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2023 Brain essay competition results
doi : 10.1093/brain/awad416
Brain, Volume 147, Issue 1, January 2024, Page 1
Who am I?
Brian Routledge
doi : 10.1093/brain/awad425
Brain, Volume 147, Issue 1, January 2024, Pages 2–4
Transdiagnostic or disorder-specific? Altered reinforcement learning in depression and schizophrenia
Jonathan S. Ryan1 and Michael T. Treadway
doi : 10.1093/brain/awad400
Brain, Volume 147, Issue 1, January 2024, Pages 5–6
Herpes viral infection and the multiple sclerosis prodrome: is HHV-6A infection a second hit?
Bruce A. C. Cree
doi : 10.1093/brain/awad418
Brain, Volume 147, Issue 1, January 2024, Pages 7–9
Extra-cranial cholinergic lesions in dementia with Lewy bodies
David S. Goldstein
doi : 10.1093/brain/awad408
Brain, Volume 147, Issue 1, January 2024, Pages 10–11
The potential of blood neurofilament light as a marker of neurodegeneration for Alzheimer's disease
Youjin Jung1,2 and Jessica S. Damoiseaux
doi : 10.1093/brain/awad267
Brain, Volume 147, Issue 1, January 2024, Pages 12–25
Review of the role of the endogenous opioid and melanocortin systems in the restless legs syndrome
Arthur S. Walters,1 Yuqing Li,2 Brian B. Koo,3,4 William G. Ondo,5 Leonard B. Weinstock,6 David Champion,7 Lawrence B. Afrin,8 Elias G. Karroum,9 Kanika Bagai1 and Karen Spruyt
doi : 10.1093/brain/awad283
Brain, Volume 147, Issue 1, January 2024, Pages 26–38
Restless legs syndrome (RLS) is responsive to opioid, dopaminergic and iron-based treatments. Receptor blocker studies in RLS patients suggest that the therapeutic efficacy of opioids is specific to the opioid receptor and mediated indirectly through the dopaminergic system. An RLS autopsy study reveals decreases in endogenous opioids, β-endorphin and perhaps Met-enkephalin in the thalamus of RLS patients.
Brain perivascular macrophages: current understanding and future prospects
Wenjie Wen,1,2,3,†Jinping Cheng1,2,3,†and Yamei Tang
doi : 10.1093/brain/awad304
Brain, Volume 147, Issue 1, January 2024, Pages 39–55
Brain perivascular macrophages are specialized populations of macrophages that reside in the space around cerebral vessels, such as penetrating arteries and venules. With the help of cutting-edge technologies, such as cell fate mapping and single-cell multi-omics, their multifaceted, pivotal roles in phagocytosis, antigen presentation, vascular integrity maintenance and metabolic regulation have more recently been further revealed under physiological conditions.
A role for the serotonin 2A receptor in the expansion and functioning of human transmodal cortex
Andrea I. Luppi,1,2,3,†Manesh Girn,4,5,†Fernando E. Rosas,6,7,8 Christopher Timmermann,6 Leor Roseman,6 David Erritzoe,6 David J. Nutt,6 Emmanuel A. Stamatakis,1 R. Nathan Spreng,4 Lei Xing,9 Wieland B. Huttner9 and Robin L. Carhart-Harris
doi : 10.1093/brain/awad311
Brain, Volume 147, Issue 1, January 2024, Pages 56–80
Integrating independent but converging lines of research on brain function and neurodevelopment across scales, this article proposes that serotonin 2A receptor (5-HT2AR) signalling is an evolutionary and developmental driver and potent modulator of the macroscale functional organization of the human cerebral cortex.
Aggregation and beyond: alpha-synuclein-based biomarkers in synucleinopathies
Avika Chopra1 and Tiago Fleming Outeiro
doi : 10.1093/brain/awad260
Brain, Volume 147, Issue 1, January 2024, Pages 81–90
Parkinson’s disease is clinically known for the loss of dopaminergic neurons in the substantia nigra pars compacta and accumulation of intraneuronal cytoplasmic inclusions rich in alpha-synuclein called ‘Lewy bodies’ and ‘Lewy neurites’. Together with dementia with Lewy bodies and multiple system atrophy, Parkinson’s disease is part of a group of disorders called synucleinopathies
Homozygous MFN2 variants causing severe antenatal encephalopathy with clumped mitochondria
Arnaud Chevrollier,1 Adeline Alice Bonnard,2,3 Lyse Ruaud,2,4 Naïg Gueguen,1,5 Laurence Perrin,2 Valérie Desquiret-Dumas,1,5 Fabien Guimiot,4,6 Pierre-Hadrien Becker,7,8 Jonathan Levy,2,7 Pascal Reynier1,5 and Pauline Gaignard
doi : 10.1093/brain/awad347
Brain, Volume 147, Issue 1, January 2024, Pages 91–99
Pathogenic variants in the MFN2 gene are commonly associated with autosomal dominant (CMT2A2A) or recessive (CMT2A2B) Charcot-Marie-Tooth disease, with possible involvement of the CNS. Here, we present a case of severe antenatal encephalopathy with lissencephaly, polymicrogyria and cerebellar atrophy.
Glymphatic dysfunction in patients with early-stage amyotrophic lateral sclerosis
Shuangwu Liu,1,2,3,†Xiaohan Sun,2,†Qingguo Ren,4 Yujing Chen,2 Tingjun Dai,2 Yiru Yang,1 Gaolang Gong,5 Wei Li,2 Yuying Zhao,2 Xiangshui Meng,4 Pengfei Lin2,‡ and Chuanzhu Yan
doi : 10.1093/brain/awad274
Brain, Volume 147, Issue 1, January 2024, Pages 100–108
Recently, an astrocytic aquaporin 4-dependent drainage system, that is, the glymphatic system, has been identified in the live murine and human brain. Growing evidence suggests that glymphatic function is impaired in patients with several neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease.
SUN1 facilitates CHMP7 nuclear influx and injury cascades in sporadic amyotrophic lateral sclerosis
Victoria Baskerville,1,2 Sampath Rapuri,1,2 Emma Mehlhop1,2 and Alyssa N. Coyne
doi : 10.1093/brain/awad291
Brain, Volume 147, Issue 1, January 2024, Pages 109–121,
We have recently identified the aberrant nuclear accumulation of the ESCRT-III protein CHMP7 as an initiating event that leads to a significant injury to the nuclear pore complex (NPC) characterized by the reduction of specific nucleoporins from the neuronal NPC in sporadic amyotrophic lateral sclerosis (sALS) and C9orf72 ALS/frontotemporal dementia (FTD)-induced pluripotent stem cell-derived neurons (iPSNs), a phenomenon also observed in post-mortem patient tissues.
Reversal of neurological deficits by painless nerve growth factor in a mouse model of Rett syndrome
Alexia Tiberi,1,2,†Giulia Borgonovo,2,†Giovanna Testa,2 Paola Pacifico,2 Ajesh Jacob,2 Mariachiara Di Caprio,2 Valentino Totaro,2 Mariantonietta Calvello,2 Antonino Cattaneo2,3 and Simona Capsoni
doi : 10.1093/brain/awad282
Brain, Volume 147, Issue 1, January 2024, Pages 122–134
Rett syndrome is a rare genetic neurodevelopmental disease, affecting 1 in over 10 000 females born worldwide, caused by de novo mutations in the X-chromosome-located methyl-CpG-binding protein 2 (MeCP2) gene. Despite the great effort put forth by the scientific community, a therapy for this devastating disease is still needed.
Prognostic value of single-subject grey matter networks in early multiple sclerosis
Vinzenz Fleischer,1,†Gabriel Gonzalez-Escamilla,1,†Deborah Pareto,2 Alex Rovira,2 Jaume Sastre-Garriga,3 Piotr Sowa,4 Einar A. H?gest?l,5,6 Hanne F. Harbo,5,6 Barbara Bellenberg,7 Carsten Lukas,7 Serena Ruggieri,8 Claudio Gasperini,9 Tomas Uher,10 Manuela Vaneckova,11 Stefan Bittner,1 Ahmed E. Othman,12 Sara Collorone,13 Ahmed T. Toosy,13 Sven G. Meuth,14 Frauke Zipp,1 Frederik Barkhof,13,15 Olga Ciccarelli13 and Sergiu Groppa1 on behalf of the MAGNIMS study group
doi : 10.1093/brain/awad288
Brain, Volume 147, Issue 1, January 2024, Pages 135–146
The identification of prognostic markers in early multiple sclerosis (MS) is challenging and requires reliable measures that robustly predict future disease trajectories. Ideally, such measures should make inferences at the individual level to inform clinical decisions.
ALCAM on human oligodendrocytes mediates CD4 T cell adhesion
Hélène Jamann,1,2,†Haritha L. Desu,1,†Qiao-Ling Cui,3 Alexandre Halaweh,1,4 Olivier Tastet,1 Wendy Klement,1 Stephanie Zandee,1,2 Florian Pernin,3 Victoria H. Mamane,1,2 Oumarou Ouédraogo,1,4 Audrey Daigneault,1 Hadjara Sidibé,1,2 Florence Millette,1,2 Evelyn Peelen,1,2 Tessa Dhaeze,1,2 Chloé Hoornaert,1,2 Rose-Marie Rébillard,1,2 Karine Thai,1,2 Camille Grasmuck,1,2 Christine Vande Velde,1,2 Alexandre Prat,1,2 Nathalie Arbour,1,2 Jo Anne Stratton,3 Jack Antel3 and Catherine Larochelle
doi : 10.1093/brain/awad286
Brain, Volume 147, Issue 1, January 2024, Pages 147–162
Multiple sclerosis is a chronic neuroinflammatory disorder characterized by demyelination, oligodendrocyte damage/loss and neuroaxonal injury in the context of immune cell infiltration in the CNS.
Soluble TREM2 triggers microglial dysfunction in neuromyelitis optica spectrum disorders
Chuan Qin,1,2,†Man Chen,1,2,†Ming-Hao Dong,1,2 Sheng Yang,1,2 Hang Zhang,1,2 Yun-Fan You,1,2 Luo-Qi Zhou,1,2 Yun-Hui Chu,1,2 Yue Tang,1,2 Xiao-Wei Pang,1,2 Long-Jun Wu,3 Dai-Shi Tian1,2 and Wei Wang
doi : 10.1093/brain/awad321
Brain, Volume 147, Issue 1, January 2024, Pages 163–176
Microglia-mediated neuroinflammation contributes to acute demyelination in neuromyelitis optica spectrum disorders (NMOSD). Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in the CSF has been associated with microglial activation in several neurodegenerative diseases.
Human herpesvirus 6A and axonal injury before the clinical onset of multiple sclerosis
Viktor Grut,1 Martin Bistr?m,1 Jonatan Salzer,1 Pernilla Stridh,2,3 Daniel Jons,4 Rasmus Gustafsson,2,3 Anna Fogdell-Hahn,2,3 Jesse Huang,2,3 Julia Butt,5 Anna Lindam,6 Lucia Alonso-Magdalena,7 Tomas Bergstr?m,8 Ingrid Kockum,2,3 Tim Waterboer,5 Tomas Olsson,2,3 Henrik Zetterberg,9,10,11,12,13,14 Kaj Blennow,9,10 Oluf Andersen,4 Staffan Nilsson15 and Peter Sundstr?m1
doi : 10.1093/brain/awad374
Brain, Volume 147, Issue 1, January 2024, Pages 177–185
Recent research indicates that multiple sclerosis is preceded by a prodromal phase with elevated levels of serum neurofilament light chain (sNfL), a marker of axonal injury. The effect of environmental risk factors on the extent of axonal injury during this prodrome is unknown
Inhibiting metabotropic glutamate receptor 5 after stroke restores brain function and connectivity
Jakob Hakon,1 Miriana J. Quattromani,1 Carin Sj?lund,1 Daniela Talhada,1 Byungchan Kim,2,†Slavianka Moyanova,3 Federica Mastroiacovo,3 Luisa Di Menna,3 Roger Olsson,4 Elisabet Englund,5 Ferdinando Nicoletti,3,6 Karsten Ruscher,1 Adam Q. Bauer2,‡ and Tadeusz Wieloch
doi : 10.1093/brain/awad293
Brain, Volume 147, Issue 1, January 2024, Pages 186–200
Stroke results in local neural disconnection and brain-wide neuronal network dysfunction leading to neurological deficits. Beyond the hyper-acute phase of ischaemic stroke, there is no clinically-approved pharmacological treatment that alleviates sensorimotor impairments.
Transdiagnostic inflexible learning dynamics explain deficits in depression and schizophrenia
Hans Kirschner,1 Matthew R. Nassar,2,3 Adrian G. Fischer,4 Thomas Frodl,5,6,7,8 Gabriela Meyer-Lotz,5 S?ren Frob?se,5 Stephanie Seidenbecher,5 Tilmann A. Klein1,9,†and Markus Ullsperger
doi : 10.1093/brain/awad362
Brain, Volume 147, Issue 1, January 2024, Pages 201–214
Deficits in reward learning are core symptoms across many mental disorders. Recent work suggests that such learning impairments arise by a diminished ability to use reward history to guide behaviour, but the neuro-computational mechanisms through which these impairments emerge remain unclear.
Impaired glucose utilization in the brain of patients with delirium following hip fracture
Irit Titlestad,1,2,3 Leiv Otto Watne,3,4,5 Gideon A. Caplan,6,7 Adrian McCann,8 Per Magne Ueland,8 Bj?rn Erik Neerland,3 Marius Myrstad,9 Nathalie Bodd Halaas,3,4 Christian Thomas Pollmann,10 Kristi Henjum,3,4 Anette Hylen Ranhoff,11,12 Lene B. Solberg,13 Wender Figved,4,14 Colm Cunningham15 and Lasse M. Giil
doi : 10.1093/brain/awad296
Brain, Volume 147, Issue 1, January 2024, Pages 215–223
Alterations in brain energy metabolism have long been proposed as one of several neurobiological processes contributing to delirium. This is supported by previous findings of altered CSF lactate and neuron-specific enolase concentrations and decreased glucose uptake on brain-PET in patients with delirium.
Correlations of receptor desensitization of gain-of-function GABRB3 variants with clinical severity
Susan X. N. Lin,1 Philip K. Ahring,1 Angelo Keramidas,2 Vivian W. Y. Liao,1 Rikke S. M?ller,3,4 Mary Chebib1 and Nathan L. Absalom
doi : 10.1093/brain/awad285
Brain, Volume 147, Issue 1, January 2024, Pages 224–239
Genetic variants associated with developmental and epileptic encephalopathies have been identified in the GABRB3 gene that encodes the β3 subunit of GABAA receptors. Typically, variants alter receptor sensitivity to GABA resulting in either gain- or loss-of-function, which correlates with patient phenotypes. However, it is unclear how another important receptor property, desensitization, contributes to the greater clinical severity of gain-of-function variants.
Cross-seeding by prion protein inactivates TDP-43
Stella A. Polido,1 Cristiana Stuani,2 Aaron Voigt,3 Papiya Banik,1 Janine Kamps,1,4 Verian Bader,1,5 Prerna Grover,1 Laura J. Krause,4,5 Inga Zerr,6 Jakob Matschke,7 Markus Glatzel,7 Konstanze F. Winklhofer,4,5 Emanuele Buratti2 and J?rg Tatzelt1,4
doi : 10.1093/brain/awad289
Brain, Volume 147, Issue 1, January 2024, Pages 240–254
A common pathological denominator of various neurodegenerative diseases is the accumulation of protein aggregates. Neurotoxic effects are caused by a loss of the physiological activity of the aggregating protein and/or a gain of toxic function of the misfolded protein conformers.
Impaired cholinergic integrity of the colon and pancreas in dementia with Lewy bodies
Niels Okkels,1,2,3 Jacob Horsager,1,2 Tatyana D. Fedorova,1,2 Karoline Knudsen,1 Casper Skj?rb?k,1,2 Katrine B. Andersen,1,2 Miguel Labrador-Espinosa,4,5 Karsten Vestergaard,6 Janne K. Mortensen,2,3 Henriette Klit,3 Mette M?ller,3 Erik H. Danielsen,3 Erik L. Johnsen,3 Goran Bekan,7 Kim V. Hansen,1 Ole L. Munk,1 Malene F. Damholdt,2 Pernille L. Kjeldsen,1,2,6 Allan K. Hansen,1,8 Hanne Gottrup,3 Michel J. Grothe4,5 and Per Borghammer
doi : 10.1093/brain/awad391
Brain, Volume 147, Issue 1, January 2024, Pages 255–266
Dementia with Lewy bodies is characterized by a high burden of autonomic dysfunction and Lewy pathology in peripheral organs and components of the sympathetic and parasympathetic nervous system.
Multimodal assessment of mitochondrial function in Parkinson's disease
Thomas Payne,1 Toby Burgess,1 Stephen Bradley,1 Sarah Roscoe,1 Matilde Sassani,1,2 Mark J. Dunning,3 Dena Hernandez,4 Sonja Scholz,5,6 Alisdair McNeill,1 Rosie Taylor,7 Li Su,1,8 Iain Wilkinson,9,†Thomas Jenkins,1,10 Heather Mortiboys1 and Oliver Bandmann
doi : 10.1093/brain/awad364
Brain, Volume 147, Issue 1, January 2024, Pages 267–280
The heterogenous aetiology of Parkinson's disease is increasingly recognized; both mitochondrial and lysosomal dysfunction have been implicated. Powerful, clinically applicable tools are required to enable mechanistic stratification for future precision medicine approaches.
Clinical and genetic characterisation of a large Indian congenital myasthenic syndrome cohort
Kiran Polavarapu,1,2,†Balaraju Sunitha,3,4,5,†Ana T?pf,3 Veeramani Preethish-Kumar,1,6 Rachel Thompson,2 Seena Vengalil,1 Saraswati Nashi,1 Mainak Bardhan,1 Sai Bhargava Sanka,1 Akshata Huddar,1,7 Gopikrishnan Unnikrishnan,1,8 Gautham Arunachal,9 Manu Santhappan Girija,1 Anna Porter,3 Yoshiteru Azuma,3 Paulo José Lorenzoni,10 Dipti Baskar,1 Ram Murthy Anjanappa,1 Madassu Keertipriya,1 Hansashree Padmanabh,1 Ganaraja Valakunja Harikrishna,1 Steve Laurie,11 Leslie Matalonga,11 Rita Horvath,4 Atchayaram Nalini1,‡ and Hanns Lochmüller2,
doi : 10.1093/brain/awad315
Brain, Volume 147, Issue 1, January 2024, Pages 281–296
Congenital myasthenic syndromes (CMS) are a rare group of inherited disorders caused by gene defects associated with the neuromuscular junction and potentially treatable with commonly available medications such as acetylcholinesterase inhibitors and β2 adrenergic receptor agonists. In this study, we identified and genetically characterized the largest cohort of CMS patients from India to date.
The parietal architecture binding cognition to sensorimotor integration: a multimodal causal study
Luca Fornia,1,†Antonella Leonetti,2,†Guglielmo Puglisi,1 Marco Rossi,1 Luca Vigan?,2 Bianca Della Santa,1 Luciano Simone,3 Lorenzo Bello2 and Gabriella Cerri
doi : 10.1093/brain/awad316
Brain, Volume 147, Issue 1, January 2024, Pages 297–310
Despite human’s praxis abilities are unique among primates, comparative observations suggest that these cognitive motor skills could have emerged from exploitation and adaptation of phylogenetically older building blocks, namely the parieto-frontal networks subserving prehension and manipulation.
TRAPPC6B biallelic variants cause a neurodevelopmental disorder with TRAPP II and trafficking disruptions
Hashem Almousa,1,†Sara A. Lewis,2,3,†Somayeh Bakhtiari,2,3 Sandra Hinz Nordlie,2,3 Alex Pagnozzi,4 Helen Magee,2,3 Stephanie Efthymiou,5 Jennifer A. Heim,2 Patricia Cornejo,6,7,8 Maha S. Zaki,9,10 Najwa Anwar,11 Shazia Maqbool,11 Fatima Rahman,11 Derek E. Neilson,12 Anusha Vemuri,13 Sheng Chih Jin,14 Xiao-Ru Yang,15 Abolfazl Heidari,16 Koen van Gassen,17 Aurélien Trimouille,18 Christel Thauvin-Robinet,19,20,21 James Liu,2,3 Ange-Line Bruel,20,21 Hoda Tomoum,22 Mennatallah O. Shata,22 Mais O. Hashem,23 Mehran Beiraghi Toosi,24,25 Ehsan Ghayoor Karimiani,26 G?zde Yes? il,27 Lokesh Lingappa,28 Debangana Baruah,28 Farnoosh Ebrahimzadeh,29 Julien Van-Gils,17 Laurence Faivre,19 Mina Zamani,30,31 Hamid Galehdari,30 Saeid Sadeghian,32 Gholamreza Shariati,31,33 Rahema Mohammad,5 Jasper van der Smagt,17 Alya Qari,34 John B. Vincent,35 A. Micheil Innes,15 Ali Dursun,36 R. K?ksal ?zgül,36 Halil Tuna Akar,36 Kaya Bilguvar,37,38 Cyril Mignot,39,40 Boris Keren,39 Claudia Raveli,41 Lydie Burglen,42 Alexandra Afenjar,42 Laura Donker Kaat,43 Marjon van Slegtenhorst,43 Fowzan Alkuraya,23 Henry Houlden,5 Sergio Padilla-Lopez,2,3 Reza Maroofian,5,‡ Michael Sacher1,44,‡ and Michael C. Kruer
doi : 10.1093/brain/awad301
Brain, Volume 147, Issue 1, January 2024, Pages 311–324
Peripherin is a biomarker of axonal damage in Guillain-Barré syndrome: a pathophysiological annotation
José Berciano
doi : 10.1093/brain/awad277
Brain, Volume 147, Issue 1, January 2024, Pages e1–e2
Reply: Peripherin is a biomarker of axonal damage in Guillain-Barré syndrome: a pathophysiological annotation
Stephen Keddie,1,2,3 Duncan Smyth,2,3 Ryan Y. S. Keh,2,3 Luuk Wieske,4 Milou Michael,4 Filip Eftimov,4 Roberto Bellanti,5 Simon Rinaldi,5 Axel Petzold4,6 and Michael P. Lunn
doi : 10.1093/brain/awad276
Brain, Volume 147, Issue 1, January 2024, Pages e3–e4
The multifaceted role of neurofilament light chain protein: emerging opportunities in primary psychiatric conditions
Francesco Bavato,1 Erich Seifritz2,3 and Boris B. Quednow
doi : 10.1093/brain/awad281
Does co-localization analysis reinforce the results of Mendelian randomization?
Qiuyuan Yin and Lei Zhu
doi : 10.1093/brain/awad295
Brain, Volume 147, Issue 1, January 2024, Pages e7–e8
Correction to: Where have prions been all our lives?
doi : 10.1093/brain/awad334
Brain, Volume 147, Issue 1, January 2024, Page e9
Correction to: A journey towards the pot of gold
doi : 10.1093/brain/awad344
Brain, Volume 147, Issue 1, January 2024, Page e10
