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2.
Int J Nanomedicine ; 19: 4857-4875, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38828195

RESUMO

Brain diseases are the most devastating problem among the world's increasingly aging population, and the number of patients with neurological diseases is expected to increase in the future. Although methods for delivering drugs to the brain have advanced significantly, none of these approaches provide satisfactory results for the treatment of brain diseases. This remains a challenge due to the unique anatomy and physiology of the brain, including tight regulation and limited access of substances across the blood-brain barrier. Nanoparticles are considered an ideal drug delivery system to hard-to-reach organs such as the brain. The development of new drugs and new nanomaterial-based brain treatments has opened various opportunities for scientists to develop brain-specific delivery systems that could improve treatment outcomes for patients with brain disorders such as Alzheimer's disease, Parkinson's disease, stroke and brain tumors. In this review, we discuss noteworthy literature that examines recent developments in brain-targeted nanomedicines used in the treatment of neurological diseases.


Assuntos
Barreira Hematoencefálica , Encéfalo , Sistemas de Liberação de Medicamentos , Nanomedicina , Humanos , Nanomedicina/métodos , Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/metabolismo , Encéfalo/efeitos dos fármacos , Sistemas de Liberação de Medicamentos/métodos , Animais , Nanopartículas/química , Encefalopatias/tratamento farmacológico , Sistemas de Liberação de Fármacos por Nanopartículas/química , Sistemas de Liberação de Fármacos por Nanopartículas/farmacocinética , Doença de Parkinson/tratamento farmacológico , Doença de Alzheimer/tratamento farmacológico
3.
Curr Neuropharmacol ; 22(13): e310524230577, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38847379

RESUMO

BACKGROUND AND OBJECTIVE: Brain disorders are one of the major global mortality issues, and their early detection is crucial for healing. Machine learning, specifically deep learning, is a technology that is increasingly being used to detect and diagnose brain disorders. Our objective is to provide a quantitative bibliometric analysis of the field to inform researchers about trends that can inform their Research directions in the future. METHODS: We carried out a bibliometric analysis to create an overview of brain disorder detection and diagnosis using machine learning and deep learning. Our bibliometric analysis includes 1550 articles gathered from the Scopus database on automated brain disorder detection and diagnosis using machine learning and deep learning published from 2015 to May 2023. A thorough bibliometric análisis is carried out with the help of Biblioshiny and the VOSviewer platform. Citation analysis and various measures of collaboration are analyzed in the study. RESULTS: According to a study, maximum research is reported in 2022, with a consistent rise from preceding years. The majority of the authors referenced have concentrated on multiclass classification and innovative convolutional neural network models that are effective in this field. A keyword analysis revealed that among the several brain disorder types, Alzheimer's, autism, and Parkinson's disease had received the greatest attention. In terms of both authors and institutes, the USA, China, and India are among the most collaborating countries. We built a future research agenda based on our findings to help progress research on machine learning and deep learning for brain disorder detection and diagnosis. CONCLUSION: In summary, our quantitative bibliometric analysis provides useful insights about trends in the field and points them to potential directions in applying machine learning and deep learning for brain disorder detection and diagnosis.

.


Assuntos
Bibliometria , Encefalopatias , Aprendizado Profundo , Aprendizado de Máquina , Humanos , Encefalopatias/diagnóstico
4.
Stem Cell Reports ; 19(6): 767-795, 2024 Jun 11.
Artigo em Inglês | MEDLINE | ID: mdl-38865969

RESUMO

Human cellular models and their neuronal derivatives have afforded unprecedented advances in elucidating pathogenic mechanisms of neuropsychiatric diseases. Notwithstanding their indispensable contribution, animal models remain the benchmark in neurobiological research. In an attempt to harness the best of both worlds, researchers have increasingly relied on human/animal chimeras by xenografting human cells into the animal brain. Despite the unparalleled potential of xenografting approaches in the study of the human brain, literature resources that systematically examine their significance and advantages are surprisingly lacking. We fill this gap by providing a comprehensive account of brain diseases that were thus far subjected to all three modeling approaches (transgenic rodents, in vitro human lineages, human-animal xenografting) and provide a critical appraisal of the impact of xenografting approaches for advancing our understanding of those diseases and brain development. Next, we give our perspective on integrating xenografting modeling pipeline with recent cutting-edge technological advancements.


Assuntos
Benchmarking , Encefalopatias , Modelos Animais de Doenças , Animais , Humanos , Xenoenxertos , Transplante Heterólogo/métodos , Encéfalo
6.
Pharmazie ; 79(6): 118-123, 2024 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-38877682

RESUMO

Encephalopathy is the most severe complication of various common infections, including influenza and herpes, and it often results in death or severe neurological disability. The risk factors for viral encephalopathy include non-steroidal anti-inflammatory drug (NSAID) use; however, studies on NSAID-related encephalopathy are limited. In this study, we aimed to investigate the characteristics of NSAID-related encephalopathy. We investigated the incidence of NSAID-related encephalopathy using data from the United States Food and Drug Administration Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) databases containing reports on spontaneous adverse effects (AEs) published by the Pharmaceuticals and Medical Devices Agency. We used these databases to detect AEs based on reported odds ratios. By separating suspicious drugs, concomitant drugs, and drug interactions involving NSAIDs, we investigated the relationship between encephalopathy pathology and AEs of NSAIDs. Significant encephalopathy signals were detected for loxoprofen and etodolac in the FAERS database and loxoprofen in the JADER database. In the JADER database, significant encephalopathy signals in loxoprofen-treated patients were detected in 70-79-year-old, ≥80-year-old, influenza viral infection, and herpes virus infection groups. Significant encephalopathy signals in patients with herpes virus infection were detected in the ≥80-year-old and loxoprofen-treated groups. Regarding the involvement of loxoprofen in the development of encephalopathy, the JADER database listed loxoprofen as a suspect drug, without indicating any concomitant drug interactions. In conclusion, our findings suggest that loxoprofen and etodolac may be associated with viral encephalopathy. Accordingly, prudence is recommended when using loxoprofen in older individuals with viral infections.


Assuntos
Sistemas de Notificação de Reações Adversas a Medicamentos , Anti-Inflamatórios não Esteroides , Bases de Dados Factuais , United States Food and Drug Administration , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Sistemas de Notificação de Reações Adversas a Medicamentos/estatística & dados numéricos , Anti-Inflamatórios não Esteroides/efeitos adversos , Encefalopatias/induzido quimicamente , Encefalopatias/epidemiologia , Japão/epidemiologia , Fenilpropionatos/efeitos adversos , Estados Unidos/epidemiologia
7.
Brain Res Bull ; 214: 110993, 2024 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-38825254

RESUMO

Subiculum is a pivotal output component of the hippocampal formation, a structure often overlooked in neuroscientific research. Here, this review aims to explore the role of the subiculum in various brain disorders, shedding light on its significance within the functional-neuroanatomical perspective on neurological diseases. The subiculum's involvement in multiple brain disorders was thoroughly examined. In Alzheimer's disease, subiculum alterations precede cognitive decline, while in epilepsy, the subiculum plays a critical role in seizure initiation. Stress involves the subiculum's impact on the hypothalamic-pituitary-adrenocortical axis. Moreover, the subiculum exhibits structural and functional changes in anxiety, schizophrenia, and Parkinson's disease, contributing to cognitive deficits. Bipolar disorder is linked to subiculum structural abnormalities, while autism spectrum disorder reveals an alteration of inward deformation in the subiculum. Lastly, frontotemporal dementia shows volumetric differences in the subiculum, emphasizing its contribution to the disorder's complexity. Taken together, this review consolidates existing knowledge on the subiculum's role in brain disorders, and may facilitate future research, diagnostic strategies, and therapeutic interventions for various neurological conditions.


Assuntos
Encefalopatias , Hipocampo , Humanos , Hipocampo/patologia , Encefalopatias/fisiopatologia , Encefalopatias/patologia , Doença de Alzheimer/patologia , Doença de Alzheimer/fisiopatologia
8.
Theranostics ; 14(8): 3221-3245, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38855177

RESUMO

The availability of non-invasive drug delivery systems capable of efficiently transporting bioactive molecules across the blood-brain barrier to specific cells at the injury site in the brain is currently limited. Delivering drugs to neurons presents an even more formidable challenge due to their lower numbers and less phagocytic nature compared to other brain cells. Additionally, the diverse types of neurons, each performing specific functions, necessitate precise targeting of those implicated in the disease. Moreover, the complex synthetic design of drug delivery systems often hinders their clinical translation. The production of nanomaterials at an industrial scale with high reproducibility and purity is particularly challenging. However, overcoming this challenge is possible by designing nanomaterials through a straightforward, facile, and easily reproducible synthetic process. Methods: In this study, we have developed a third-generation 2-deoxy-glucose functionalized mixed layer dendrimer (2DG-D) utilizing biocompatible and cost-effective materials via a highly facile convergent approach, employing copper-catalyzed click chemistry. We further evaluated the systemic neuronal targeting and biodistribution of 2DG-D, and brain delivery of a neuroprotective agent pioglitazone (Pio) in a pediatric traumatic brain injury (TBI) model. Results: The 2DG-D exhibits favorable characteristics including high water solubility, biocompatibility, biological stability, nanoscale size, and a substantial number of end groups suitable for drug conjugation. Upon systemic administration in a pediatric mouse model of traumatic brain injury (TBI), the 2DG-D localizes in neurons at the injured brain site, clears rapidly from off-target locations, effectively delivers Pio, ameliorates neuroinflammation, and improves behavioral outcomes. Conclusions: The promising in vivo results coupled with a convenient synthetic approach for the construction of 2DG-D makes it a potential nanoplatform for addressing brain diseases.


Assuntos
Dendrímeros , Desoxiglucose , Sistemas de Liberação de Medicamentos , Neurônios , Animais , Dendrímeros/química , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Sistemas de Liberação de Medicamentos/métodos , Desoxiglucose/farmacologia , Desoxiglucose/farmacocinética , Fármacos Neuroprotetores/farmacocinética , Fármacos Neuroprotetores/administração & dosagem , Fármacos Neuroprotetores/farmacologia , Camundongos , Pioglitazona/farmacologia , Pioglitazona/administração & dosagem , Pioglitazona/farmacocinética , Barreira Hematoencefálica/metabolismo , Barreira Hematoencefálica/efeitos dos fármacos , Lesões Encefálicas Traumáticas/tratamento farmacológico , Lesões Encefálicas Traumáticas/metabolismo , Encéfalo/metabolismo , Encéfalo/efeitos dos fármacos , Encefalopatias/tratamento farmacológico , Humanos , Modelos Animais de Doenças , Distribuição Tecidual , Masculino
9.
R I Med J (2013) ; 107(6): 7-9, 2024 Jun 03.
Artigo em Inglês | MEDLINE | ID: mdl-38810006

RESUMO

Raoultella ornithinolytica is a rare, gram-negative environmental enterobacterium. Although infections in humans caused by R. ornithinolytica are uncommon, there are increasing reports implicating it in urinary tract infections, hepatobiliary infections, and bacteremia, designating it as an emerging pathogen. Its habitat is primarily in aquatic environments and soil, with seafood frequently identified as a potential source of infection. While these infections have predominantly been described in immunocompromised patients previously, our case suggests that advanced age may be a significant risk factor. We describe a case of a 73-year-old man presenting with encephalopathy who then was found to have R. ornithinolytica bacteremia from a genitourinary source. Following antibiotic treatment, the infection resolved and the neurologic symptoms improved. To the best of our knowledge, this is the first documented case in the medical literature of R. ornithinolytica featuring a primary neurologic presentation.


Assuntos
Antibacterianos , Encefalopatias , Infecções por Enterobacteriaceae , Enterobacteriaceae , Humanos , Idoso , Masculino , Infecções por Enterobacteriaceae/diagnóstico , Infecções por Enterobacteriaceae/tratamento farmacológico , Antibacterianos/uso terapêutico , Enterobacteriaceae/isolamento & purificação , Encefalopatias/microbiologia , Encefalopatias/tratamento farmacológico , Encefalopatias/diagnóstico , Bacteriemia/tratamento farmacológico , Bacteriemia/microbiologia , Bacteriemia/diagnóstico
11.
BMJ Case Rep ; 17(5)2024 May 02.
Artigo em Inglês | MEDLINE | ID: mdl-38697679

RESUMO

Ornithine transcarbamylase deficiency (OTCD) is a rare, X linked disorder that can manifest in late adulthood in heterozygous females as severe hyperammonaemia following environmental stressors. We present a case of hyperammonaemic encephalopathy that was triggered by glucocorticoid administration in an adult woman with heterozygous OTCD with clinical response to haemodialysis, ammonia scavengers and a high-calorie, low-protein diet.


Assuntos
Hiperamonemia , Doença da Deficiência de Ornitina Carbomoiltransferase , Humanos , Feminino , Doença da Deficiência de Ornitina Carbomoiltransferase/complicações , Doença da Deficiência de Ornitina Carbomoiltransferase/diagnóstico , Hiperamonemia/induzido quimicamente , Glucocorticoides/uso terapêutico , Glucocorticoides/efeitos adversos , Diálise Renal , Encefalopatias/induzido quimicamente , Encefalopatias/etiologia , Pessoa de Meia-Idade , Dieta com Restrição de Proteínas/efeitos adversos
12.
Clin Neurophysiol ; 163: 160-173, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38754181

RESUMO

OBJECTIVE: We investigated how electroencephalography (EEG) quantitative measures and dysglycemia relate to neurodevelopmental outcomes following neonatal encephalopathy (NE). METHODS: This retrospective study included 90 neonates with encephalopathy who received therapeutic hypothermia. EEG absolute spectral power was calculated during post-rewarming and 2-month follow-up. Measures of dysglycemia (hypoglycemia, hyperglycemia, and glycemic lability) and glucose variability were computed for the first 48 h of life. We evaluated the ability of EEG and glucose measures to predict neurodevelopmental outcomes at ≥ 18 months, using logistic regressions (with area under the receiver operating characteristic [AUROC] curves). RESULTS: The post-rewarming global delta power (average all electrodes), hyperglycemia and glycemic lability predicted moderate/severe neurodevelopmental outcome separately (AUROC = 0.8, 95%CI [0.7,0.9], p < .001) and even more so when combined (AUROC = 0.9, 95%CI [0.8,0.9], p < .001). After adjusting for NE severity and magnetic resonance imaging (MRI) brain injury, only global delta power remained significantly associated with moderate/severe neurodevelopmental outcome (odds ratio [OR] = 0.9, 95%CI [0.8,1.0], p = .04), gross motor delay (OR = 0.9, 95%CI [0.8,1.0], p = .04), global developmental delay (OR = 0.9, 95%CI [0.8,1.0], p = .04), and auditory deficits (OR = 0.9, 95%CI [0.8,1.0], p = .03). CONCLUSIONS: In NE, global delta power post-rewarming was predictive of outcomes at ≥ 18 months. SIGNIFICANCE: EEG markers post-rewarming can aid prediction of neurodevelopmental outcomes following NE.


Assuntos
Eletroencefalografia , Hipotermia Induzida , Humanos , Masculino , Feminino , Recém-Nascido , Eletroencefalografia/métodos , Estudos Retrospectivos , Transtornos do Neurodesenvolvimento/fisiopatologia , Transtornos do Neurodesenvolvimento/etiologia , Transtornos do Neurodesenvolvimento/diagnóstico , Hiperglicemia/fisiopatologia , Hiperglicemia/complicações , Hipoglicemia/fisiopatologia , Hipoglicemia/complicações , Encefalopatias/fisiopatologia , Glicemia/metabolismo , Lactente
13.
Sleep Med ; 119: 201-209, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38703603

RESUMO

BACKGROUND: There is a profound connection between abnormal sleep patterns and brain disorders, suggesting a shared influential association. However, the shared genetic basis and potential causal relationships between sleep-related traits and brain disorders are yet to be fully elucidated. METHODS: Utilizing linkage disequilibrium score regression (LDSC) and bidirectional two-sample univariable Mendelian Randomization (UVMR) analyses with large-scale GWAS datasets, we investigated the genetic correlations and causal associations across six sleep traits and 24 prevalent brain disorders. Additionally, a multivariable Mendelian Randomization (MVMR) analysis evaluated the cumulative effects of various sleep traits on each brain disorder, complemented by genetic loci characterization to pinpoint pertinent genes and pathways. RESULTS: LDSC analysis identified significant genetic correlations in 66 out of 144 (45.8 %) pairs between sleep-related traits and brain disorders, with the most pronounced correlations observed in psychiatric disorders (66 %, 48/72). UVMR analysis identified 29 causal relationships (FDR<0.05) between sleep traits and brain disorders, with 19 associations newly discovered according to our knowledge. Notably, major depression, attention-deficit/hyperactivity disorder, bipolar disorder, cannabis use disorder, and anorexia nervosa showed bidirectional causal relations with sleep traits, especially insomnia's marked influence on major depression (IVW beta 0.468, FDR = 5.24E-09). MVMR analysis revealed a nuanced interplay among various sleep traits and their impact on brain disorders. Genetic loci characterization underscored potential genes, such as HOXB2, while further enrichment analyses illuminated the importance of synaptic processes in these relationships. CONCLUSIONS: This study provides compelling evidence for the causal relationships and shared genetic backgrounds between common sleep-related traits and brain disorders.


Assuntos
Encefalopatias , Estudo de Associação Genômica Ampla , Desequilíbrio de Ligação , Análise da Randomização Mendeliana , Humanos , Encefalopatias/genética , Transtornos do Sono-Vigília/genética , Predisposição Genética para Doença/genética
14.
Chem Rev ; 124(11): 7106-7164, 2024 Jun 12.
Artigo em Inglês | MEDLINE | ID: mdl-38760012

RESUMO

The identification and detection of disease-related biomarkers is essential for early clinical diagnosis, evaluating disease progression, and for the development of therapeutics. Possessing the advantages of high sensitivity and selectivity, fluorescent probes have become effective tools for monitoring disease-related active molecules at the cellular level and in vivo. In this review, we describe current fluorescent probes designed for the detection and quantification of key bioactive molecules associated with common diseases, such as organ damage, inflammation, cancers, cardiovascular diseases, and brain disorders. We emphasize the strategies behind the design of fluorescent probes capable of disease biomarker detection and diagnosis and cover some aspects of combined diagnostic/therapeutic strategies based on regulating disease-related molecules. This review concludes with a discussion of the challenges and outlook for fluorescent probes, highlighting future avenues of research that should enable these probes to achieve accurate detection and identification of disease-related biomarkers for biomedical research and clinical applications.


Assuntos
Biomarcadores , Corantes Fluorescentes , Corantes Fluorescentes/química , Humanos , Biomarcadores/análise , Biomarcadores/metabolismo , Animais , Neoplasias/diagnóstico , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/metabolismo , Inflamação/diagnóstico , Encefalopatias/diagnóstico , Encefalopatias/diagnóstico por imagem
15.
Epilepsy Behav ; 156: 109840, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38788662

RESUMO

PURPOSE: We aimed to describe risks of status epilepticus (SE) after different brain disorders in adults using population-wide register data. Our hypothesis was that SE would be more common in disorders with widespread pathology and that the risk would increase with disorder severity. METHODS: We analyzed five large datasets created from the Swedish National Patient Register, the Cause of Death Register, and national quality registers with adults in Sweden with brain infections, dementia, multiple sclerosis (MS), stroke, and traumatic brain injury (TBI). Risk factors were assessed using Cox regression. RESULTS: In adults with TBI, stroke, dementia, MS, or brain infections, the incidence rate of SE was highest in survivors of brain infections (64/100,000 person years) and stroke (64/100,000), followed by TBI (37/100,000), dementia (36/100,000), and MS (26/100,000). SE was considerably more common in patients with epilepsy after their brain disorder. Across all datasets severe disorder increased SE-risk. Herpes simplex encephalitis (HR 5.5 95 % CI: 2.6-12), progressive MS (HR 2.3, 95 % CI: 1.1-4.7), structural TBI (2.0, 95 % CI: 1.6-2.6), and intracerebral hemorrhage (HR 1.5, 95 % CI: 1.2-2.0) were the subtypes of brain disorders with the highest relative risk of SE. Having another CNS disorder increased SE-risk in TBI (HR 2.9, 95 % CI: 2.3-3.7), brain infections (HR 2.8, 95 % CI: 1.7-4.5), and dementia (HR 2.5, 95 % CI: 1.5-4.2). CONCLUSION: SE-risk increases with disorder severity and number of CNS comorbidities. These findings can guide treatment strategy by allowing identification of high-risk patients. Pathophysiological studies are needed to better understand remote symptomatic SE.


Assuntos
Sistema de Registros , Estado Epiléptico , Humanos , Feminino , Masculino , Estado Epiléptico/epidemiologia , Estado Epiléptico/etiologia , Fatores de Risco , Pessoa de Meia-Idade , Adulto , Suécia/epidemiologia , Idoso , Estudos de Coortes , Encefalopatias/epidemiologia , Idoso de 80 Anos ou mais , Incidência , Adulto Jovem
16.
Ugeskr Laeger ; 186(20)2024 May 13.
Artigo em Dinamarquês | MEDLINE | ID: mdl-38808758

RESUMO

This review investigates that there has been an increase in incidental brain MRI findings due to better technology and more scans. These unexpected, asymptomatic anomalies range from harmless to serious, requiring careful clinical and ethical handling. The prevalence of incidental findings with brain MRI is 4.2% and even higher when including white matter hyperintensities. There is a significant variation in this number dependent on the age of the person being scanned and the MRI quality.


Assuntos
Encéfalo , Achados Incidentais , Imageamento por Ressonância Magnética , Humanos , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Encefalopatias/diagnóstico por imagem
17.
Science ; 384(6698): eadh4265, 2024 May 24.
Artigo em Inglês | MEDLINE | ID: mdl-38781378

RESUMO

Nucleotide variants in cell type-specific gene regulatory elements in the human brain are risk factors for human disease. We measured chromatin accessibility in 1932 aliquots of sorted neurons and non-neurons from 616 human postmortem brains and identified 34,539 open chromatin regions with chromatin accessibility quantitative trait loci (caQTLs). Only 10.4% of caQTLs are shared between neurons and non-neurons, which supports cell type-specific genetic regulation of the brain regulome. Incorporating allele-specific chromatin accessibility improves statistical fine-mapping and refines molecular mechanisms that underlie disease risk. Using massively parallel reporter assays in induced excitatory neurons, we screened 19,893 brain QTLs and identified the functional impact of 476 regulatory variants. Combined, this comprehensive resource captures variation in the human brain regulome and provides insights into disease etiology.


Assuntos
Encefalopatias , Encéfalo , Cromatina , Regulação da Expressão Gênica , Elementos Reguladores de Transcrição , Humanos , Alelos , Encéfalo/metabolismo , Encefalopatias/genética , Cromatina/metabolismo , Neurônios/metabolismo , Locos de Características Quantitativas , Masculino , Feminino
18.
Neurosci Biobehav Rev ; 162: 105731, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38763180

RESUMO

Fragile X messenger ribonucleoprotein 1 (FMRP) is a widely expressed RNA binding protein involved in several steps of mRNA metabolism. Mutations in the FMR1 gene encoding FMRP are responsible for fragile X syndrome (FXS), a leading genetic cause of intellectual disability and autism spectrum disorder, and fragile X-associated tremor-ataxia syndrome (FXTAS), a neurodegenerative disorder in aging men. Although FMRP is mainly expressed in neurons, it is also present in glial cells and its deficiency or altered expression can affect functions of glial cells with implications for the pathophysiology of brain disorders. The present review focuses on recent advances on the role of glial subtypes, astrocytes, oligodendrocytes and microglia, in the pathophysiology of FXS and FXTAS, and describes how the absence or reduced expression of FMRP in these cells can impact on glial and neuronal functions. We will also briefly address the role of FMRP in radial glial cells and its effects on neural development, and gliomas and will speculate on the role of glial FMRP in other brain disorders.


Assuntos
Proteína do X Frágil da Deficiência Intelectual , Síndrome do Cromossomo X Frágil , Neuroglia , Humanos , Proteína do X Frágil da Deficiência Intelectual/metabolismo , Proteína do X Frágil da Deficiência Intelectual/genética , Neuroglia/metabolismo , Animais , Síndrome do Cromossomo X Frágil/metabolismo , Síndrome do Cromossomo X Frágil/fisiopatologia , Síndrome do Cromossomo X Frágil/patologia , Encefalopatias/metabolismo , Encefalopatias/fisiopatologia , Encefalopatias/genética , Ataxia/metabolismo , Ataxia/fisiopatologia , Ataxia/genética , Tremor/metabolismo , Tremor/fisiopatologia , Tremor/genética
19.
Clin Neuropharmacol ; 47(3): 104-107, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38743605

RESUMO

OBJECTIVES: Metronidazole central nervous system toxicity is a rare finding in patients receiving the medication. We report a peculiar case of metronidazole central nervous system toxicity in which both the underlying condition (Crohn disease) and the drugs used to treat it are potential causes of encephalopathy. METHODS: A 26-year-old female with 6-year history of Crohn's disease for 6 years presented acute-onset encephalopathy. We provide bibliographic evidence to support metronidazole toxicity and potential Crohn disease-associated neurologic involvement. RESULTS: The patient presented dystonia, cerebellar ataxia, and altered mental status. Magnetic resonance imaging of the brain revealed typical findings of metronidazole toxicity and white matter involvement of the centrum semiovale. Immunoelectrophoresis and immunofixation of serum and cerebrospinal fluid proteins were consistent with a systemic inflammatory process. We concluded on an association between drug toxicity and probable Crohn-associated neurologic involvement. Metronidazole was stopped and the patient was placed on vitamin therapy and diazepam to control dystonia. She deteriorated and was transferred to the intensive care unit where she expired. CONCLUSIONS: Acute behavioral changes in a young patient constitute an emergency and differential diagnoses should include infective, inflammatory, metabolic, and toxic causes. Metronidazole is a potential toxic etiology.


Assuntos
Doença de Crohn , Encefalite , Metronidazol , Humanos , Metronidazol/efeitos adversos , Feminino , Doença de Crohn/tratamento farmacológico , Doença de Crohn/complicações , Adulto , Encefalite/induzido quimicamente , Encefalopatias/induzido quimicamente , Imageamento por Ressonância Magnética , Evolução Fatal
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