Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 2.029
Filtrar
1.
Cell Adh Migr ; 15(1): 261-271, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34494935

RESUMO

Serotonin is well known as a neurotransmitter. Its roles in neuronal processes such as learning, memory or cognition are well established, and also in disorders such as depression, schizophrenia, bipolar disorder, and dementia. However, its effects on adhesion and cytoskeletal remodelling which are strongly affected by 5-HT receptors, are not as well studied with some exceptions for e.g. platelet aggregation. Neuronal function is strongly dependent on cell-cell contacts and adhesion-related processes. Therefore the role played by serotonin in psychiatric illness, as well as in the positive and negative effects of neuropsychiatric drugs through cell-related adhesion can be of great significance. In this review, we explore the role of serotonin in some of these aspects based on recent findings.


Assuntos
Adesão Celular/fisiologia , Movimento Celular/fisiologia , Citoesqueleto/fisiologia , Neurotransmissores/fisiologia , Serotonina/fisiologia , Animais , Humanos , Transtornos Mentais/metabolismo
2.
Int J Mol Sci ; 22(17)2021 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-34502322

RESUMO

Vasopressin is a ubiquitous molecule playing an important role in a wide range of physiological processes thereby implicated in the pathomechanism of many disorders. Its effect is well characterized through V2 receptors, which regulates the water resorption in kidney, while its vasoconstrictory effect through V1a receptor also received a lot of attention in the maintenance of blood pressure during shock. However, the most striking is its central effect both through the V1b receptors in stress-axis regulation as well as through V1a receptors regulating many aspects of our behavior (e.g., social behavior, learning and memory). Vasopressin has been implicated in the development of depression, due to its connection with chronic stress, as well as schizophrenia because of its involvement in social interactions and memory processes. Epigenetic changes may also play a role in the development of these disorders. The possible mechanism includes DNA methylation, histone modification and/or micro RNAs, and these possible regulations will be in the focus of our present review.


Assuntos
Epigênese Genética , Homeostase , Transtornos Mentais/patologia , Receptores de Vasopressinas/metabolismo , Vasopressinas/metabolismo , Animais , Humanos , Transtornos Mentais/genética , Transtornos Mentais/metabolismo , Receptores de Vasopressinas/genética , Transdução de Sinais , Vasopressinas/genética
3.
Chem Biol Interact ; 345: 109564, 2021 Aug 25.
Artigo em Inglês | MEDLINE | ID: mdl-34161785

RESUMO

Suppressive effect of bis (3-amino-2-pyridine) diselenide (BAPD) on psychiatric disorders - atopic dermatitis (AD) comorbidity in mice was investigated. To sensitize the animals, 2,4-dinitrochlorobenzene (DNCB) was applied to their dorsal skin on days 1-3. Mice were challenged with DNCB on their ears and dorsal skin on days 14, 17, 20, 23, 26, and 29. BAPD and Dexamethasone were administered to the animals, from days 14-29, and skin severity scores and behavioral tests were determined. Oxidative stress and inflammatory parameters were evaluated on the dorsal skin of mice. Na+, K+-ATPase activity and corticosterone levels were determined in hippocampus/cerebral cortex and plasma of mice, respectively. BAPD improved cutaneous damage, scratching behavior, inflammatory and oxidative stress markers. BAPD showed anxiolytic- and antidepressant-like effects and restored Na+, K+-ATPase activity and corticosterone levels. The present study was performed using female mice due the susceptibility for this disease. But, the evaluation of AD model in male mice would help to verify whether the male gender has the same predisposition to present this pathology. Our data demonstrated the suppressive effect of BAPD on psychiatric disorders - AD comorbidity by regulating inflammatory and oxidative status in mice.


Assuntos
Dermatite Atópica/tratamento farmacológico , Dermatite Atópica/epidemiologia , Transtornos Mentais/tratamento farmacológico , Transtornos Mentais/epidemiologia , Siloxanas/farmacologia , Animais , Comportamento Animal/efeitos dos fármacos , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Comorbidade , Corticosterona/sangue , Corticosterona/metabolismo , Dermatite Atópica/complicações , Dermatite Atópica/metabolismo , Feminino , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Inflamação/complicações , Transtornos Mentais/complicações , Transtornos Mentais/metabolismo , Camundongos , Oxirredução/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Siloxanas/uso terapêutico
4.
Biomolecules ; 11(5)2021 05 11.
Artigo em Inglês | MEDLINE | ID: mdl-34064602

RESUMO

Biomolecules has launched a Special Issue entitled "Dopamine D3 Receptor: Contemporary Views of Its Function and Pharmacology for Neuropsychiatric Diseases [...].


Assuntos
Transtornos Mentais/tratamento farmacológico , Neuropsiquiatria/métodos , Receptores de Dopamina D3/metabolismo , Animais , Humanos , Transtornos Mentais/metabolismo , Publicações/estatística & dados numéricos
5.
CNS Drugs ; 35(4): 345-384, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33866523

RESUMO

As many patients with underlying psychiatric disorders may be infected with COVID-19, and COVID-19-affected subjects may frequently experience a new onset of psychiatric manifestations, concomitant use of psychotropic medications and COVID-19 therapies is expected to be highly likely and raises concerns of clinically relevant drug interactions. In this setting, four major mechanisms responsible for drug interactions involving psychotropic agents and COVID-19 therapies may be identified: (1) pharmacokinetic drug-drug interactions mainly acting on cytochrome P450; (2) pharmacodynamic drug-drug interactions resulting in additive or synergistic toxicity; (3) drug-disease interactions according to stage and severity of the disease; and (4) pharmacogenetic issues associated with polymorphisms of cytochrome P450 isoenzymes. In this review, we summarise the available literature on relevant drug interactions between psychotropic agents and COVID-19 therapies, providing practical clinical recommendations and potential management strategies according to severity of illness and clinical scenario.


Assuntos
COVID-19/tratamento farmacológico , Reposicionamento de Medicamentos/tendências , Transtornos Mentais/metabolismo , Psicotrópicos/efeitos adversos , Psicotrópicos/metabolismo , Antivirais/efeitos adversos , Antivirais/farmacocinética , COVID-19/genética , COVID-19/metabolismo , Interações Medicamentosas/fisiologia , Humanos , Transtornos Mentais/tratamento farmacológico , Transtornos Mentais/genética , Farmacogenética/tendências
6.
Biomolecules ; 11(2)2021 02 20.
Artigo em Inglês | MEDLINE | ID: mdl-33672636

RESUMO

The prevalence of patients suffering from mental disorders is substantially increasing in recent years and represents a major burden to society. The underlying causes and neuronal circuits affected are complex and difficult to unravel. Frequent disorders such as depression, schizophrenia, autism, and bipolar disorder share links to the habenular neural circuit. This conserved neurotransmitter system relays cognitive information between different brain areas steering behaviors ranging from fear and anxiety to reward, sleep, and social behaviors. Advances in the field using the zebrafish model organism have uncovered major genetic mechanisms underlying the formation of the habenular neural circuit. Some of the identified genes involved in regulating Wnt/beta-catenin signaling have previously been suggested as risk genes of human mental disorders. Hence, these studies on habenular genetics contribute to a better understanding of brain diseases. We are here summarizing how the gained knowledge on the mechanisms underlying habenular neural circuit development can be used to introduce defined manipulations into the system to study the functional behavioral consequences. We further give an overview of existing behavior assays to address phenotypes related to mental disorders and critically discuss the power but also the limits of the zebrafish model for identifying suitable targets to develop therapies.


Assuntos
Habenula/fisiologia , Transtornos Mentais/genética , Peixe-Zebra/genética , Animais , Ansiedade , Axônios/metabolismo , Comportamento Animal , Depressão/tratamento farmacológico , Depressão/metabolismo , Depressão/fisiopatologia , Modelos Animais de Doenças , Habenula/metabolismo , Transtornos Mentais/metabolismo , Mutação , Rede Nervosa , Neurogênese , Neurônios/metabolismo , Neurotransmissores , Fenótipo , Comportamento Social , Proteínas Wnt/metabolismo , Via de Sinalização Wnt , Peixe-Zebra/fisiologia , Proteínas de Peixe-Zebra/genética
7.
Commun Biol ; 4(1): 301, 2021 03 08.
Artigo em Inglês | MEDLINE | ID: mdl-33686216

RESUMO

Network architecture is a brain-organizational motif present across spatial scales from cell assemblies to distributed systems. Structural pathology in some neurodegenerative disorders selectively afflicts a subset of functional networks, motivating the network degeneration hypothesis (NDH). Recent evidence suggests that structural pathology recapitulating physiology may be a general property of neuropsychiatric disorders. To test this possibility, we compared functional and structural network meta-analyses drawing upon the BrainMap database. The functional meta-analysis included results from >7,000 experiments of subjects performing >100 task paradigms; the structural meta-analysis included >2,000 experiments of patients with >40 brain disorders. Structure-function network concordance was high: 68% of networks matched (pFWE < 0.01), confirming the broader scope of NDH. This correspondence persisted across higher model orders. A positive linear association between disease and behavioral entropy (p = 0.0006;R2 = 0.53) suggests nodal stress as a common mechanism. Corroborating this interpretation with independent data, we show that metabolic 'cost' significantly differs along this transdiagnostic/multimodal gradient.


Assuntos
Encéfalo/patologia , Encéfalo/fisiopatologia , Transtornos Mentais/patologia , Transtornos Mentais/fisiopatologia , Degeneração Neural , Doenças Neurodegenerativas/patologia , Doenças Neurodegenerativas/fisiopatologia , Encéfalo/diagnóstico por imagem , Encéfalo/metabolismo , Mapeamento Encefálico , Estudos de Casos e Controles , Humanos , Transtornos Mentais/diagnóstico por imagem , Transtornos Mentais/metabolismo , Rede Nervosa/patologia , Rede Nervosa/fisiopatologia , Metanálise em Rede , Doenças Neurodegenerativas/diagnóstico por imagem , Doenças Neurodegenerativas/metabolismo
8.
Biochim Biophys Acta Mol Basis Dis ; 1867(5): 166098, 2021 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-33545299

RESUMO

Astrocytes represent the reticular part of the central nervous system; gap junctions formed by connexins Cx43, Cx30- and Cx26 provide for homocellular astrocyte-astrocyte coupling, whereas connexins Cx30, Cx32, Cx43, and Cx47 connect astrocytes and oligodendrocytes. Astroglial networks are anatomically and functionally segregated being homologous to neuronal ensembles. Connexons, gap junctions and hemichannels (unpaired connexons) are affected in various neuropathologies from neuropsychiatric to neurodegenerative diseases. Manipulation of astrocytic connexins modulates the size and outreach of astroglial syncytia thus affecting astroglial homeostatic support. Modulation of astrocytic connexin significantly modifies pharmacological profile of many CNS drugs, which represents an innovative therapeutic approach for CNS disorders; this approach is now actively tested in pre-clinical and clinical studies. Wide combination of connexin modulators with CNS drugs open new promising perspectives for fundamental studies and therapeutic strategies.


Assuntos
Conexinas/antagonistas & inibidores , Transtornos Mentais/terapia , Doenças do Sistema Nervoso/terapia , Animais , Conexinas/metabolismo , Humanos , Transtornos Mentais/metabolismo , Transtornos Mentais/patologia , Terapia de Alvo Molecular , Doenças do Sistema Nervoso/metabolismo , Doenças do Sistema Nervoso/patologia
9.
Anat Sci Int ; 96(3): 333-342, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33604770

RESUMO

Polyunsaturated fatty acids (PUFAs) are essential for brain development and function. Increasing evidence has shown that an imbalance of PUFAs is associated with various human psychiatric disorders, including autism and schizophrenia. However, the mechanisms underlying the effects of PUFAs on brain functions at cellular and molecular levels remain unclear. Since PUFAs are insoluble in water, specific transporters are required to deliver PUFAs to appropriate intracellular compartments. Fatty acid-binding proteins (FABPs), the cellular chaperones of PUFAs, are involved in PUFA intracellular trafficking, signal transduction, and gene transcription. Therefore, we focused on the relationship between FABP-regulated PUFA homeostasis in the brain and neuronal plasticity. The authors previously reported that FABP3, which preferentially binds to n-6 PUFAs, is strongly expressed in the gamma-aminobutyric acid (GABAergic) inhibitory interneurons of the adult mouse anterior cingulate cortex (ACC), which is a component of the limbic cortex and is important for the coordination of cognitive and emotional behaviors. Interestingly, Fabp3 KO mice show increased GABA synthesis and abnormal excitatory/inhibitory balance in the ACC. In addition, studies have indicated that FABP7, which preferentially binds to n-3 PUFAs, controls lipid raft function in astrocytes, and astrocytic Fabp7 deficiency results in an altered response of astrocytes to external stimuli. Furthermore, Fabp7 KO mice exhibit aberrant dendritic morphology, and decreased spine density and excitatory synaptic transmission in pyramidal neurons. This review summarizes relationship between PUFAs or FABPs and human psychiatric disorders and discusses recent progress in elucidating the function of FABPs, especially FABP3 and 7, in the brain.


Assuntos
Encéfalo/metabolismo , Proteínas de Ligação a Ácido Graxo/metabolismo , Transtornos Mentais/metabolismo , Animais , Proteína 3 Ligante de Ácido Graxo/genética , Proteína 3 Ligante de Ácido Graxo/metabolismo , Proteínas de Ligação a Ácido Graxo/genética , Humanos , Transtornos Mentais/genética , Camundongos , Camundongos Knockout
10.
Cell Mol Life Sci ; 78(9): 4189-4200, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33558994

RESUMO

Mammalian brain presents extraordinary complexity reflected in the structure, function, and dynamic changes in the biological and physiological processes of development, maturity, and aging. Recent transcriptomic profiles from the brain tissues of distinct species have described a novel class of transcripts with a covalently closed-loop structure, called circular RNAs (circRNAs), which are produced by alternative back-splicing and derived from genes associated with synaptogenesis and neural activities. Brain is a tightly regulated and largely unexplored organ where circRNAs are highly enriched and expressed in the cell type-, spatiotemporal-specific, sex-biased, and age-related manner. Although the biological functions of most of the circRNAs in the brain remain elusive, increased evidence suggests that dynamic changes in circRNA expression are critical for brain function and the maintenance of physiological homeostasis in the brain. Here, we review the latest immense progresses in the understanding of circRNA expression and function in the mammalian brain. We also discuss possibly biological functions of circRNAs in the brain, which may provide new sights of understanding brain development and aging, as well as the pathogenesis of mental diseases.


Assuntos
Encéfalo/metabolismo , RNA Circular/metabolismo , Envelhecimento , Animais , Biomarcadores/metabolismo , Encéfalo/citologia , Encéfalo/crescimento & desenvolvimento , Humanos , Transtornos Mentais/genética , Transtornos Mentais/metabolismo , Transtornos Mentais/patologia , Células-Tronco Neurais/citologia , Células-Tronco Neurais/metabolismo , Doenças Neurodegenerativas/genética , Doenças Neurodegenerativas/metabolismo , Doenças Neurodegenerativas/patologia
11.
Clin Neurophysiol ; 132(2): 429-448, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33465534

RESUMO

OBJECTIVE: Repetitive transcranial magnetic stimulation (rTMS) is an evidenced based treatment for depression and an emerging treatment for several other neuropsychiatric disorders. The objective of this systematic review was to assess molecular changes produced by rTMS or molecular markers that predict treatment response in neuropsychiatric disorders. METHODS: PubMed, PsycINFO, and Embase were searched through July 2019 for studies published in peer-reviewed journals. Eighty-nine studies were identified examining healthy adults and patients with neuropsychiatric disorders including depression, chronic pain, post-stroke deficits, and movement disorders. RESULTS: Our ability to synthesize the information was limited by the large variability in treatment parameters and a limited number of placebo-controlled studies. While few findings were replicated by multiple strong studies, brain derived neurotrophic factor (BDNF) and gamma aminobutyric acid (GABA) in depression, BDNF in post-stroke deficits, and ß-endorphin in chronic pain may be altered by rTMS. CONCLUSION: BDNF, GABA and ß-endorphin were identified as potential molecular markers of rTMS and warrant further exploration. SIGNIFICANCE: This study, which is the first systematic review to examine molecular markers of rTMS in both neurological and psychiatric disorders, provides an updated review of this subject and highlight the need for more placebo-controlled and adequately powered studies to identify biomarkers of rTMS.


Assuntos
Transtornos Mentais/terapia , Doenças do Sistema Nervoso/terapia , Estimulação Magnética Transcraniana/métodos , Biomarcadores/metabolismo , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Humanos , Transtornos Mentais/metabolismo , Doenças do Sistema Nervoso/metabolismo , beta-Endorfina/metabolismo , Ácido gama-Aminobutírico/metabolismo
12.
Neuron ; 109(4): 576-596, 2021 02 17.
Artigo em Inglês | MEDLINE | ID: mdl-33385325

RESUMO

Astrocytes are a large and diverse population of morphologically complex cells that exist throughout nervous systems of multiple species. Progress over the last two decades has shown that astrocytes mediate developmental, physiological, and pathological processes. However, a long-standing open question is how astrocytes regulate neural circuits in ways that are behaviorally consequential. In this regard, we summarize recent studies using Caenorhabditis elegans, Drosophila melanogaster, Danio rerio, and Mus musculus. The data reveal diverse astrocyte mechanisms operating in seconds or much longer timescales within neural circuits and shaping multiple behavioral outputs. We also refer to human diseases that have a known primary astrocytic basis. We suggest that including astrocytes in mechanistic, theoretical, and computational studies of neural circuits provides new perspectives to understand behavior, its regulation, and its disease-related manifestations.


Assuntos
Astrócitos/metabolismo , Transtornos Mentais/metabolismo , Rede Nervosa/metabolismo , Neurônios/metabolismo , Animais , Astrócitos/patologia , Caenorhabditis elegans , Drosophila , Humanos , Transtornos Mentais/genética , Transtornos Mentais/patologia , Camundongos , Rede Nervosa/patologia , Neurônios/patologia , Especificidade da Espécie , Peixe-Zebra
13.
Science ; 371(6527)2021 Jan 22.
Artigo em Inglês | MEDLINE | ID: mdl-33479124

RESUMO

The cerebral cortex is an intricate structure that controls human features such as language and cognition. Cortical functions rely on specialized neurons that emerge during development from complex molecular and cellular interactions. Neurodevelopmental disorders occur when one or several of these steps is incorrectly executed. Although a number of causal genes and disease phenotypes have been identified, the sequence of events linking molecular disruption to clinical expression mostly remains obscure. Here, focusing on human malformations of cortical development, we illustrate how complex interactions at the genetic, cellular, and circuit levels together contribute to diversity and variability in disease phenotypes. Using specific examples and an online resource, we propose that a multilevel assessment of disease processes is key to identifying points of vulnerability and developing new therapeutic strategies.


Assuntos
Córtex Cerebral/anormalidades , Transtornos Mentais/metabolismo , Doenças do Sistema Nervoso/metabolismo , Neurogênese/fisiologia , Neurônios/fisiologia , Animais , Comportamento , Movimento Celular/genética , Movimento Celular/fisiologia , Córtex Cerebral/metabolismo , Córtex Cerebral/ultraestrutura , Regulação da Expressão Gênica no Desenvolvimento , Humanos , Transtornos Mentais/genética , Camundongos , Doenças do Sistema Nervoso/genética , Vias Neurais/anormalidades , Vias Neurais/metabolismo , Vias Neurais/ultraestrutura , Neurogênese/genética , Neurônios/citologia , Especificidade de Órgãos/genética , Especificidade de Órgãos/fisiologia
14.
Neurosci Lett ; 746: 135618, 2021 02 16.
Artigo em Inglês | MEDLINE | ID: mdl-33429002

RESUMO

Stress is a common seizure trigger in persons with epilepsy. The body's physiological response to stress is mediated by the hypothalamic-pituitary-adrenal (HPA) axis and involves a hormonal cascade that includes corticotropin releasing hormone (CRH), adrenocorticotropin releasing hormone (ACTH) and the release of cortisol (in humans and primates) or corticosterone (in rodents). The prolonged exposure to stress hormones may not only exacerbate pre-existing medical conditions including epilepsy, but may also increase the predisposition to psychiatric comorbidities. Hyperactivity of the HPA axis negatively impacts the structure and function of the temporal lobe of the brain, a region that is heavily involved in epilepsy and mood disorders like anxiety and depression. Seizures themselves damage temporal lobe structures, further disinhibiting the HPA axis, setting off a vicious cycle of neuronal damage and increasing susceptibility for subsequent seizures and psychiatric comorbidity. Treatments targeting the HPA axis may be beneficial both for epilepsy and for associated stress-related comorbidities such as anxiety or depression. This paper will highlight the evidence demonstrating dysfunction in the HPA axis associated with epilepsy which may contribute to the comorbidity of psychiatric disorders and epilepsy, and propose treatment strategies that may dually improve seizure control as well as alleviate stress related psychiatric comorbidities.


Assuntos
Epilepsia/metabolismo , Sistema Hipotálamo-Hipofisário/metabolismo , Transtornos Mentais/metabolismo , Sistema Hipófise-Suprarrenal/metabolismo , Hormônio Adrenocorticotrópico/antagonistas & inibidores , Hormônio Adrenocorticotrópico/metabolismo , Animais , Anticonvulsivantes/administração & dosagem , Corticosterona/antagonistas & inibidores , Corticosterona/metabolismo , Desoxicorticosterona/antagonistas & inibidores , Desoxicorticosterona/metabolismo , Epilepsia/tratamento farmacológico , Epilepsia/epidemiologia , Humanos , Sistema Hipotálamo-Hipofisário/efeitos dos fármacos , Transtornos Mentais/tratamento farmacológico , Transtornos Mentais/epidemiologia , Sistema Hipófise-Suprarrenal/efeitos dos fármacos , Resultado do Tratamento
15.
Scott Med J ; 66(1): 3-10, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32718266

RESUMO

BACKGROUND & AIMS: Though viewed as a critical measure to prevent the spread of the virus, a prolonged homestay may result in unfavourable sedentary behaviour and chronic disease risk. This systematic review focuses on sedentary behaviour resulting from this quarantine period which may elevate the cardiovascular disease risk, obesity, hypertension, cancer and mental health illness. METHODS: Evidence of breaking sedentary behaviour and global recommendations were investigated. Potential unanswered questions regarding sedentary behaviour and physical activity during lockdown were explored. RESULTS: Five systematic reviews and six prospective trials explored the effect of sedentarism affecting chronic disease through potential pathophysiological mechanisms. Sedentary behaviour especially prolonged sitting is found to be a pleiotropic risk factor with altered energy expenditure, adipogenic signalling, immunomodulation, autonomic stability and hormonal dysregulation perpetuating underlying chronic diseases such as obesity, cardiovascular disease, cancer and mental health disorders. CONCLUSION: Breaking sitting and physical activity are found to reverse the adverse effects associated with excessive sitting during the lockdown.


Assuntos
COVID-19/prevenção & controle , Doenças Cardiovasculares/epidemiologia , Controle de Doenças Transmissíveis , Transtornos Mentais/epidemiologia , Obesidade/epidemiologia , Política Pública , Comportamento Sedentário , Fatores de Risco Cardiometabólico , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Doença Crônica , Exercício Físico , Humanos , Transtornos Mentais/metabolismo , Transtornos Mentais/fisiopatologia , Neoplasias/epidemiologia , Neoplasias/metabolismo , Neoplasias/fisiopatologia , Obesidade/metabolismo , Obesidade/fisiopatologia , SARS-CoV-2
16.
Neurosci Lett ; 741: 135540, 2021 01 10.
Artigo em Inglês | MEDLINE | ID: mdl-33278505

RESUMO

Dopamine (DA), a critical neurotransmitter of both the central and peripheral nerve system, plays important roles in a series of biological processes. Dysfunction of dopaminergic signalling may lead to a series of developmental disorders, including attention deficit/hyperactivity disorder, autism and schizophrenia. However, the exact roles of dopaminergic signalling in these diseases are far from fully understood. We analyse the roles of dopaminergic signalling in multiple physiological and pathological processes, focusing on brain development and related disorders. By summarizing current research in this area, we provide guidance for future studies. This review seeks to deepen our understanding of dopaminergic signalling in developmental disorders, which may offer clues for developing more effective therapeutic drugs.


Assuntos
Encéfalo/crescimento & desenvolvimento , Encéfalo/metabolismo , Dopamina/metabolismo , Transtornos Mentais/metabolismo , Doenças do Sistema Nervoso/metabolismo , Animais , Transtorno do Deficit de Atenção com Hiperatividade/metabolismo , Transtorno do Espectro Autista/metabolismo , Humanos , Neurogênese , Neurônios/metabolismo , Esquizofrenia/metabolismo , Transdução de Sinais
17.
J Neurosci ; 41(5): 891-900, 2021 02 03.
Artigo em Inglês | MEDLINE | ID: mdl-33257322

RESUMO

A revamped interest in the study of hallucinogens has recently emerged, especially with regard to their potential application in the treatment of psychiatric disorders. In the last decade, a plethora of preclinical and clinical studies have confirmed the efficacy of ketamine in the treatment of depression. More recently, emerging evidence has pointed out the potential therapeutic properties of psilocybin and LSD, as well as their ability to modulate functional brain connectivity. Moreover, MDMA, a compound belonging to the family of entactogens, has been demonstrated to be useful to treat post-traumatic stress disorders. In this review, the pharmacology of hallucinogenic compounds is summarized by underscoring the differences between psychedelic and nonpsychedelic hallucinogens as well as entactogens, and their behavioral effects in both animals and humans are described. Together, these data substantiate the potentials of these compounds in treating mental diseases.


Assuntos
Alucinógenos/administração & dosagem , Ketamina/administração & dosagem , Dietilamida do Ácido Lisérgico/administração & dosagem , Transtornos Mentais/tratamento farmacológico , N-Metil-3,4-Metilenodioxianfetamina/administração & dosagem , Psilocibina/administração & dosagem , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Humanos , Transtornos Mentais/metabolismo , Transtornos Mentais/psicologia , Saúde Mental/tendências , Ensaios Clínicos Controlados Aleatórios como Assunto/métodos
18.
Mol Psychiatry ; 26(1): 66-69, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33099577

RESUMO

There is an increasing body of knowledge on the influence of differential DNA methylation of specific genomic regions in psychiatric disorders. However, fewer studies have addressed global DNA methylation (GMe) levels. GMe is an estimative of biological functioning that is regulated by pervasive mechanisms able to capture the big picture of metabolic and environmental influences upon gene expression. In the present perspective article, we highlighted evidence for the relationships between cortisol and sex hormones and GMe in psychiatric disorders. We argue that the far-reaching effects of cortisol and sexual hormones on GMe may lie on the pathways linking stress and mental health. Further research on these endocrine-epigenetic links may help to explain the role of environmental stress as well as sex differences in the prevalence of psychiatric disorders.


Assuntos
Metilação de DNA , Hormônios Esteroides Gonadais/metabolismo , Hidrocortisona/metabolismo , Transtornos Mentais/genética , Transtornos Mentais/metabolismo , Metilação de DNA/genética , Epigênese Genética , Humanos , Caracteres Sexuais
19.
Food Chem Toxicol ; 148: 111945, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33359022

RESUMO

Glutathione peroxidase (GPx) acts in co-ordination with other signaling molecules to exert its own antioxidant role. We have demonstrated the protective effects of GPx,/GPx-1, a selenium-dependent enzyme, on various neurodegenerative disorders (i.e., Parkinson's disease, Alzheimer's disease, cerebral ischemia, and convulsive disorders). In addition, we summarized the recent findings indicating that GPx-1 might play a role as a neuromodulator in neuropsychiatric conditions, such as, stress, bipolar disorder, schizophrenia, and drug intoxication. In this review, we attempted to highlight the mechanistic scenarios mediated by the GPx/GPx-1 gene in impacting these neurodegenerative and neuropsychiatric disorders, and hope to provide new insights on the therapeutic interventions against these disorders.


Assuntos
Glutationa Peroxidase/metabolismo , Transtornos Mentais/metabolismo , Doenças Neurodegenerativas/metabolismo , Neuroproteção/fisiologia , Animais , Azóis/uso terapêutico , Glutationa Peroxidase/genética , Humanos , Raios Infravermelhos , Transtornos Mentais/tratamento farmacológico , Transtornos Mentais/terapia , Doenças Neurodegenerativas/tratamento farmacológico , Doenças Neurodegenerativas/terapia , Óxido Nítrico Sintase Tipo III/metabolismo , Compostos Organosselênicos/uso terapêutico , Fototerapia , Proteína Quinase C-delta/metabolismo , Receptor Muscarínico M1/metabolismo , Regulação para Cima/efeitos da radiação
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...