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Brain 2023 essay competition
Masud Husain
doi : 10.1093/brain/awad160
Brain, Volume 146, Issue 7, July 2023, Page 2657
A journey towards the pot of gold
Vale�rie Godefroy, Arabella Bouzigues
doi : 10.1093/brain/awad156
Brain, Volume 146, Issue 7, July 2023, Pages 2658–2660
Functional network reorganization precedes apathy in Parkinson’s disease: a neural marker of risk?
Philip E Mosley, Gail A Robinson
doi : 10.1093/brain/awad180
Brain, Volume 146, Issue 7, July 2023, Pages 2661–2662
Thalamic stereo-EEG in epilepsy surgery: where do we stand?
John M Bernabei, Brian Litt, Iahn Cajigas
doi : 10.1093/brain/awad178
Brain, Volume 146, Issue 7, July 2023, Pages 2663–2665
Precision diagnosis and staging of TDP-43 proteinopathies: harnessing the power of artificial intelligence
Richard A Hickman, Sonja W Scholz
doi : 10.1093/brain/awad175
Brain, Volume 146, Issue 7, July 2023, Pages 2666–2668
Multistage neurosurgical mapping of low-grade glioma relapses reveals cortical remodelling
Luca Viganò, Lorenzo Bello
doi : 10.1093/brain/awad190
Brain, Volume 146, Issue 7, July 2023, Pages 2669–2671
Cell therapies for spinal cord injury: a review of the clinical trials and cell-type therapeutic potential
Beatriz F Ribeiro, Bruna C da Cruz, Bárbara M de Sousa, PatrÃcia D Correia, Nuno David, Camila Rocha, Ramiro D Almeida, Maria Ribeiro da Cunha, António A Marques Baptista, Sandra I Vieira
doi : 10.1093/brain/awad047
Brain, Volume 146, Issue 7, July 2023, Pages 2672–2693
Spinal cord injury (SCI) is an as yet untreatable neuropathology that causes severe dysfunction and disability. Cell-based therapies hold neuroregenerative and neuroprotective potential, but, although being studied in SCI patients for more than two decades, long-term efficacy and safety remain unproven, and which cell types result in higher neurological and functional recovery remains under debate.
Epileptogenesis in tuberous sclerosis complex-related developmental and epileptic encephalopathy
Eleonora Aronica, Nicola Specchio, Mark J Luinenburg, Paolo Curatolo
doi : 10.1093/brain/awad048
Brain, Volume 146, Issue 7, July 2023, Pages 2694–2710
Epileptogenesis in infants with tuberous sclerosis complex (TSC) is a gradual and dynamic process, leading to early onset and difficult-to-treat seizures. Several cellular, molecular and pathophysiologic mechanisms, including mammalian target of rapamycin (mTOR) dysregulation, GABAergic dysfunction and abnormal connectivity, may play a role in this epileptogenic process and may also contribute to the associated developmental encephalopathy.
Neurofilament light chain in drug development for amyotrophic lateral sclerosis: a critical appraisal
Michael Benatar, Joanne Wuu, Martin R Turner
doi : 10.1093/brain/awac394
Brain, Volume 146, Issue 7, July 2023, Pages 2711–2716
Interest in amyotrophic lateral sclerosis (ALS) biomarkers has grown exponentially over the course of the last 25 years, with great hope that they might serve as tools to facilitate the development of meaningful therapies for this otherwise inexorably progressive and invariably fatal disease.
Towards a multi-arm multi-stage platform trial of disease modifying approaches in Parkinson’s disease
Tom Foltynie, Sonia Gandhi, Cristina Gonzalez-Robles, Marie-Louise Zeissler, Georgia Mills, Roger Barker, James Carpenter, Anette Schrag, Anthony Schapira, Oliver Bandmann, Stephen Mullin, Joy Duffen, Kevin McFarthing, Jeremy Chataway, Mahesh Parmar, Camille Carroll, the EJS ACT-PD Consortium
doi : 10.1093/brain/awad063
Brain, Volume 146, Issue 7, July 2023, Pages 2717–2722
An increase in the efficiency of clinical trial conduct has been successfully demonstrated in the oncology field, by the use of multi-arm, multi-stage trials allowing the evaluation of multiple therapeutic candidates simultaneously, and seamless recruitment to phase 3 for those candidates passing an interim signal of efficacy.
Unexpected frequency of the pathogenic AR CAG repeat expansion in the general population
Matteo Zanovello, Kristina Ibáñez, Anna-Leigh Brown, Prasanth Sivakumar, Alessandro Bombaci, Liana Santos, Joke J F A van Vugt, Giuseppe Narzisi, Ramita Karra, Sonja W Scholz, Jinhui Ding, J Raphael Gibbs, Adriano Chiò, Clifton Dalgard, Ben Weisburd, The American Genome Center (TAGC) consortium, Genomics England Research Consortium, Project MinE ALS Sequencing Consortium, The NYGC ALS Consortium , Michael G Hanna, Linda Greensmith, Hemali Phatnani, Jan H Veldink, Bryan J Traynor, James Polke, Henry Houlden, Pietro Fratta, Arianna Tucci
doi : 10.1093/brain/awad050
Brain, Volume 146, Issue 7, July 2023, Pages 2723–2729
CAG repeat expansions in exon 1 of the AR gene on the X chromosome cause spinal and bulbar muscular atrophy, a male-specific progressive neuromuscular disorder associated with a variety of extra-neurological symptoms. The disease has a reported male prevalence of approximately 1:30 000 or less, but the AR repeat expansion frequency is unknown.
Variants in ATP5F1B are associated with dominantly inherited dystonia
Alessia Nasca, Niccolò E Mencacci, Federica Invernizzi, Michael Zech, Ignacio J Keller Sarmiento, Andrea Legati, Chiara Frascarelli, Bernabe I Bustos, Luigi M Romito, Dimitri Krainc, Juliane Winkelmann, Miryam Carecchio, Nardo Nardocci, Giovanna Zorzi, Holger Prokisch, Steven J Lubbe, Barbara Garavaglia, Daniele Ghezzi
doi : 10.1093/brain/awad068
Brain, Volume 146, Issue 7, July 2023, Pages 2730–2738
ATP5F1B is a subunit of the mitochondrial ATP synthase or complex V of the mitochondrial respiratory chain. Pathogenic variants in nuclear genes encoding assembly factors or structural subunits are associated with complex V deficiency, typically characterized by autosomal recessive inheritance and multisystem phenotypes. Movement disorders have been described in a subset of cases carrying autosomal dominant variants in structural subunits genes ATP5F1A and ATP5MC3.
Altered nucleus accumbens functional connectivity precedes apathy in Parkinson’s disease
Lee-Anne Morris, Samuel J Harrison, Tracy R Melzer, John C Dalrymple-Alford, Tim J Anderson, Michael R MacAskill, Campbell J Le Heron
doi : 10.1093/brain/awad113
Brain, Volume 146, Issue 7, July 2023, Pages 2739–2752
Work in animal and human neuroscience has identified neural regions forming a network involved in the production of motivated, goal-directed behaviour. In particular, the nucleus accumbens and anterior cingulate cortex are recognized as key network nodes underlying decisions of whether to exert effort for reward, to drive behaviour.
Mitochondrial DNA heteroplasmy distinguishes disease manifestation in PINK1/PRKN-linked Parkinson’s disease
Joanne Trinh, Andrew A Hicks, Inke R König, Sylvie Delcambre, Theresa Lüth, Susen Schaake, Kobi Wasner, Jenny Ghelfi, Max Borsche, Carles Vilariño-Güell, Faycel Hentati, Elisabeth L Germer, Peter Bauer, Masashi Takanashi, Vladimir Kostić, Anthony E Lang, Norbert Brüggemann, Peter P Pramstaller, Irene Pichler, Alex Rajput, Nobutaka Hattori, Matthew J Farrer, Katja Lohmann, Hansi Weissensteiner, Patrick May, Christine Klein, Anne Grünewald
doi : 10.1093/brain/awac464
Brain, Volume 146, Issue 7, July 2023, Pages 2753–2765
Biallelic mutations in PINK1/PRKN cause recessive Parkinson’s disease. Given the established role of PINK1/Parkin in regulating mitochondrial dynamics, we explored mitochondrial DNA integrity and inflammation as disease modifiers in carriers of mutations in these genes. Mitochondrial DNA integrity was investigated in a large collection of biallelic (n = 84) and monoallelic (n = 170) carriers of PINK1/PRKN mutations, idiopathic Parkinson’s disease patients (n = 67) and controls (n = 90).
Subthalamic and nigral neurons are differentially modulated during parkinsonian gait
Alessandro Gulberti, Jonas R Wagner, Martin A Horn, Jacob H Reuss, Miriam Heise, Johannes A Koeppen, Hans O Pinnschmidt, Manfred Westphal, Andreas K Engel, Christian Gerloff, Andrew Sharott, Wolfgang Hamel, Christian K E Moll, Monika Pötter-Nerger
doi : 10.1093/brain/awad006
Brain, Volume 146, Issue 7, July 2023, Pages 2766–2779
The parkinsonian gait disorder and freezing of gait are therapeutically demanding symptoms with considerable impact on quality of life. The aim of this study was to assess the role of subthalamic and nigral neurons in the parkinsonian gait control using intraoperative microelectrode recordings of basal ganglia neurons during a supine stepping task.
Subthalamic stimulation modulates motor network in Parkinson’s disease: recover, relieve and remodel
Chunguang Chu, Shang Liu, Naying He, Zhitong Zeng, Jiang Wang, Zhen Zhang, Kristina Zeljic, Odin van der Stelt, Bomin Sun, Fuhua Yan, Chen Liu, Dianyou Li, Chencheng Zhang
doi : 10.1093/brain/awad004
Brain, Volume 146, Issue 7, July 2023, Pages 2780–2791
Aberrant dynamic switches between internal brain states are believed to underlie motor dysfunction in Parkinson’s disease. Deep brain stimulation of the subthalamic nucleus is a well-established treatment for the motor symptoms of Parkinson’s disease, yet it remains poorly understood how subthalamic stimulation modulates the whole-brain intrinsic motor network state dynamics.
Multisite thalamic recordings to characterize seizure propagation in the human brain
Teresa Q Wu, Neda Kaboodvand, Ryan J McGinn, Mike Veit, Zachary Davey, Anjali Datta, Kevin D Graber, Kimford J Meador, Robert Fisher, Vivek Buch, Josef Parvizi
doi : 10.1093/brain/awad121
Brain, Volume 146, Issue 7, July 2023, Pages 2792–2802
Neuromodulation of the anterior nuclei of the thalamus (ANT) has shown to be efficacious in a subset of patients with refractory focal epilepsy. One important uncertainty is to what extent thalamic subregions other than the ANT could be recruited more prominently in the propagation of focal onset seizures.
Sleep and seizure risk in epilepsy: bed and wake times are more important than sleep duration
Rachel E Stirling, Cindy M Hidajat, David B Grayden, Wendyl J D’Souza, Jodie Naim-Feil, Katrina L Dell, Logan D Schneider, Ewan Nurse, Dean Freestone, Mark J Cook, Philippa J Karoly
doi : 10.1093/brain/awac476
Brain, Volume 146, Issue 7, July 2023, Pages 2803–2813
Sleep duration, sleep deprivation and the sleep–wake cycle are thought to play an important role in the generation of epileptic activity and may also influence seizure risk. Hence, people diagnosed with epilepsy are commonly asked to maintain consistent sleep routines.
Optogenetic stimulation reveals a latent tipping point in cortical networks during ictogenesis
Robert T Graham, R Ryley Parrish, Laura Alberio, Emily L Johnson, Laura Owens, Andrew J Trevelyan
doi : 10.1093/brain/awac487
Brain, Volume 146, Issue 7, July 2023, Pages 2814–2827
Brain-state transitions are readily apparent from changes in brain rhythms,1 but are difficult to predict, suggestive that the underlying cause is latent to passive recording methods. Among the most important transitions, clinically, are the starts of seizures.
The Interictal Suppression Hypothesis in focal epilepsy: network-level supporting evidence
Graham W Johnson, Derek J Doss, Victoria L Morgan, Danika L Paulo, Leon Y Cai, Jared S Shless, Aarushi S Negi, Abhijeet Gummadavelli, Hakmook Kang, Shilpa B Reddy, Robert P Naftel, Sarah K Bick, Shawniqua Williams Roberson, Benoit M Dawant, Mark T Wallace, Dario J Englot
doi : 10.1093/brain/awad016
Brain, Volume 146, Issue 7, July 2023, Pages 2828–2845
Why are people with focal epilepsy not continuously having seizures? Previous neuronal signalling work has implicated gamma-aminobutyric acid balance as integral to seizure generation and termination, but is a high-level distributed brain network involved in suppressing seizures? Recent intracranial electrographic evidence has suggested that seizure-onset zones have increased inward connectivity that could be associated with interictal suppression of seizure activity.
Cortical interneuron development is affected in 4H leukodystrophy
Stephanie Dooves, Liza M L Kok, Dwayne B Holmes, Nicole Breeuwsma, Marjolein Breur, Marianna Bugiani, Nicole I Wolf, Vivi M Heine
doi : 10.1093/brain/awad017
Brain, Volume 146, Issue 7, July 2023, Pages 2846–2860
4H leukodystrophy is a rare genetic disorder classically characterized by hypomyelination, hypodontia and hypogonadotropic hypogonadism. With the discovery that 4H is caused by mutations that affect RNA polymerase III, mainly involved in the transcription of small non-coding RNAs, patients with atypical presentations with mainly a neuronal phenotype were also identified.
Genome-wide association analysis identifies a susceptibility locus for sporadic vestibular schwannoma at 9p21
Katherine V Sadler, John Bowes, Charlie F Rowlands, Cristina Perez-Becerril, C Mwee van der Meer, Andrew T King, Scott A Rutherford, Omar N Pathmanaban, Charlotte Hammerbeck-Ward, Simon K W Lloyd, Simon R Freeman, Ricky Williams, Cathal John Hannan, Daniel Lewis, Steve Eyre, D Gareth Evans, Miriam J Smith
doi : 10.1093/brain/awac478
Brain, Volume 146, Issue 7, July 2023, Pages 2861–2868
Vestibular schwannomas are benign nerve sheath tumours that arise on the vestibulocochlear nerves. Vestibular schwannomas are known to occur in the context of tumour predisposition syndromes NF2-related and LZTR1-related schwannomatosis. However, the majority of vestibular schwannomas present sporadically without identification of germline pathogenic variants.
Functional genomics provide key insights to improve the diagnostic yield of hereditary ataxia
Zhongbo Chen, Arianna Tucci, Valentina Cipriani, Emil K Gustavsson, Kristina Ibañez, Regina H Reynolds, David Zhang, Letizia Vestito, Alejandro Cisterna GarcÃa, Siddharth Sethi, Jonathan W Brenton, Sonia GarcÃa-Ruiz, Aine Fairbrother-Browne, Ana-Luisa Gil-Martinez, Genomics England Research Consortium , Nick Wood, John A Hardy, Damian Smedley, Henry Houlden, Juan BotÃa, Mina Ryten
doi : 10.1093/brain/awad009
Brain, Volume 146, Issue 7, July 2023, Pages 2869–2884
Improvements in functional genomic annotation have led to a critical mass of neurogenetic discoveries. This is exemplified in hereditary ataxia, a heterogeneous group of disorders characterised by incoordination from cerebellar dysfunction.
Downregulation of PMP22 ameliorates myelin defects in iPSC-derived human organoid cultures of CMT1A
Jonas Van Lent, Leen Vendredy, Elias Adriaenssens, Tatiana Da Silva Authier, Bob Asselbergh, Marcus Kaji, Sarah Weckhuysen, Ludo Van Den Bosch, Jonathan Baets, Vincent Timmerman
doi : 10.1093/brain/awac475
Brain, Volume 146, Issue 7, July 2023, Pages 2885–2896
Charcot–Marie–Tooth disease is the most common inherited disorder of the PNS. CMT1A accounts for 40–50% of all cases and is caused by a duplication of the PMP22 gene on chromosome 17, leading to dysmyelination in the PNS. Patient-derived models to study such myelination defects are lacking as the in vitro generation of human myelinating Schwann cells has proved to be particularly challenging.
Impaired ribosome-associated quality control of C9orf72 arginine-rich dipeptide-repeat proteins
Ashley P Viera Ortiz, Gregory Cajka, Olamide A Olatunji, Bailey Mikytuck, Ophir Shalem, Edward B Lee
doi : 10.1093/brain/awac479
Brain, Volume 146, Issue 7, July 2023, Pages 2897–2912
Protein quality control pathways have evolved to ensure the fidelity of protein synthesis and efficiently clear potentially toxic protein species. Defects in ribosome-associated quality control and its associated factors have been implicated in the accumulation of aberrant proteins and neurodegeneration.
Three-tiered EGFr domain risk stratification for individualized NOTCH3-small vessel disease prediction
Remco J Hack, Gido Gravesteijn, Minne N Cerfontaine, Mark A Santcroos, Laura Gatti, Anna Kopczak, Anna Bersano, Marco Duering, Julie W Rutten, Saskia A J Lesnik Oberstein
doi : 10.1093/brain/awac486
Brain, Volume 146, Issue 7, July 2023, Pages 2913–2927
Cysteine-altering missense variants (NOTCH3cys) in one of the 34 epidermal growth-factor-like repeat (EGFr) domains of the NOTCH3 protein are the cause of NOTCH3-associated small vessel disease (NOTCH3-SVD). NOTCH3-SVD is highly variable, ranging from cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) at the severe end of the spectrum to non-penetrance.
Brain network decoupling with increased serum neurofilament and reduced cognitive function in Alzheimer’s disease
Muriah D Wheelock, Jeremy F Strain, Patricia Mansfield, Jiaxin Cindy Tu, Aaron Tanenbaum, Oliver Preische, Jasmeer P Chhatwal, David M Cash, Carlos Cruchaga, Anne M Fagan, Nick C Fox, Neill R Graff-Radford, Jason Hassenstab, Clifford R Jack, Jr, Celeste M Karch, Johannes Levin, Eric M McDade, Richard J Perrin, Peter R Schofield, Chengjie Xiong, John C Morris, Randal J Bateman, Mathias Jucker, Tammie L S Benzinger, Beau M Ances, Adam T Eggebrecht, Brian A Gordon, the Dominantly Inherited Alzheimer Network
doi : 10.1093/brain/awac498
Brain, Volume 146, Issue 7, July 2023, Pages 2928–2943
Neurofilament light chain, a putative measure of neuronal damage, is measurable in blood and CSF and is predictive of cognitive function in individuals with Alzheimer’s disease.
Proteomic clusters underlie heterogeneity in preclinical Alzheimer’s disease progression
Julie K Wisch, Omar H Butt, Brian A Gordon, Suzanne E Schindler, Anne M Fagan, Rachel L Henson, Chengran Yang, Anna H Boerwinkle, Tammie L S Benzinger, David M Holtzman, John C Morris, Carlos Cruchaga, Beau M Ances
doi : 10.1093/brain/awac484
Brain, Volume 146, Issue 7, July 2023, Pages 2944–2956
Heterogeneity in progression to Alzheimer's disease (AD) poses challenges for both clinical prognosis and clinical trial implementation. Multiple AD-related subtypes have previously been identified, suggesting differences in receptivity to drug interventions.
Visualizing reactive astrocyte-neuron interaction in Alzheimer’s disease using 11C-acetate and 18F-FDG
Min-Ho Nam, Hae Young Ko, Dongwoo Kim, Sangwon Lee, Yongmin Mason Park, Seung Jae Hyeon, Woojin Won, Jee-In Chung, Seon Yoo Kim, Han Hee Jo, Kyeong Taek Oh, Young-Eun Han, Gwan-Ho Lee, Yeon Ha Ju, Hyowon Lee, Hyunjin Kim, Jaejun Heo, Mridula Bhalla, Ki Jung Kim, Jea Kwon, Thor D Stein, Mingyu Kong, Hyunbeom Lee, Seung Eun Lee, Soo-Jin Oh, Joong-Hyun Chun, Mi-Ae Park, Ki Duk Park, Hoon Ryu, Mijin Yun, C Justin Lee
doi : 10.1093/brain/awad037
Brain, Volume 146, Issue 7, July 2023, Pages 2957–2974
Reactive astrogliosis is a hallmark of Alzheimer’s disease (AD). However, a clinically validated neuroimaging probe to visualize the reactive astrogliosis is yet to be discovered. Here, we show that PET imaging with 11C-acetate and 18F-fluorodeoxyglucose (18F-FDG) functionally visualizes the reactive astrocyte-mediated neuronal hypometabolism in the brains with neuroinflammation and AD.
Data-driven neuropathological staging and subtyping of TDP-43 proteinopathies
Alexandra L Young, Jacob W Vogel, John L Robinson, Corey T McMillan, Rik Ossenkoppele, David A Wolk, David J Irwin, Lauren Elman, Murray Grossman, Virginia M Y Lee, Edward B Lee, Oskar Hansson
doi : 10.1093/brain/awad145
Brain, Volume 146, Issue 7, July 2023, Pages 2975–2988
TAR DNA-binding protein-43 (TDP-43) accumulation is the primary pathology underlying several neurodegenerative diseases. Charting the progression and heterogeneity of TDP-43 accumulation is necessary to better characterize TDP-43 proteinopathies, but current TDP-43 staging systems are heuristic and assume each syndrome is homogeneous.
Neuronal NLRP3 inflammasome mediates spreading depolarization-evoked trigeminovascular activation
Pin-Yu Chen, Jiin-Cherng Yen, Tzu-Ting Liu, Szu-Ting Chen, Shuu-Jiun Wang, Shih-Pin Chen
doi : 10.1093/brain/awad045
Brain, Volume 146, Issue 7, July 2023, Pages 2989–3002
Spreading depolarization (SD), the underlying mechanism of migraine aura, may trigger the opening of the pannexin 1 (PANX1) pore to sustain the cortical neuroinflammatory cascades involved in the genesis of headache. Yet, the mechanism underlying SD-evoked neuroinflammation and trigeminovascular activation remains incompletely understood.
BCKDK deficiency: a treatable neurodevelopmental disease amenable to newborn screening
Trine Tangeraas, Juliana R Constante, Paul Hoff Backe, Alfonso Oyarzábal, Julia Neugebauer, Natalie Weinhold, Francois Boemer, François G Debray, Burcu Ozturk-Hism, Gumus Evren, Eminoglu F Tuba, Oncul Ummuhan, Emma Footitt, James Davison, Caroline Martinez, Clarissa Bueno, Irene Machado, Pilar RodrÃguez-Pombo, Nouriya Al-Sannaa, Mariela De Los Santos, Jordi Muchart López, Hatice Ozturkmen-Akay, Meryem Karaca, Mustafa Tekin, Sonia Pajares, Aida Ormazabal, Stephanie D Stoway, Rafael Artuch, Marjorie Dixon, Lars Mørkrid, Angeles GarcÃa-Cazorla
doi : 10.1093/brain/awad010
Brain, Volume 146, Issue 7, July 2023, Pages 3003–3013
There are few causes of treatable neurodevelopmental diseases described to date. Branched-chain ketoacid dehydrogenase kinase (BCKDK) deficiency causes branched-chain amino acid (BCAA) depletion and is linked to a neurodevelopmental disorder characterized by autism, intellectual disability and microcephaly.
Reduced endothelial caveolin-1 underlies deficits in brain insulin signalling in type 2 diabetes
Aashutosh U Shetti, Abhirami Ramakrishnan, Liudmila Romanova, Wenping Li, Khanh Vo, Ipsita Volety, Ishara Ratnayake, Terilyn Stephen, Richard D Minshall, Stephanie M Cologna, Orly Lazarov
doi : 10.1093/brain/awad028
Brain, Volume 146, Issue 7, July 2023, Pages 3014–3028
Patients with type 2 diabetes exhibit severe impairments in insulin signalling in the brain and are five times more likely to develop Alzheimer’s disease. However, what leads to these impairments is not fully understood.
Tamoxifen improves muscle structure and function of Bin1- and Dnm2-related centronuclear myopathies
Charlotte Gineste, Alix Simon, Marie Braun, David Reiss, Jocelyn Laporte
doi : 10.1093/brain/awac489
Brain, Volume 146, Issue 7, July 2023, Pages 3029–3048
Congenital myopathies define a genetically heterogeneous group of disorders associated with severe muscle weakness, for which no therapies are currently available.
Integrative miRNA–mRNA profiling of human epidermis: unique signature of SCN9A painful neuropathy
Mirna Andelic, Erika Salvi, Stefania Marcuzzo, Margherita Marchi, Raffaella Lombardi, Daniele Cartelli, Daniele Cazzato, Elkadia Mehmeti, Andrea Gelemanovic, Matilde Paolini, Carlotta Pardo, Ilaria D’Amato, Janneke G J Hoeijmakers, Sulayman Dib-Hajj, Stephen G Waxman, Catharina G Faber, Giuseppe Lauria
doi : 10.1093/brain/awad025
Brain, Volume 146, Issue 7, July 2023, Pages 3049–3062
Personalized management of neuropathic pain is an unmet clinical need due to heterogeneity of the underlying aetiologies, incompletely understood pathophysiological mechanisms and limited efficacy of existing treatments. Recent studies on microRNA in pain preclinical models have begun to yield insights into pain-related mechanisms, identifying nociception-related species differences and pinpointing potential drug candidates.
The biomechanical signature of loss of consciousness: computational modelling of elite athlete head injuries
Karl A Zimmerman, Janie Cournoyer, Helen Lai, Samuel B Snider, David Fischer, Simon Kemp, Clara Karton, Thomas B Hoshizaki, Mazdak Ghajari, David J Sharp
doi : 10.1093/brain/awac485
Brain, Volume 146, Issue 7, July 2023, Pages 3063–3078
Sports related head injuries can cause transient neurological events including loss of consciousness and dystonic posturing. However, it is unknown why head impacts that appear similar produce distinct neurological effects. The biomechanical effect of impacts can be estimated using computational models of strain within the brain.
Decreased water exchange rate across blood–brain barrier in hereditary cerebral small vessel disease
Yingying Li, Yunqing Ying, Tingyan Yao, Xuejia Jia, Huilou Liang, Weijun Tang, Xiuqin Jia, Haiqing Song, Xingfeng Shao, Danny J J Wang, Chaodong Wang, Xin Cheng, Qi Yang
doi : 10.1093/brain/awac500
Brain, Volume 146, Issue 7, July 2023, Pages 3079–3087
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and heterozygous HTRA1 mutation-related cerebral small vessel disease (CSVD) are the two types of dominant hereditary CSVD.
Intraoperative functional remapping unveils evolving patterns of cortical plasticity
Sam Ng, Pablo A Valdes, Sylvie Moritz-Gasser, Anne-Laure Lemaitre, Hugues Duffau, Guillaume Herbet
doi : 10.1093/brain/awad116
Brain, Volume 146, Issue 7, July 2023, Pages 3088–3100
The efficiency with which the brain reorganizes following injury not only depends on the extent and the severity of the lesion, but also on its temporal features. It is established that diffuse low-grade gliomas (DLGG), brain tumours with a slow-growth rate, induce a compensatory modulation of the anatomo-functional architecture, making this kind of tumours an ideal lesion model to study the dynamics of neuroplasticity
Are recovery of fluency and recovery of phonology antagonistic?
Grant M Walker, Gregory Hickok
doi : 10.1093/brain/awad026
Brain, Volume 146, Issue 7, July 2023, Pages e48–e51
Reply: Are recovery of fluency and recovery of phonology antagonistic?
Matthew A Lambon Ralph, James D Stefaniak, Ajay D Halai, Fatemeh Geranmayeh
doi : 10.1093/brain/awad027
Brain, Volume 146, Issue 7, July 2023, Pages e52–e54
Correction to: Local brain environment changes associated with epileptogenesis
doi : 10.1093/brain/awad091
Brain, Volume 146, Issue 7, July 2023, Page e55
Correction to: Blood–brain barrier opening of the default mode network in Alzheimer's disease with magnetic resonance-guided focused ultrasound
doi : 10.1093/brain/awad082
Brain, Volume 146, Issue 7, July 2023, Page e56
