TDP-43) proteinopathies are accompanied by the pathological hallmark of cytoplasmic inclusions in the neurodegenerative diseases, including frontal temporal lobar degeneration-TDP and amyotrophic lateral sclerosis.
Brain region-specific synaptic function of FUS underlies the FTLD-linked behavioural disinhibition
Jun-Ying Wang, Guo-Ming Ma, Xiao-Qiang Tang, Qi-Li Shi, Ming-Can Yu, Min-Min Lou, Kai-Wen He, Wen-Yuan Wang
doi : 10.1093/brain/awac411
Brain, Volume 146, Issue 5, May 2023, Pages 2107–2119
Synaptic dysfunction is one of the earliest pathological processes that contribute to the development of many neurological disorders, including Alzheimer’s disease and frontotemporal lobar degeneration. However, the synaptic function of many disease-causative genes and their contribution to the pathogenesis of the related diseases remain unclear.
Neurodevelopmental effects of genetic frontotemporal dementia in young adult mutation carriers
Elizabeth Finger, Rubina Malik, Martina Bocchetta, Kristy Coleman, Caroline Graff, Barbara Borroni, Mario Masellis, Robert Laforce, Caroline V Greaves, Lucy L Russell, Rhian S Convery, Arabella Bouzigues, David M Cash, Markus Otto, Matthis Synofzik, James B Rowe, Daniela Galimberti, Pietro Tiraboschi, Robert Bartha, Christen Shoesmith, Maria Carmela Tartaglia, John C van Swieten, Harro Seelaar, Lize C Jiskoot, Sandro Sorbi, Chris R Butler, Alexander Gerhard, Raquel Sanchez-Valle, Alexandre de Mendonça, Fermin Moreno, Rik Vandenberghe, Isabelle Le Ber, Johannes Levin, Florence Pasquier, Isabel Santana, Jonathan D Rohrer, Simon Ducharme, the Genetic FTD Initiative, GENFI
doi : 10.1093/brain/awac446
Brain, Volume 146, Issue 5, May 2023, Pages 2120–2131
While frontotemporal dementia has been considered a neurodegenerative disease that starts in mid-life or later, it is now clearly established that cortical and subcortical volume loss is observed more than a decade prior to symptom onset and progresses with ageing.
Extremes of baseline cognitive function determine the severity of delirium: a population study
Alex Tsui, Natalie Yeo, Samuel D Searle, Helen Bowden, Katrin Hoffmann, Joanne Hornby, Arley Goslett, Maryse Weston-Clarke, David Lanham, Patrick Hogan, Anna Seeley, Mark Rawle, Nish Chaturvedi, Elizabeth L Sampson, Kenneth Rockwood, Colm Cunningham, E Wesley Ely, Sarah J Richardson, Carol Brayne, Graciela Muniz Terrera, Zoë Tieges, Alasdair M J MacLullich, Daniel Davis
doi : 10.1093/brain/awad062
Brain, Volume 146, Issue 5, May 2023, Pages 2132–2141
Although delirium is a significant clinical and public health problem, little is understood about how specific vulnerabilities underlie the severity of its presentation. Our objective was to quantify the relationship between baseline cognition and subsequent delirium severity.
Multimodal neuroimaging in post-COVID syndrome and correlation with cognition
MarÃa DÃez-Cirarda, Miguel Yus, Natividad Gómez-Ruiz, Carmen Polidura, Lidia Gil-MartÃnez, Cristina Delgado-Alonso, Manuela Jorquera, Ulises Gómez-Pinedo, Jorge Matias-Guiu, Juan Arrazola, Jordi A Matias-Guiu
doi : 10.1093/brain/awac384
Brain, Volume 146, Issue 5, May 2023, Pages 2142–2152
Brain changes have been reported in the first weeks after SARS-CoV-2 infection. However, limited literature exists about brain alterations in post-COVID syndrome, a condition increasingly associated with cognitive impairment.
Lesions to both somatic and affective pain pathways lead to decreased salience network connectivity
Itamar Jalon, Assaf Berger, Ben Shofty, Noam Goldway, Moran Artzi, Guy Gurevitch, Uri Hochberg, Rotem Tellem, Talma Hendler, Tal Gonen, Ido Strauss
doi : 10.1093/brain/awac403
Brain, Volume 146, Issue 5, May 2023, Pages 2153–2162
Human pain is a salient stimulus composed of two main components: a sensory/somatic component, carrying peripheral nociceptive sensation via the spinothalamic tract and brainstem nuclei to the thalamus and then to sensory cortical regions, and an affective (suffering) component, where information from central thalamic nuclei is carried to the anterior insula, dorsal anterior cingulate cortex and other regions.
Social cognition deficits and biometric signatures in the behavioural variant of Alzheimer’s disease
Ellen H Singleton, Jay L P Fieldhouse, Jochum J van ’t Hooft, Marta Scarioni, Marie-Paule E van Engelen, Sietske A M Sikkes, Casper de Boer, Diana I Bocancea, Esther van den Berg, Philip Scheltens, Wiesje M van der Flier, Janne M Papma, Yolande A L Pijnenburg, Rik Ossenkoppele
doi : 10.1093/brain/awac382
Brain, Volume 146, Issue 5, May 2023, Pages 2163–2174
The behavioural variant of Alzheimer’s disease (bvAD) is characterized by early predominant behavioural changes, mimicking the behavioural variant of frontotemporal dementia (bvFTD), which is characterized by social cognition deficits and altered biometric responses to socioemotional cues. These functions remain understudied in bvAD.
Mnk1/2 kinases regulate memory and autism-related behaviours via Syngap1
Kleanthi Chalkiadaki, Mehdi Hooshmandi, Gilliard Lach, Elpida Statoulla, Konstanze Simbriger, Ines S Amorim, Stella Kouloulia, Maria Zafeiri, Panagiotis Pothos, Éric Bonneil, Ilse Gantois, Jelena Popic, Sung-Hoon Kim, Calvin Wong, Ruifeng Cao, Noboru H Komiyama, Yaser Atlasi, Seyed Mehdi Jafarnejad, Arkady Khoutorsky, Christos G Gkogkas
doi : 10.1093/brain/awac398
Brain, Volume 146, Issue 5, May 2023, Pages 2175–2190,
MAPK interacting protein kinases 1 and 2 (Mnk1/2) regulate a plethora of functions, presumably via phosphorylation of their best characterized substrate, eukaryotic translation initiation factor 4E (eIF4E) on Ser209.
Reduced grid-like theta modulation in schizophrenia
Laura Convertino, Daniel Bush, Fanfan Zheng, Rick A Adams, Neil Burgess
doi : 10.1093/brain/awac416
Brain, Volume 146, Issue 5, May 2023, Pages 2191–2198
The hippocampal formation has been implicated in the pathophysiology of schizophrenia, with patients showing impairments in spatial and relational cognition, structural changes in entorhinal cortex and reduced theta coherence with medial prefrontal cortex. Both the entorhinal cortex and medial prefrontal cortex exhibit a 6-fold (or ‘hexadirectional’) modulation of neural activity during virtual navigation that is indicative of grid cell populations and associated with accurate spatial navigation.
Biallelic variants in the COQ7 gene cause distal hereditary motor neuropathy in two Chinese families
Xiao-xuan Liu, Ning Wang, Yi-kun Chen, Wen-qi Lv, Jing-Mei Hong, Guo-Rong Xu, Lin-Ying Zhou, Wan-Jin Chen, Dong-Sheng Fan, Jin He
doi : 10.1093/brain/awad040
Brain, Volume 146, Issue 5, May 2023, Pages e27–e30
Reply: Biallelic variants in the COQ7 gene cause distal hereditary motor neuropathy in two Chinese families
Arnaud Jacquier, Julian Theuriet, Shams Ribault, Nicolas Lacoste, Antoine Pegat, Philippe Latour, Laurent Schaeffer
doi : 10.1093/brain/awad041
Brain, Volume 146, Issue 5, May 2023, Pages e31–e32
Correction to: Variants in the SK2 channel gene (KCNN2) lead to dominant neurodevelopmental movement disorders
doi : 10.1093/brain/awad029
Brain, Volume 146, Issue 5, May 2023, Page e33
