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1.
Int. j. clin. health psychol. (Internet) ; 24(1): [100433], Ene-Mar, 2024. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-230376

RESUMO

Background: The exact causal mechanisms of depression remain unclear due to the complexity of the triggers, which has led to limitations in treating depression using modern drugs. High-intensity interval training (HIIT) is as effective as medication in treating depression without toxic side effects. Typically, HIIT requires less time commitment (i.e., shorter exercise duration) and exhibits pronounced benefits on depressive symptoms than other forms of physical exercise. This review summarizes the risk reduction and clinical effects of HIIT for depression and discusses the underlying mechanisms, providing a theoretical basis for utilizing HIIT in treating depression. Methods: A database search was conducted in PubMed, Embase, Web of Science, and Scopus from inception up to October 2022. The methodological quality of the included literature was evaluated by the physiotherapy evidence database (PEDro) scale criteria. The review focused on evaluating the changes in depression risk or symptoms of HIIT interventions in healthy individuals, patients with depression, and patients with other disorders co-morbid with depression. Consequently, the mechanisms associated with depression related HIIT were summarized. Results: A total of 586 participants (52 % female; mean age: 43.58±8.93 years) from 22 studies were included. Implementing HIIT using different exercise types alleviates depressive symptoms in individuals with depression and in individuals with depression who have exhibited comorbidities and reduced depression scale scores in subjects immediately after acute exercise. In addition, the long-interval HIIT and short-interval HIIT in the treatment of patients with cardiovascular or psychiatric disorders may reduce depressive symptoms via complex exercise-related changes on several levels, including by effecting the following measures: releasing monoamines, reducing neuronal death, inducing neurogenesis, modulating the functional...(AU)


Assuntos
Humanos , Masculino , Feminino , Depressão , Inflamação/reabilitação , Fatores de Crescimento Neural , Sistema Hipotálamo-Hipofisário , Treinamento Intervalado de Alta Intensidade , Tratamento Farmacológico
2.
Int. j. clin. health psychol. (Internet) ; 23(3)jul.-sep. 2023. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-218530

RESUMO

Background: Major depressive disorder (MDD) is a serious mood disorder and leading cause of disability. Despite treatment advances, approximately 30% of individuals with MDD do not achieve adequate clinical response. Better understanding the biological mechanism(s) underlying clinical response to specific psychopharmacological interventions may help fine tune treatments in order to further modulate their underlying mechanisms of action. However, little is known regarding the effect of non-pharmacological treatments (NPTs) on candidate molecular biomarker levels in MDD. This review aims to identify molecular biomarkers that may elucidate NPT response for MDD. Methods: We performed a systematic review and a multilevel linear mixed-effects meta-analyses, and a meta-regression. Searches were performed in PubMed, Scopus, and PsycINFO in October 2020 and July 2021. Results: From 1387 retrieved articles, 17 and six studies were included in the systematic review and meta-analyses, respectively. Although there was little consensus associating molecular biomarker levels with symptomology and/or treatment response, brain metabolites accessed via molecular biomarker-focused neuroimaging techniques may provide promising information on whether an individual with MDD would respond positively to NPTs. Furthermore, non-invasive brain stimulation interventions significantly increased the expression of neurotrophic factors (NTFs) compared to sham/placebo, regardless of add-on pharmacological treatment. Conclusions: NTFs are candidate biomarkers to fine-tune NIBS for MDD treatment. (AU)


Assuntos
Humanos , Transtorno Depressivo Maior , Terapia Cognitivo-Comportamental , Biomarcadores , Terapia por Estimulação Elétrica , Fatores de Crescimento Neural
3.
Rev. neurol. (Ed. impr.) ; 68(5): 181-189, 1 mar., 2019. graf, tab
Artigo em Espanhol | IBECS | ID: ibc-180387

RESUMO

Introducción. La inmersión vertical induce una variedad de respuestas fisiológicas en diferentes sistemas corporales, dependiendo de las propiedades de la mecánica de fluidos, las cuales son la base que sustenta los programas de terapia acuática en diferentes patologías. Objetivo. Realizar una revisión sistemática para analizar y describir los efectos que la inmersión vertical produce en el sistema nervioso en sujetos sanos. Sujetos y métodos. Se llevó a cabo una búsqueda sistemática de la bibliografía existente en las bases de datos BRAIN, PubMed, PEDro y Web of Science. Se evaluó metodológicamente la calidad mediante la guía CASPe y el nivel de evidencia se categorizó mediante la escala Oxford. Se incluyó un total de 12 artículos, con un rango de puntuación de 7-10 según CASPe, niveles de evidencia 1b-2b y grado de recomendación B. Resultados. Todos los estudios mostraron resultados positivos a las diferentes formas de exposición de la inmersión vertical en el agua y a la suma de estímulos empleados, sin referir efectos adversos en ningún caso. Conclusiones. La inmersión vertical en el agua genera efectos positivos sobre los flujos circulatorios cerebrales, la activación cortical, las funciones ejecutivas y la producción de neurotrofinas en sujetos sanos


Introduction. Vertical immersion induces a variety of physiological responses in different body systems, depending on the properties of fluid mechanics, which are the basis that underpins aquatic therapy programs in different pathologies. Aim. To perform a systematic review to analyze and describe the effects that vertical immersion produces on the nervous system in healthy subjects. Subjects and methods. A systematic search of the existing literature was conducted in the databases BRAIN, PubMed, PEDro and Web of Science. Quality was methodologically assessed using the CASPe guideline and the level of evidence was categorized using the Oxford scale. A total of 12 articles were included, with a score range of 7-10 according to CASPe, levels of evidence 1b-2b and grade of recommendation B. Results. All studies showed positive results to the different forms of exposure of vertical immersion in water and the summation of the stimuli used; no adverse effects were reported in any case. Conclusions. The vertical immersion in the water generates positive effects on cerebral blood flows, cortical activation, executive functions and the production of neurotrophins in healthy subjects


Assuntos
Humanos , Imersão , Hidroterapia/métodos , Doenças do Sistema Nervoso Central/terapia , Fatores de Crescimento Neural , Fenômenos Fisiológicos do Sistema Nervoso , Mecânica dos Fluidos , Nível de Alerta/fisiologia
4.
Eur. j. psychiatry ; 30(2): 109-118, abr.-jun. 2016. tab, graf
Artigo em Inglês | IBECS | ID: ibc-155809

RESUMO

Background and Objectives: Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) are neurotrophic neuropeptides that play important roles in the synaptic plasticity, neuronal growth, survival and function. A possible neuroprotective role of neurotrophic factors against alcohol-induced cell damage has been suggested, and dysregulations in neurotrophic factors may be involved in the vulnerability to addiction. The aim of this study was to investigate the alterations of BDNF and GDNF serum levels in alcohol-addicted patients during alcohol withdrawal compared to healthy controls. Methods: BDNF and GDNF serum levels of 34 male inpatients diagnosed with alcohol addiction according to DSM-IV-TR were investigated during alcohol withdrawal (day 1, 7 and 14) in comparison to 32 healthy controls using an enzyme-linked immunosorbent assay (ELISA). Severity of alcohol withdrawal was measured by Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar), and intensity of alcohol craving was measured by Penn Alcohol Craving Scale (PACS) during alcohol withdrawal (day 1, 7 and 14). Results: BDNF serum levels increased significantly during alcohol withdrawal (p = 0.020). They were negatively correlated to the severity of alcohol withdrawal, and the correlation was close to being statistically significant (p = 0.058). BDNF and GDNF serum levels did not differ significantly between the patient and control groups. GDNF serum levels did not change significantly during alcohol withdrawal. Conclusions: Our results may provide support for the previously hypothesized role of BDNF in the neuroadaptation during alcohol withdrawal (AU)


No disponible


Assuntos
Humanos , Alcoolismo/fisiopatologia , Síndrome de Abstinência a Substâncias/fisiopatologia , Fator Neurotrófico Derivado do Encéfalo/análise , Fator Neurotrófico Derivado de Linhagem de Célula Glial/análise , Fatores de Crescimento Neural/análise , Estudos de Casos e Controles
5.
Acta otorrinolaringol. esp ; 66(5): 286-295, sept.-oct. 2015. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-143924

RESUMO

La hipoacusia neurosensorial es un problema que se debe principalmente a la pérdida de células ciliadas cocleares, con la consecuente desaferenciación de las neuronas del ganglio espiral. En los humanos no existe regeneración celular endógena en el oído interno, ni una terapia exógena que permita la sustitución de las células dañadas. El tratamiento actual se basa en las prótesis auditivas y los implantes cocleares. Estos dispositivos presentan resultados variables entre pacientes, con limitaciones en la discriminación auditiva y una vida útil limitada. La tecnología, cada vez más avanzada, está limitada por la capacidad funcional de las neuronas restantes del ganglio espiral. Las terapias emergentes, con células madre y reprogramación celular, han desarrollado varias posibilidades para inducir la regeneración endógena o para trasplantar células madre que puedan sustituir las células dañadas y restaurar la función auditiva. El conocimiento de la biología celular y molecular del oído interno y su desarrollo embrionario permite plantear el uso de células madre inducidas como modelos in vitro de enfermedad y terapia celular sustitutiva. La investigación traslacional en la hipoacusia neurosensorial está orientada al desarrollo de una terapia celular con aplicación clínica para el tratamiento de la hipoacusia neurosensorial profunda (AU)


Sensorineural hearing loss is a caused by the loss of the cochlear hair cells with the consequent deafferentation of spiral ganglion neurons. Humans do not show endogenous cellular regeneration in the inner ear and there is no exogenous therapy that allows the replacement of the damaged hair cells. Currently, treatment is based on the use of hearing aids and cochlear implants that present different outcomes, some difficulties in auditory discrimination and a limited useful life. More advanced technology is hindered by the functional capacity of the remaining spiral ganglion neurons. The latest advances with stem cell therapy and cellular reprogramming have developed several possibilities to induce endogenous regeneration or stem cell transplantation to replace damaged inner ear hair cells and restore hearing function. With further knowledge of the cellular and molecular biology of the inner ear and its embryonic development, it will be possible to use induced stem cells as in vitro models of disease and as replacement cellular therapy. Investigation in this area is focused on generating cellular therapy with clinical use for the treatment of profound sensorineural hearing loss (AU)


Assuntos
Perda Auditiva Neurossensorial/cirurgia , Células Ciliadas Auditivas/patologia , Gânglio Espiral da Cóclea/fisiopatologia , Nervo Coclear/fisiopatologia , Órgão Espiral/fisiopatologia , Reprogramação Celular , Regeneração , Transplante de Células-Tronco Hematopoéticas , Transplante de Células-Tronco Mesenquimais , Células-Tronco Embrionárias/transplante , Células-Tronco Neurais/transplante , Células-Tronco Pluripotentes Induzidas/transplante , Terapia Genética , Fatores de Crescimento Neural/uso terapêutico , Implantes Cocleares , Terapia Baseada em Transplante de Células e Tecidos
6.
Rev. neurol. (Ed. impr.) ; 58(supl.1): 19-24, 24 feb., 2014.
Artigo em Espanhol | IBECS | ID: ibc-119457

RESUMO

Se revisa la bibliografía existente sobre los hallazgos de la implicación de los factores neurotróficos en el trastorno por déficit de atención/hiperactividad (TDAH). Las neurotrofinas, una familia de factores neurotróficos, son un tipo de proteínas específicas del sistema nervioso con un papel esencial en la supervivencia, diferenciación y proliferación neuronal durante el desarrollo del sistema nervioso central y periférico. Estas moléculas estimulan el crecimiento axonal e influyen en las conexiones con el tejido diana para el establecimiento de las conexiones sinápticas. El interés por el estudio de las neurotrofinas en el TDAH, un trastorno del neurodesarrollo, deriva principalmente de las funciones que estas proteínas ejercen en el sistema nervioso central. Existen evidencias derivadas de estudios en modelos animales, farmacológicos y de genética molecular que relacionan a las neurotrofinas con el trastorno. En el presente trabajo se revisan los resultados de los estudios realizados hasta el momento sobre TDAH y factores neurotróficos, principalmente factor neurotrófico derivado de cerebro (BDNF). Así, aunque estudios farmacológicos sugieren que la respuesta a la atomoxetina en adultos con TDAH no está directamente mediada por el efecto sobre el BDNF, se han descrito disminuciones en los niveles plasmáticos de BDNF en pacientes adultos con TDAH. Se requieren estudios con muestras más amplias y mayor control de factores ambientales que pueden regular la expresión de la neurotrofinas, como la dieta, el ejercicio físico y situaciones de riesgo social, con el fin de determinar el papel de éstas en la etiología del TDAH (AU)


The existing literature that reports findings linked with the involvement of neurotrophic factors in attention deficit hyperactivity disorder (ADHD) is reviewed. Neurotrophins, a family of neurotrophic factors, are a kind of proteins that are specific to the nervous system and play an essential role in neuron survival, differentiation and proliferation during the development of the central and peripheral nervous system. These molecules stimulate axonal growth and exert an influence on the connections with the target tissue in order to establish the synaptic connections. The study of neurotrophins in ADHD, a neurodevelopmental disorder, is of interest mainly due to the functions that these proteins perform in the central nervous system. Studies on animal, pharmacological and molecular genetic models yield evidence that relates neurotrophins with the disorder. This work reviews the results from the studies conducted to date on ADHD and neurotrophic factors, especially brain-derived neurotrophic factor (BDNF). Thus, although pharmacological studies suggest that the response to atomoxetine in adults with ADHD is not directly mediated by the effect on the BDNF, reductions in BDNF levels in the plasma of adult patients with ADHD have been reported. Further studies with broader samples and greater control of environmental factors that can regulate neurotrophin expression, such as diet, physical exercise and situations of social risk, are needed to be able to determine the role they play in the aetiology of ADHD (AU)


Assuntos
Humanos , Masculino , Feminino , Adulto , Fatores de Crescimento Neural/análise , Transtorno do Deficit de Atenção com Hiperatividade/fisiopatologia , Estimulantes do Sistema Nervoso Central/uso terapêutico , Deficiências do Desenvolvimento/fisiopatologia , Sistema Nervoso Central/crescimento & desenvolvimento
7.
Inf. psiquiátr ; (213): 261-273, sept. 2013. tab
Artigo em Espanhol | IBECS | ID: ibc-118360

RESUMO

La depresión mayor es uno de los trastornos afectivos con mayor prevalencia en clínica. A pesar de todos los procesos neurobiológicos implicados en esta patología, el tratamiento actual de la depresión se centra en los neurotransmisores NA y 5Ht a nivel de sistema nervioso central, y en menor medida, dopamina. el tratamiento con antidepresivos y su respuesta requiere una revaloración sistemática del paciente debido a que existe un 25 % de la población que no responde al tratamiento con estos fármacos, del 26-50 % responden solo parcialmente y tan solo un 50 % responde favorablemente, o al menos, disminuyen significativamente los síntomas más graves de la enfermedad. Las estrategias usadas en pacientes resistentes a la depresión, consiste en la administración de otros agentes en combinación con antidepresivos para aumentar su efecto. La depresión es característica no solo por ser un trastorno afectivo sino que posee una dimensión somática caracterizada por la pérdida de peso, fatiga, trastornos del sueño, dolores de cabeza y estómago y otros síntomas de dolor. La teoría que explica la prevalencia de estas enfermedades se basa en el hecho de que ambas patologías comparten sustratos neurobiológicos como, por ejemplo, ocurre en el caso de los neurotransmisores implica-dos en la depresión (5Ht y NA) que, a su vez, juegan un papel fundamental en la modulación del dolor. La hipótesis neurotrófica de la depresión es otra hipótesis más reciente (que postula una disminución en la producción de nuevas neuronas en el giro dentado del hipocampo) está relacionada con la etiopatogenia de la depresión. Varios estudios han demostrado que la mayoría de los antidepresivos estimulan la neurogénesis en el giro dentado del hipocampo


Major depression is one of the affective disorders with higher prevalence in clinical. Although major depression comprises many neurobiological pro cesses, the current treatment is focusing in the increase of NA and 5Ht neurotransmitters in the cNS, and even less dopamine. Both treatment and response of patients to antidepressants require high monitoring due to the fact that 25 % of population result resistant to the treatment, 25-50 % respond partially and only the 50 % improve the symptom of depression. Another pharmacological strategies used in patients resistant to depression, involves the administration of other agents in combination with antidepressants to enhance their effect. Depression is widely known by its affective component characterized by moods, feelings of worthless-ness, diminished interest in pleasurable stimuli, and impaired decision-making abilities, although it can also have a somatic dimension characterized by weight change, fatigue, sleep disturbances, and pain. the prevalence of pain in major depression is a common situation in clinical. According to the earlier theories, the presence of pain symptoms in depression is due to the fact that both pathologies share neuroanatomical substrates such as the neurotransmitter involved in depression (NA and 5Ht) which play an important role in the modulation of pain. Major depression have been explained for many theories, one of the most important at the present is called «the neurotropic hypothesis of depression» which postulates that the production of new neurons in the dentate gyrus of the hippocampus is related to the pathogenesis of depression and accordingly to this theory, many studies have demonstrated an increase of neurogenesis in the hippocampus after antidepressant treatment


Assuntos
Humanos , Transtorno Depressivo Maior/tratamento farmacológico , Antidepressivos/uso terapêutico , Neurogênese , Hipocampo , Psicotrópicos/uso terapêutico , Dopamina , Resistência a Medicamentos , Manejo da Dor/métodos , Fatores de Crescimento Neural/farmacocinética , Monoaminas Biogênicas/farmacocinética
9.
J. physiol. biochem ; 67(2): 235-241, jun. 2011.
Artigo em Inglês | IBECS | ID: ibc-122623

RESUMO

No disponible


We investigated the effects of treadmill exercise performed regularly for 6 weeks on the levels of nerve growth factor (NGF), tyrosine kinase A and p75 receptors, phosphatidylinositol 3-kinase (PI3-K), mitogen-activated protein kinase/extracellular signal-regulated kinase (Erk) 1,2, cyclic AMP response element-binding protein (CREB), and caspase-3 in the soleus of rats with streptozotocin (STZ)-induced diabetes. Thirty-two male Sprague–Dawley rats were divided into the following four groups: (1) normal control group (NCG; n = 8), (2) normal exercise group (NEG; n = 8), (3) diabetes control group (DCG; n = 8), and (4) diabetes exercise group (..) (AU)


Assuntos
Humanos , Condicionamento Físico Animal/fisiologia , Diabetes Mellitus/fisiopatologia , Fatores de Crescimento Neural/fisiologia , Apoptose/fisiologia , Células Musculares/fisiologia , Fosfatidilinositol 3-Quinases/fisiologia , Proteínas Tirosina Quinases , Morte Celular/fisiologia , Músculo Esquelético/fisiologia
11.
Actas dermo-sifiliogr. (Ed. impr.) ; 100(supl.2): 70-74, dic. 2009.
Artigo em Inglês | IBECS | ID: ibc-78818

RESUMO

Neurotrophins (NTs) belong to a family of structurally and functionally related proteins that, depending on the tissue context and the receptors involved, promote neuronal cell survival and differentiation or cell death. NTs also exert important functions in other organs besides the nervous system, including the skin. The presence in the skin of diverse cell types which are able to secrete and/or to respond to stimulation by NTs creates a unique network of molecular signaling in the cutaneous microenvironment. This review summarizes currently available data on the expression and function of NTs and their receptors in several cell types in the skin (namely, keratinocytes, melanocytes and fibroblasts). The role of the skin NT network in the development and maintenance of some relevant skin diseases is presented and the potential implications for therapeutic intervention are discussed (AU)


Las neurotrofinas (NT) pertenecen a una familia de proteínas relacionadas estructural y funcionalmente que, dependiendo del tejido y del receptor implicados, promueven la supervicencia y diferenciación neuronal o la apoptosis. Las NT también ejercen importantes funciones en otros órganos, aparte del sistema nervioso, incluyendo la piel. La presencia de diversos tipos celulares en la piel que son capaces de segregar o responder al estímulo de las NT, crea una red única de señalización molecular en el microambiente cutáneo. Esta revisión resume los datos disponibles actualmente sobre la expresión y función de las NT y sus receptores en diversos tipos celulares de la piel (a saber: queratinocitos, melanocitos, fibroblastos). Se discute el papel de la red de NT cutáneas en el desarrollo y mantenimiento de algunas enfermedades cutáneas relevantes, así como las implicaciones potenciales para una intervención terapéutica (AU)


Assuntos
Humanos , Fatores de Crescimento Neural/imunologia , Psoríase/imunologia , Melanoma/imunologia , Fatores de Crescimento Neural , Psoríase/diagnóstico , Melanoma/diagnóstico , Apoptose/imunologia
13.
Rev. neurol. (Ed. impr.) ; 45(7): 409-417, 1 oct., 2007. ilus
Artigo em Es | IBECS | ID: ibc-65923

RESUMO

Se ha propuesto que las modificaciones de larga duración que tienen lugar en la transmisión sinápticaconstituyen la base de los procesos de almacenamiento de información. La neurotrofina denominada factor neurotrófico derivado del cerebro (BDNF) ha emergido recientemente como un potente mediador molecular de la plasticidad sináptica central. Desarrollo. En este trabajo se revisan los estudios que han representado un avance significativo en el esclarecimientodel papel que desempeña el BDNF en la plasticidad sináptica de larga duración. Los efectos del BDNF en la plasticidad sináptica pueden ser de naturaleza tanto permisiva, estableciendo las condiciones para que los cambios plásticos puedan llevarse a cabo, como instructiva, ejerciendo efectos directos que producen cambios en la comunicación y morfología de las sinapsis.Entre las acciones del BDNF se encuentra su capacidad de coadyuvar en la estabilización y maduración de las sinapsis ya existentes, así como de generar nuevos contactos sinápticos. Un hallazgo de gran relevancia que subraya la participación de esta neurotrofina en la plasticidad sináptica lo constituye la observación de que la adición de BDNF produce drásticosincrementos de larga duración en la transmisión sináptica, similares a la potenciación a largo plazo en el hipocampo y la neocorteza de los mamíferos. Conclusión. En virtud de que el BDNF modula tanto las propiedades eléctricas como la organizaciónestructural de la sinapsis, esta neurotrofina se ha considerado como un importante señalizador durante los procesos de aprendizaje y memoria


It has been suggested that the long-term modifications that take place in synaptic transmission constitutethe foundation of the processes by which information stored. The neurotrophin called brain-derived neurotrophic factor (BDNF) has recently emerged as a powerful molecular mediator in central synaptic plasticity. Development. In this work wereview the studies that have represented a significant step forward in explaining the role played by BDNF in long-term synaptic plasticity. The effects of BDNF on synaptic plasticity can be of a permissive nature, whereby it establishes the conditions under which plastic changes can take place, or it may be instructive. In this latter case it exerts direct effects that bring about changes in the communication and morphology of the synapses. The actions carried out by BDNF include its capacity to contribute to the stabilisation and maturation of already-existing synapses, as well as to generate new synapticcontacts. One important finding that highlights the participation of this neurotrophin in synaptic plasticity is the observation that adding BDNF gives rise to drastic long-term increases in synaptic transmission, similar to the long-term potentiation inthe hippocampus and neocortex of mammals. Conclusions. Because BDNF modulates both the electrical properties and the structural organisation of the synapse, this neurotrophin has been considered to be an important marker during learning andmemory processes


Assuntos
Humanos , Memória/fisiologia , Fator Neurotrófico Derivado do Encéfalo/fisiologia , Transmissão Sináptica/fisiologia , Fatores de Crescimento Neural/fisiologia , Aprendizagem/fisiologia
14.
Rev. neurol. (Ed. impr.) ; 45(4): 245-250, 16 ago., 2007. graf
Artigo em Es | IBECS | ID: ibc-69803

RESUMO

Introducción. La pérdida de audición constituye una de las deficiencias sensoriales invalidantes más frecuentes en el mundo desarrollado. En la actualidad se estudian diferentes abordajes terapéuticos, entre los que se incluyen el tratamiento con células madre, la manipulación genética y la protección farmacológica. Objetivo. Evaluar el papel del factor de crecimientosimilar a la insulina de tipo I (IGF-I) en el desarrollo, el mantenimiento y la reparación de la función auditiva. Desarrollo. El desarrollo del oído interno depende de la adecuada coordinación de los procesos celulares de proliferación, diferenciación, neurogénesis y muerte celular programada, que se encuentran regulados por distintos factores entre los que se encuentra el IGF-I. Durante la embriogénesis del oído interno, este factor se expresa abundantemente y es fundamental para la supervivencia celular y el mantenimiento de los precursores neuronales. El estudio del ratón nulo Igf-1–/– ha puesto de manifiesto su importancia en el desarrollo y mantenimiento funcional del oído interno. Los ratones deficientes en este gen presentan alteraciones morfológicas que se corresponden con graves deficiencias funcionales, confirmadas mediante el análisis de los potenciales evocados auditivos de tronco cerebral. El déficit de IGF-I en humanos también se acompaña de hipoacusia sensorial profunda. Conclusión. En este escenario, se perfila el IGF-I como un factor clave para el desarrollo de la función auditiva y un candidato para la terapia regenerativa del oído interno


Introduction. Loss of hearing constitutes one of the most frequent disabling sensory impairments in the developed world. Different therapeutic approaches are currently being studied, including treatment with stem cells, genetic manipulation and pharmacological protection. Aim. To evaluate the role played by insulin-like growth factor-I (IGF-I) in the development, maintenance and repair of auditory functioning. Development. Proper development of the inner ear is dependent on a suitable coordination of the cell processes of proliferation, differentiation, neurogenesis and programmed cell death, which are regulated by different factors, one of which is IGF-I. During the embryogenesis of the inner ear, this factor is expressed in abundance and is essential for cell survival and maintaining neuronal precursors. Studies conducted in Igf-1–/– null mice have highlighted its importance in the development and continued functioning of the inner ear. Mice with a deficit in this gene display morphological disorders that correspond to severe functional deficiencies, which are confirmed by analysing brainstem auditory evoked potentials. A deficit of IGF-I in humans is also accompanied by profound sensory hypoacusis. Conclusions. In a scenario like this, IGF-I appears as a key factor in the development of auditory functioning and a candidate for regenerative therapy of the inner ear


Assuntos
Humanos , Orelha Interna/fisiologia , Fator de Crescimento Insulin-Like I/metabolismo , Fatores de Crescimento Neural/metabolismo , Audição/fisiologia , Transdução de Sinais/fisiologia , Orelha Interna/metabolismo , Orelha Interna/citologia
15.
Clin. transl. oncol. (Print) ; 9(8): 478-483, ago. 2007. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-123344

RESUMO

Neuroblastoma is one of the most frequently occurring solid tumours in children, especially in the first year of life, when it accounts for 50% of all tumours. It is the second most common cause of death in children, only preceded by accidents. The most peculiar characteristic of neuroblastoma is its clinical heterogeneity. Approximately half of the cases are classified as high risk, with overall survival rates around 40% despite intensive multimodal therapy. Nevertheless, other subsets of neuroblastomas will undergo spontaneous regression and others will show very slow progression. Despite many advances in the past three decades, neuroblastoma has remained an enigmatic challenge to clinical and basic scientists. Elucidation of the exact molecular pathways of neuroblastoma will enable researchers and clinicians to stratify the disease and adapt therapy to the risk of relapse or progression. This review focuses on recent advances in our understanding of the biology of this complex paediatric tumour. Neuroblastoma is already one of the first examples for the use of tumoral genetic markers as a tool for defining tumour behaviour and to aid clinical staging (AU)


Assuntos
Humanos , Masculino , Feminino , Neuroblastoma/diagnóstico , Neuroblastoma/genética , Estadiamento de Neoplasias/classificação , Estadiamento de Neoplasias/métodos , Apoptose , Perfilação da Expressão Gênica/métodos , Perfilação da Expressão Gênica , Marcadores Genéticos , Neuroblastoma/fisiopatologia , Transdução de Sinais , Fatores de Crescimento Neural/genética , Fatores de Crescimento Neural/metabolismo
16.
An. sist. sanit. Navar ; 29(3): 325-335, sept.-dic. 2006. ilus
Artigo em Es | IBECS | ID: ibc-052250

RESUMO

La enfermedad de Parkinson es la segunda enfermedad neurodegenerativa más común después del Alzheimer. Actualmente se dispone únicamente de terapias sintomáticas que, aunque son muy eficaces en las primeras etapas de la enfermedad poseen a largo plazo considerables efectos secundarios. La terapia ideal sería aquella que permitiese frenar o detener la progresión de la enfermedad. Este es el caso de las terapias neuroprotectoras y neurorestauradoras. De entre todas ellas, la terapia celular y la terapia con factores tróficos tipo GDNF son las que mayores expectativas han generado en la comunidad científica. Aunque ya se ha planteado el uso de GDNF para el tratamiento de la enfermedad de Parkinson, es necesario buscar nuevas estrategias que permitan administrar dicho factor neurotrófico en las zonas concretas del cerebro donde vaya a ejercer su acción. Aquí se discute el uso de micropartículas como el sistema más apropiado para la administración de dicho factor neurotrófico


Parkinson´s disease is the second most common neurodegenerative disorder after Alzheimer´s disease. Current therapies are symptomatic and, although these therapies are efficacious during the early stages of the disease, they present important side effects when they are used for a long time. The ideal therapy would be the one that would slow down or stop the progression of the disease. This can be achieved, for instance, with neuroprotective and neurorestorative therapies. Among them, cell therapy and therapy with trophic factors such as glial cell line derived neurotrophic factor (GDNF) are the most challenging and promising ones for the scientific community. Although the use of GDNF as a treatment for Parkinson ´s disease was proposed several years ago, it is necessary to develop alternative strategies to deliver GDNF appropriately to concrete areas of the brain. Here, the use of microspheres as the most suitable tool for the administration of this neurotrophic factor is discussed


Assuntos
Humanos , Doença de Parkinson/terapia , Fármacos Neuroprotetores/administração & dosagem , Di-Hidroxifenilalanina/farmacocinética , Terapia Baseada em Transplante de Células e Tecidos/métodos , Ubiquinona/farmacocinética , Fatores de Crescimento Neural/uso terapêutico
17.
Rev. neurol. (Ed. impr.) ; 43(7): 409-415, 1 oct., 2006. ilus
Artigo em Es | IBECS | ID: ibc-049632

RESUMO

Objetivo. Analizar datos y conceptos que se han generadoen torno a una de las funciones propuestas para el sueño: la restauraciónneuronal. Desarrollo. El sueño es un estado de concienciadiferente de la vigilia. Los mamíferos invierten una buena partede su vida en dormir; por ejemplo, los humanos dormimos una terceraparte de nuestra vida, pero ¿para qué invertir tanto tiempo enun estado donde perdemos contacto con el entorno?, ¿qué pasaríasi no durmiéramos? La privación de sueño total altera procesoscognitivos, como la memoria o la atención; si esta privación seprolonga, el sujeto se deteriora y muere. Se ha propuesto que elsueño sirve para restaurar a los organismos del desgaste ocurridodurante la vigilia y, dado que los primeros efectos de la ausenciade sueño se observan en procesos que dependen directamente delcerebro, se ha sugerido que la restauración neuronal es su principalobjetivo. En este trabajo se analizan algunos estudios sobre losefectos de la privación de sueño total en humanos y ratas, así comola relación entre el sueño y el sistema de las neurotrofinas, el cualpromueve la supervivencia y la restauración neuronal. Finalmente,se discuten teorías recientes sobre la función del sueño. Conclusiones.La restauración de las neuronas no es el fin último del sueño,sino mantener y reorganizar los circuitos neuronales, incluyendo laneoformación de sinapsis, que permiten modificar redes neuronalesexistentes, por efecto de la experiencia, y todo esto para el adecuadofuncionamiento del cerebro y su adaptación al ambiente


Aim. To analyse the data and concepts that have been produced in relation to one of the functions that have beensuggested for sleep, namely, neuronal recovery. Development. Sleep is a state of consciousness that is different to that ofarousal. Mammals devote an important part of their lives to sleeping; for example, as humans, we sleep for a third of our lives,but why do we spend so much time in a state where we lose contact with our surroundings? What would happen if we didn’tsleep? Total sleep deprivation alters cognitive processes such as memory or attention, and if this deprivation is prolonged, theindividual deteriorates and dies. It has been suggested that sleep provides the organism with time to recover from the wear andtear that occurs during the waking state and, given that the first effects of the absence of sleep are seen to affect processes thatare directly dependent on the brain, it has been claimed that its main purpose is to allow neuronal recovery. In this work weanalyse some of the studies on the effects of total sleep deprivation in humans and rats, as well as the relationship betweensleep and the neurotrophin system, which promotes neuronal survival and recovery. Finally, the latest theories about thefunction of sleep are discussed. Conclusions. Neuron recovery is not the ultimate purpose of sleep; rather it is to allow formaintenance and reorganisation of neuronal circuits, including new synapse formation, which enables existing neuronalnetworks to be modified by the effect of experience, and all this makes it possible for the brain to work properly and to adaptitself to the environment


Assuntos
Humanos , Sono/fisiologia , Neurônios/fisiologia , Privação do Sono , Sinapses/fisiologia , Fatores de Crescimento Neural/fisiologia , Plasticidade Neuronal
18.
Rev. neurol. (Ed. impr.) ; 41(11): 684-693, 1 dic., 2005. ilus
Artigo em Es | IBECS | ID: ibc-042672

RESUMO

Objetivo. Revisar, desde una perspectiva fundamentalmente clínica, las diferentes estrategias que tienen como finalidad la regeneración o restauración del sistema dopaminérgico nigroestriatal en la enfermedad de Parkinson (EP). En una primera parte se analizaron los resultados de los trasplantes de médula adrenal y de mesencéfalo fetal humano, y en este artículo se continúa con los trasplantes de otras estirpes celulares, la administración de factor estróficos y la terapia génica. Desarrollo. Como alternativa al trasplante fetal humano se han planteado otros procedimientos con similar mecanismo de acción 'dopaminérgico' (xenotrasplante porcino, células retinianas microencapsuladas), aunque con resultados poco consistentes. El trasplante de agregados celulares del cuerpo carotídeo podría ser una terapia prometedora por su mecanismo de acción neurotrófico. Se revisan también las perspectivas de la terapia celular basada en células modificadas genéticamente y en células precursoras de distinta procedencia. Entre otras estrategias neurorregenerativas, se analizan los resultados clínicos dela administración directa de factores neurotróficos y las perspectivas de la terapia génica in vivo. Conclusiones. El objetivo de una auténtica terapia neurorregenerativa para la EP debería ser, no sólo incrementar la función dopaminérgica estriatal, sino promoverla restauración trófica de los sistemas neuronales dañados. Tras el reciente fracaso de los métodos de administración directa(intraventricular e intraputaminal) de factor neurotrófico derivad o de una línea celular glial (GDNF), ha cobrado una mayor relevancia la investigación de otros métodos indirectos, como el trasplante de células productoras de GDNF -agregados celulares del cuerpo carotídeo, distintas células modificadas genéticamente- y la terapia génica in vivo (AU)


Objective. To review, from a mainly clinical standpoint, the different strategies applied to regenerate or restore the nigrostriatal dopaminergic system in Parkinson’s disease (PD). A previous first part focused on the results of adrenal medulla and human fetal mesencephalic transplants, and this second part addresses transplants of other cell types, administration of trophic factors, and gene therapy. Development. As an alternative to human fetal mesencephalic neurons, other donor cells types (porcine mesencephalic neurons, retinal pigment epithelial cells) with similar ‘dopaminergic’ action mechanism have been tried, although with heterogeneous results. Transplantation of carotid body cell aggregates may be a promising therapy because of its neurotrophic action mechanism. The perspectives of cell therapies based on genetically modified cells and precursor cells of different origin are also reviewed. Among other neuroregenerative approaches, the clinical outcomes of direct administration of neurotrophic factors and the perspectives for in vivo gene therapy are also addressed. Conclusions. The objective of neuroregenerative therapy for PD should include trophic restoration of damaged neuronal systems, since improvement in striatal dopaminergic function is not sufficient. After the recent failure of the direct (intraventricular orintraputaminal) administration of glial cell line-derived neurotrophic factor (GDNF), attention of researchers has focused on indirect methods, including transplantation of GDNF-producing cells (carotid body cell aggregates or different genetically modified cells), and in vivo gene therapy (AU)


Assuntos
Humanos , Terapia Genética , Doença de Parkinson/terapia , Terapia Baseada em Transplante de Células e Tecidos , Transplante de Tecido Encefálico , Corpo Estriado/metabolismo , Corpo Estriado/patologia , Dopamina/metabolismo , Fatores de Crescimento Neural/uso terapêutico , Regeneração Nervosa/fisiologia , Fármacos Neuroprotetores/uso terapêutico
19.
Rev. neurol. (Ed. impr.) ; 41(10): 604-614, nov. 2005. tab
Artigo em Es | IBECS | ID: ibc-042990

RESUMO

Objetivo. Revisar, desde una perspectiva fundamentalmente clínica, las diferentes estrategias que tienen como finalidad la regeneración o restauración del sistema dopaminérgico nigroestriatal en la enfermedad de Parkinson. En esta primera parte se analizan los resultados de los trasplantes de médula adrenal y de mesencéfalo fetal humano, y se continúa en una segunda parte con los trasplantes de otras estirpes celulares, la administración de factores tróficos y la terapia génica. Desarrollo. Los trasplantes de médula adrenal se abandonaron por la inconsistencia de sus resultados y su elevada morbilidad. Los trasplantes de mesencéfalo fetal poseen capacidad para restaurar a largo plazo el déficit de dopamina estriatal; sin embargo, este efecto neuroquímico ha demostrado ser clínicamente insuficiente en presencia de una degeneración neuronal progresiva. En este contexto, otras estrategias con similar mecanismo de acción ‘dopaminérgico’ no suponen una alternativa. Conclusiones. El objetivo de una auténtica terapia neurorregenerativa para la enfermedad de Parkinson debería ser no sólo incrementar la función dopaminérgica estriatal, sino promover la restauración trófica de los sistemas neuronales dañados. Tras el reciente fracaso de los métodos de administración directa (intraventricular e intraputaminal) de factor neurotrófico derivado de una línea celular glial (GDNF), ha cobrado una mayor relevancia la investigación de otros métodos indirectos, como el trasplante de células productoras de GDNF (agregados celulares del cuerpo carotídeo, distintas células modificadas genéticamente) y la terapia génica in vivo


Objective. To review, from a mainly clinical standpoint, the different strategies applied to regenerate or restore the nigrostriatal dopaminergic system in Parkinson’s disease. This first part focuses on the results of adrenal medulla and human fetal mesencephalic transplants, and a second part will address transplants of other cell types, administration of trophic factors, and gene therapy. Development. Adrenal medulla transplants were abandoned because of their inconsistent results and high morbidity. Although fetal mesencephalic transplantation can produce long-term restoration of striatal dopamine deficiency, this neurochemical effect is clinically inadequate in presence of progressive neuronal loss. Other strategies with similar ‘dopaminergic’ action mechanism are not a therapeutic option in this setting. Conclusions. The objective of neuroregenerative therapy for Parkinson’s disease should include trophic restoration of damaged neuronal systems, since improvement in striatal dopaminergic function is not sufficient. After the recent failure of the direct (intraventricular or intraputaminal) administration of glial cell line-derived neurotrophic factor (GDNF), attention of researchers has focused on indirect methods, including transplantation of GDNF-producing cells (carotid body cell aggregates or different genetically modified cells, including stem cells), and in vivo gene therapy


Assuntos
Humanos , Transplante de Tecido Fetal , Regeneração Nervosa/fisiologia , Doença de Parkinson/patologia , Doença de Parkinson/terapia , Medula Suprarrenal/transplante , Corpo Estriado/patologia , Corpo Estriado/fisiologia , Dopamina/metabolismo , Terapia Genética , Fatores de Crescimento Neural/metabolismo , Fatores de Crescimento Neural/uso terapêutico , Doença de Parkinson/fisiopatologia , Resultado do Tratamento
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