Brain disorders (Amsterdam, Netherlands)最新文献

{"title":"Progestogens reduce tau phosphorylation via ERK 1/2 in a tau overexpression cell model","authors":"Taysa Bervian Bassani ,&nbsp;Rafaela Brito Oliveira ,&nbsp;Giulia Ventura Portella ,&nbsp;Michelle Sayuri Nishino ,&nbsp;Angelica Jardim Costa ,&nbsp;Rodrigo Portes Ureshino","doi":"10.1016/j.dscb.2025.100236","DOIUrl":"10.1016/j.dscb.2025.100236","url":null,"abstract":"<div><div>Several studies have suggested the neuroprotective effects of progestogens in neurodegenerative diseases. Among the most common neurodegenerative diseases are tauopathies. Tauopathies are characterized by the formation of neurofibrillary tangles within neurons, resulting from the aggregation of hyperphosphorylated tau protein, cytoskeleton impairment and, ultimately, cell death. However, the effect of progestogens on those processes needs to be further explored. Thus, this work aims to investigate the effect of progesterone and allopregnanolone on tau hyperphosphorylation in a cellular model of tau overexpression. We used a neuronal cellular model overexpressing the human tau protein (isoform 0N4R) fused with EGFP. The data showed that progesterone effectively decreased the accumulation of overexpressed EGFP-tau. In addition, both compounds reduced tau phosphorylation in different sites, as progesterone reduced at the AT8 and allopregnanolone at AT180 site. The attenuation of its phosphorylation appears to be related to inhibiting the kinase activity of enzymes involved in tau phosphorylation, such as ERK 1/2. Thus, the progestogens tested showed promising neuroprotective potential for the treatment of tauopathies, especially by attenuating hyperphosphorylated forms that give rise to paired helical filaments and neurofibrillary tangles, probably due to modulation of intracellular pathways.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"19 ","pages":"Article 100236"},"PeriodicalIF":0.0,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma macrophage migration inhibitory factor and matrix metalloproteinase-9 levels, and their related factors in Alzheimer’s disease","authors":"Zhengchuang Fu ,&nbsp;Min Wang ,&nbsp;Ming Yu,&nbsp;Quanfeng Zhu,&nbsp;Yali Zheng","doi":"10.1016/j.dscb.2025.100237","DOIUrl":"10.1016/j.dscb.2025.100237","url":null,"abstract":"<div><div>Previous studies have shown that the levels of macrophage migration inhibitory factor (MIF) and matrix metalloproteinase-9 (MMP-9) in its downstream signaling pathway are related to the occurrence and development of Alzheimer’s disease (AD); some studies have suggested that plasma levels of MIF and MMP-9 could be used as potential biomarkers for AD. This study aimed to explore the changes in MIF and MMP-9 levels in the plasma of patients with AD and whether they were correlated with other clinical indicators and cognitive function. Altogether, 43 patients with AD and 40 healthy controls (HCs) were enrolled in this study. Socio-demographic information of the subjects was collected, and their cognitive function was assessed using Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Further, the biochemical indicators and plasma MIF and MMP-9 levels were detected. Our study found that plasma MIF levels were not significantly altered in patients with AD compared to HCs, while MMP-9 levels were significantly increased, and prolactin levels had significant effects on MMP-9 levels. In addition, plasma levels of MIF and MMP-9 in patients with AD had no significant correlation with cognitive function. In summary, plasma levels of MIF and MMP-9 in AD patients may be influenced by multiple factors and could vary significantly across different disease stages. Further studies are needed to elucidate their roles and underlying mechanisms in AD.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100237"},"PeriodicalIF":0.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144089443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemihypomimia and lingual tremor in Parkinson’s disease: A case report","authors":"Anita Senthinathan,&nbsp;Sharon Tudorovsky","doi":"10.1016/j.dscb.2025.100234","DOIUrl":"10.1016/j.dscb.2025.100234","url":null,"abstract":"<div><div>Parkinson's disease is a progressive nervous system disorder that can cause many other non-motor and motor symptoms in addition to tremors and stiffness (Emamzadeh et al., 2018). Hemihypomimia and lingual abnormalities are rare occurrences in Parkinson’s disease (PD). The following report describes a unique case of this dual symptomology in a case of short disease duration and early onset PD. In addition, prior case reports have shown a predominantly right-sided effect (Panichelli &amp; Spitz, 2021; Ozekmekçi et al., 2007; Zingler et al., 2005). Hemihypomimia (HH) can persist for several years and is consistent with normal asymmetrical involvement of the limbs (Ozekmekçi et al., 2007). HH mostly appears in the lower portion of the right side of the face (Bologna et al., 2016). Lingual tremor and strength deficits are a rare phenomenon in PD, and the implications for speech and swallowing are important for QOL considerations.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"19 ","pages":"Article 100234"},"PeriodicalIF":0.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Navigating multiple sclerosis: From clinical categories to clinical management","authors":"Isra Omar ,&nbsp;Ahmed Alakhras ,&nbsp;Samahir Mutwali ,&nbsp;Moiz Bakhiet","doi":"10.1016/j.dscb.2025.100235","DOIUrl":"10.1016/j.dscb.2025.100235","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a chronic, immune-mediated neurological disorder that continues to challenge both researchers and clinicians. While advances in understanding its pathophysiology have led to improved disease-modifying therapies, these treatments primarily focus on immunosuppression and relapse prevention, leaving progressive forms of MS with limited options. Neurodegeneration, myelin loss, and long-term disability remain major hurdles, underscoring the urgent need for therapies that go beyond symptom management to actively repair damage and alter disease progression. With emerging breakthroughs in regenerative medicine, including stem cell-based therapies and novel immune-targeting treatments, we are entering a new era of MS research that prioritizes neuroprotection and repair. This review explores the latest insights into MS classification, pathogenesis, and treatment approaches, with a particular focus on cutting-edge therapies that hold the potential to shift MS care from disease suppression to long-term recovery. By bridging research and clinical application, this study aims to highlight the most promising avenues for future innovation and improved patient outcomes.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100235"},"PeriodicalIF":0.0,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational discovery of plant-derived flavonoids as potential amyloid-β fibril disaggregating agents for alzheimer’s disease","authors":"Uthirapathi Logeswari Rakesh ,&nbsp;Golla Anil Kumar ,&nbsp;Theivendren Panneerselvam ,&nbsp;Parasuraman Pavadai ,&nbsp;Suganthan Veerachamy ,&nbsp;Ponnusamy Palanisamy ,&nbsp;SunilKumar Bandral ,&nbsp;Selvaraj Kunjiappan","doi":"10.1016/j.dscb.2025.100233","DOIUrl":"10.1016/j.dscb.2025.100233","url":null,"abstract":"<div><div>The neurological hallmark of Alzheimer's disease (AD) is a pathogenic deposition of amyloid-β peptide in the brain. Amyloid-β aggregation is neurotoxic and ultimately results in dysfunction of the nervous system. The present study aims to find potential amyloid-β fibrils disaggregating molecules from plant sources through molecular modeling techniques, which seems to be a promising and attractive therapeutic approach. Here, 500 flavonoids from various plants were considered, initially undergoing ADME studies to screen molecules that could cross the blood-brain barrier. Later, potential Amyloid-β-disaggregating molecules were predicted by molecular docking and molecular dynamics studies. Five molecules, prenylmethoxy flavonol (-7.3 kcal × mol^-1), isopentenyl flavonol (-7.3 kcal × mol^-1), 7,3′-Dihydroxyflavone (-7.2 kcal × mol^-1), 7-Hydroxy-5-methyl-4′-methoxyflavone (-7.2 kcal × mol^-1), 8‑hydroxy-7-methoxyflavone (-7 kcal × mol^-1) exhibited top binding score against Alzheimer's Aβ (1–42) fibrils, and these are very close to the standard drug (Donepezil) (-7.90 kcal × mol^-1). Further, the MD simulation studies confirmed the stability of the five selected ligands-Amyloid-β oligomer protein complex. Based on these findings, the selected five compounds might be used as potential Amyloid-β fibril disaggregating agents, and <em>in vitro</em> and <em>in vivo</em> studies are necessary to confirm the promising therapeutic capability.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100233"},"PeriodicalIF":0.0,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential role of magnolol: A comprehensive review on its efficacy in managing neurological disorders","authors":"Nasrin Sultana ,&nbsp;Mohammed Abu Sayeed ,&nbsp;Marajul Islam ,&nbsp;S.M. Asadul Karim Azad ,&nbsp;Sumaiya Binte Tareq ,&nbsp;Miskhat-Ul- Jannat ,&nbsp;Farzana Yeasmin","doi":"10.1016/j.dscb.2025.100231","DOIUrl":"10.1016/j.dscb.2025.100231","url":null,"abstract":"<div><div>Magnolol (MG) is a lignan compound isolated from Magnolia officinalis, renowned for its significant neuroprotective properties include the reduction of amyloid-beta toxicity and the inhibition of apoptotic pathways in neuronal cells. MG has demonstrated beneficial effects in models of Alzheimer’s disease and Parkinson’s disease. Approximately 2–10 % MG was found from the bark of Magnolia species. MG has been a cornerstone of traditional Japanese and Chinese medicine, revered for its therapeutic benefits. This bioactive ingredient is a focal point in neuropharmacological research because it promotes neurite outgrowth, enhances neuronal survival, and mitigates neurological impairments. Such properties underscore its potential in addressing a myriad of neurological conditions, including neurodegenerative diseases, stroke, epilepsy, traumatic brain and spinal cord injuries, and neuropathies. MG is not only potent in alleviating neurological impairments but also exhibits robust protective effects against nervous system damage and toxicity. This comprehensive review elucidates the neuropharmacological potential of MG, exploring into its sources, chemical composition, pharmacokinetics, and toxicity, while addressing the challenges and prospects associated with its therapeutic applications. MG's multifaceted benefits underscore its promise as a pivotal agent in neuropharmacology.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100231"},"PeriodicalIF":0.0,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traumatic brain injury as a precursor to neurodegenerative diseases: Mechanisms linking TBI to Alzheimer’s disease","authors":"Kirti Bamel ,&nbsp;Anil Panwar ,&nbsp;Mukesh Kumar ,&nbsp;Sunil Kumar ,&nbsp;Varruchi Sharma ,&nbsp;Anil Sharma","doi":"10.1016/j.dscb.2025.100232","DOIUrl":"10.1016/j.dscb.2025.100232","url":null,"abstract":"<div><div>Bioinformatics has become an essential field of interest for examining intricate biological data and revealing the possible mechanisms that have significant contribution to various diseases. The field encompasses diverse applications, such as genomic, transcriptomic, proteomic, and network analysis, which hold significant promise for uncovering critical pathways and molecules implicated in the TBI-AD mechanism. Numerous studies have indicated that bioinformatics has yielded significant insights into inflammation, immune response, tau pathology, amyloid-β pathology, and changes in neuroplasticity following TBI, potentially contributing to the onset of AD. Building on this, systems biology approaches are essential for integrating multi-omics data, which aids in the discovery of biomarkers, drug targets, and treatment strategies. Recent advancements in high-throughput and high-content screens (HCS) for neurodegenerative diseases have primarily focused on inherited neurodegenerative disorders. Traumatic brain injury (TBI) is increasingly recognized as a major risk factor for the development of neurodegenerative diseases (NDDs), particularly Alzheimer’s disease (AD). The molecular and cellular responses triggered by TBI–such as oxidative stress, mechanical deformation, and excitotoxicity—disrupt critical homeostatic processes, including axonal transport, protein folding, and clearance. These disruptions contribute to hallmark AD pathologies, including amyloid-beta (Aβ) plaque deposition and tau hyperphosphorylation leading to neurofibrillary tangle formation. Furthermore, neuroinflammatory responses and the overproduction of reactive oxygen species (ROS) exacerbate neuronal injury and accelerate neurodegenerative progression. Advances in bioinformatics, particularly through high-throughput omics analyses, have illuminated differentially expressed genes (DEGs), dysregulated pathways, and key molecular players involved in these processes. These insights are guiding the development of targeted therapeutic strategies, including NMDAR modulators to alleviate excitotoxicity, beta-secretase inhibitors to limit Aβ aggregation, and anti-inflammatory agents aimed at suppressing COX2-mediated inflammation. By integrating findings from clinical data and preclinical models, bioinformatics continues to deepen our understanding of the complex interplay between TBI and AD. Ultimately, this integrative approach is essential for identifying early diagnostic markers, optimizing treatment strategies, and improving long-term outcomes for individuals affected by TBI-induced neurodegeneration.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100232"},"PeriodicalIF":0.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lymphocyte dynamics in patients with multiple sclerosis who were treated with dimethyl fumarate and subsequently switched to diroximel fumarate","authors":"Shauna M. Gales ,&nbsp;Ahmed Z. Obeidat ,&nbsp;Andreina Neall ,&nbsp;Kermit A. Lloyd ,&nbsp;Nicholas Belviso ,&nbsp;Seth Levin ,&nbsp;Ivan Bozin ,&nbsp;Jason P. Mendoza ,&nbsp;James B. Lewin ,&nbsp;Michael D. Kornberg","doi":"10.1016/j.dscb.2025.100229","DOIUrl":"10.1016/j.dscb.2025.100229","url":null,"abstract":"<div><h3>Objective</h3><div>Dimethyl fumarate (DMF) and diroximel fumarate (DRF) are oral multiple sclerosis (MS) disease-modifying therapies (DMTs). Absolute lymphocyte count (ALC) dynamics are similar for DMF and DRF, but have not been investigated in patients who switched from DMF to DRF. This retrospective, observational study of the US Komodo Health Claims Database characterized ALC dynamics and outcomes in patients who switched DMF-DRF (“Switchers”) versus patients who stayed on DMF (“Stayers”).</div></div><div><h3>Methods</h3><div>Eligible patients aged 18–64 years, with a diagnosis of MS and ≥1 DMT claim during the study period (01Jan2015<img>31Aug2022) had ≥1 year on DMF before switching to DRF and ≥6 months on DRF. Switchers were propensity score-matched 1:2 to Stayers. Assessments included ALC, relapses, and infection-related healthcare encounters (HCEs) and healthcare costs (HCCs).</div></div><div><h3>Results</h3><div>Of 94 eligible Switchers, 62 were matched with 124 Stayers. Mean (SD) duration of DMF exposure was 36.0 (16.0) months prior to index date/switch and 15.0 (4.9) months post-index date/switch. Over 12 months, mean ALC change from index date was –26.9 % (Switchers) versus +3.5 % (Stayers). In Switchers, mean ALC remained stable thereafter. Proportions remaining relapse-free during 15 months mean follow-up were similar between Switchers (95 %) and Stayers (91 %). Outcomes were similar for annualized rates of infection-related HCEs (mean [SD]: Switchers, 0.70 [1.03]; Stayers, 0.74 [1.57]) and HCCs (mean [SD]: Switchers, $285 [$856]; Stayers, $346 [$2299]).</div></div><div><h3>Conclusion</h3><div>Over 12 months, ALC declined by 26.9 % in Switchers but increased by 3.5 % in Stayers. Despite this difference in ALC dynamics, infection-related HCEs and HCCs remained low and comparable between cohorts.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100229"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tongue crushing trismus following brainstem stroke","authors":"Prince Thakkar ,&nbsp;Hussam Elkambergy ,&nbsp;Syed Irteza Hussain","doi":"10.1016/j.dscb.2025.100230","DOIUrl":"10.1016/j.dscb.2025.100230","url":null,"abstract":"<div><div>38-year-old female presented to emergency with history of dizziness followed by loss of consciousness. She was intubated in ED due to low GCS E3 M4 V1 and admitted to neuro intensive care unit. MRI Brain showed left and right pontine paramedian and right cerebellar infarcts. On day 7 after tracheostomy tube placement, trial of weaning was started and tongue bites were noted with difficulty to open the mouth due to masseter tightness. The tongue is crushed between the upper and lower teeth. She had a swollen left side of the tongue with a large laceration and slough formation suggestive of a severe tongue injury. Oral baclofen trial failed, and she needed sedation for muscle relaxation and prevention of tongue injury. Botulinum toxin was injected in the masseter (50 units per side) and temporalis (25 units per side) bilaterally. There was minimal improvement (5 mm) at two weeks, with intermittent tongue bites requiring a mouth gag and sedation. Due to intermittent severe trismus persisting into the 3rd week, she underwent dental extraction of the upper incisors to prevent further tongue damage. At about 60 days, interincisal distance improved satisfactory, she was then able to open and close her mouth voluntarily, allowing adequate oral care. Trismus resulting in functional impairment should receive prompt treatment with Botulinum toxin to the oromandibular muscles for prevention of complications.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100230"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"One-year cognitive follow-up in patients hospitalized for COVID-19 in a cohort from Mexico","authors":"Rodríguez-Agudelo Yaneth ,&nbsp;Paz-Rodríguez Francisco ,&nbsp;Chávez-Oliveros Mireya ,&nbsp;Lozano-Tovar Susana ,&nbsp;Rodríguez-Rodríguez Mónica ,&nbsp;Soto-Moreno Francisco-Javier ,&nbsp;García-Santos Anwar ,&nbsp;López-González Diana ,&nbsp;González-Navarro Mauricio ,&nbsp;Fuentes-Dominguez Mauro Fernando ,&nbsp;Carrillo-Mezo Roger ,&nbsp;Marrufo-Meléndez Oscar ,&nbsp;Gutiérrez-Romero Alonso ,&nbsp;Del Río Quiñones Manuel ,&nbsp;Arauz-Góngora Antonio ,&nbsp;Avila-Rios Santiago","doi":"10.1016/j.dscb.2025.100228","DOIUrl":"10.1016/j.dscb.2025.100228","url":null,"abstract":"<div><div>Cognitive symptoms have been identified as a prevalent sequela of Covid-19 disease, that it they persist beyond the acute phase of infection. This situation has consequences for the general and emotional functionality of patients. The aim of this work was to explore the prevalence of both global and specific impairments in various cognitive domains in a group of SARS-CoV-2 infection survivors with subjective memory-related complaints from the COVID-19 clinic of the National Institute of Respiratory Diseases. Study subjects underwent a neuropsychological assessment three months after hospital discharge (first assessment T1) and again twelve months later (second assessment T2). The results show that although in the second assessment there was a significant improvement (<em>p</em> &lt; 0.05) in several domains: attention, gnosias, visual memory and language, however, we noted a high persistence of impairments in executive functions (20.8 % at T2). On the other hand, in the analysis of the complete assessment we observed deficits in at least three tests, 73.7 % at T1 and 60.4 % at T2. While in memory and semantic and phonological verbal fluency tasks, we observed improvement without being statistically significant. Our results show that although symptoms such as depression and anxiety decreased significantly, cognitive impairment may still be observed after one year, so we suggest that those patients with severe COVID-19 should receive cognitive follow-up through periodic cognitive assessments.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"18 ","pages":"Article 100228"},"PeriodicalIF":0.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}