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1.
Int J Mol Sci ; 22(19)2021 Oct 02.
Artigo em Inglês | MEDLINE | ID: mdl-34639048

RESUMO

Cognitive function decline is strictly related to age, resulting in the loss of the ability to perform daily behaviors and is a fundamental clinical neurodegeneration symptom. It has been proven that an adequate diet, comprehensive nutrition, and a healthy lifestyle may significantly inhibit neurodegenerative processes, improving cognitive functions. Therefore, intensive research has been conducted on cognitive-enhancing treatment for many years, especially with substances of natural origin. There are several intervention programs aimed at improving cognitive functions in elderly adults. Cognitive functions depend on body weight, food consumed daily, the quality of the intestinal microflora, and the supplements used. The effectiveness in the prevention of dementia is particularly high before the onset of the first symptoms. The impact of diet and nutrition on age-associated cognitive decline is becoming a growing field as a vital factor that may be easily modified, and the effects may be observed on an ongoing basis. The paper presents a review of the latest preclinical and clinical studies on the influence of natural antioxidants on cognitive functions, with particular emphasis on neurodegenerative diseases. Nevertheless, despite the promising research results in animal models, the clinical application of natural compounds will only be possible after solving a few challenges.


Assuntos
Envelhecimento , Antioxidantes/uso terapêutico , Produtos Biológicos/uso terapêutico , Transtornos Cognitivos/tratamento farmacológico , Transtornos Cognitivos/etiologia , Doenças Neurodegenerativas/complicações , Animais , Antioxidantes/farmacologia , Produtos Biológicos/farmacologia , Ensaios Clínicos como Assunto , Cognição/efeitos dos fármacos , Transtornos Cognitivos/diagnóstico , Disfunção Cognitiva/diagnóstico , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/etiologia , Suplementos Nutricionais , Avaliação Pré-Clínica de Medicamentos , Humanos , Doenças Neurodegenerativas/tratamento farmacológico , Doenças Neurodegenerativas/etiologia , Resultado do Tratamento
2.
Artigo em Russo | MEDLINE | ID: mdl-34481437

RESUMO

OBJECTIVE: To investigate whether visual processing abnormalities are the result of visual dysfunction involving cognitive impairment or independent abnormalities and to identify the relationship of visual impairments with cognitive functions and severity of psychopathological symptoms. MATERIAL AND METHODS: We compared results of visual size perception and actions on objects (motor assessment) in patients with schizophrenia (n=37), including patients with non-resistant schizophrenia (n=19) and healthy individuals (n=20). Cognitive impairments were assessed with BACS. Severity of schizophrenia symptoms was assessed with PANSS. RESULTS: The error in the visual size perception test was smaller in healthy controls compared with non-resistant patients (p<0.03). There are no significant differences between non-resistant patients and other groups. Also, there are no significant differences in motor assessment between healthy controls and patients with schizophrenia. In the visual size perception test, the amount of error correlates with cognitive impairments (r= -0.84, p<0.001), and the severity of psychotic symptoms on PANSS (r=0.55, p<0.05). CONCLUSION: Changes in visual threshold in patients with schizophrenia are correlated with cognitive dysfunction and reflect dysfunction in the parvocellular system.


Assuntos
Transtornos Cognitivos , Disfunção Cognitiva , Esquizofrenia , Cognição , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Disfunção Cognitiva/diagnóstico , Disfunção Cognitiva/etiologia , Humanos , Testes Neuropsicológicos , Esquizofrenia/complicações
3.
Artigo em Russo | MEDLINE | ID: mdl-34481451

RESUMO

On June 25-26, 2021, a round table was held in Kazan with the participation of leading neurologists of Russia, where the issues of treatment of patients with cognitive impairment due to cerebrovascular diseases were discussed. Cognitive disorders of vascular genesis (VCD) are widespread in the population, are a common cause of a decrease in the quality of life and restriction of daily activity. The cause of VCD is both acute and chronic cerebrovascular diseases. An effective way to prevent VCD is to control cardiovascular risk factors, ensure a sufficient level of cognitive and physical activity throughout life. The role of drug therapy, aimed, among other things, at normalizing metabolic processes in the brain, is extremely important. The data on the mechanisms of action of the new domestic drug prospecta, the results of its clinical trials in patients with VCD are presented.


Assuntos
Transtornos Cerebrovasculares , Transtornos Cognitivos , Disfunção Cognitiva , Encéfalo , Transtornos Cerebrovasculares/complicações , Transtornos Cerebrovasculares/tratamento farmacológico , Transtornos Cognitivos/tratamento farmacológico , Transtornos Cognitivos/etiologia , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/etiologia , Humanos , Qualidade de Vida
4.
Acta Clin Croat ; 60(1): 127-130, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-34588732

RESUMO

High incidence and significance of repercussions on patient health and healthcare system make postoperative cognitive dysfunction (POCD) a major problem following cardiac surgery. POCD frequency drops over time since surgery and its occurrence are related to different aspects of cognitive deterioration that markedly impair the patient quality of life. Therefore, a substantial number of papers have focused on this complex postoperative complication, however, with limited achievement in clarifying it. The underlying mechanisms of POCD development and contributing factors are still unclear. A significant issue in POCD research is the lack of uniformity in defining cognitive impairment among investigators, including unique terminology of cognitive changes, a battery of appropriate neuropsychological tests, timing of assessment, and statistical approach. Thus, the aim of this review is to address the difficulties in establishing POCD definition, with inclusion of specific recommendations based on recent publications.


Assuntos
Procedimentos Cirúrgicos Cardíacos , Transtornos Cognitivos , Disfunção Cognitiva , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Disfunção Cognitiva/diagnóstico , Disfunção Cognitiva/etiologia , Humanos , Testes Neuropsicológicos , Complicações Pós-Operatórias/diagnóstico , Qualidade de Vida
5.
Am J Physiol Endocrinol Metab ; 321(5): E652-E664, 2021 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-34569271

RESUMO

Mitochondrial dysfunction is evident in diseases affecting cognition and metabolism such as Alzheimer's disease and type 2 diabetes. Human studies of brain mitochondrial function are limited to postmortem tissue, preventing the assessment of bioenergetics by respirometry. Here, we investigated the effect of two diets on mitochondrial bioenergetics in three brain regions: the prefrontal cortex (PFC), the entorhinal cortex (ERC), and the cerebellum (CB), using middle-aged nonhuman primates. Eighteen female cynomolgus macaques aged 12.3 ± 0.7 yr were fed either a Mediterranean diet that is associated with healthy outcomes or a Western diet that is associated with poor cognitive and metabolic outcomes. Average bioenergetic capacity within each brain region did not differ between diets. Distinct brain regions have different metabolic requirements related to their function and disease susceptibility. Therefore, we also examined differences in bioenergetic capacity between brain regions. Mitochondria isolated from animals fed a Mediterranean diet maintained distinct differences in mitochondrial bioenergetics between brain regions, whereas animals fed the Western diet had diminished distinction in bioenergetics between brain regions. Notably, fatty acid ß-oxidation was not affected between regions in animals fed a Western diet. In addition, bioenergetics in animals fed a Western diet had positive associations with fasting blood glucose and insulin levels in PFC and ERC mitochondria but not in CB mitochondria. Altogether, these data indicate that a Western diet disrupts bioenergetic patterns across brain regions and that circulating blood glucose and insulin levels in Western-diet fed animals influence bioenergetics in brain regions susceptible to Alzheimer's disease and type 2 diabetes.NEW & NOTEWORTHY We show that compared with cynomolgus macaques fed a Mediterranean diet, a Western diet resulted in diminished bioenergetic pattern between brain regions related to blood glucose and insulin levels, specifically in brain regions susceptible to neurodegeneration and diabetes. In addition, fatty acid metabolism not directly linked to the TCA cycle and glucose metabolism did not show differences in bioenergetics due to diet.


Assuntos
Encéfalo/metabolismo , Dieta Mediterrânea , Dieta Ocidental , Metabolismo Energético/fisiologia , Mitocôndrias/metabolismo , Animais , Glicemia/análise , Glicemia/metabolismo , Citrato (si)-Sintase/metabolismo , Transtornos Cognitivos/etiologia , Córtex Entorrinal/embriologia , Ácidos Graxos/metabolismo , Feminino , Insulina/sangue , Macaca fascicularis , Córtex Pré-Frontal/metabolismo
6.
Scand J Med Sci Sports ; 31(12): 2291-2299, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34487582

RESUMO

Recurrent contact and concussion in rugby union remains a significant public health concern given the potential increased risk of neurodegeneration in later life. This study determined to what extent prior-recurrent contact impacts molecular-hemodynamic biomarkers underpinning cognition in current professional rugby union players with a history of concussion. Measurements were performed in 20 professional rugby union players with an average of 16 (interquartile range [IQR] 13-19) years playing history reporting 3 (IQR 1-4) concussions. They were compared to 17 sex-age-physical activity-and education-matched non-contact controls with no prior history of self-reported concussion. Venous blood was assayed directly for the ascorbate free radical (A•- electron paramagnetic resonance spectroscopy) nitric oxide metabolites (NO reductive ozone-based chemiluminescence) and select biomarkers of neurovascular unit integrity (NVU chemiluminescence/ELISA). Middle cerebral artery blood flow velocity (MCAv doppler ultrasound) was employed to determine basal perfusion and cerebrovascular reactivity (CVR) to hyper/hypocapnia ( CVR CO 2 Hyper / Hypo ). Cognition was assessed by neuropsychometric testing. Elevated systemic oxidative-nitrosative stress was confirmed in the players through increased A•- (p < 0.001) and suppression of NO bioavailability (p < 0.001). This was accompanied by a lower CVR range ( CVR CO 2 Range ; p = 0.045) elevation in neurofilament light-chain (p = 0.010) and frontotemporal impairments in immediate-memory (p = 0.001) delayed-recall (p = 0.048) and fine-motor coordination (p < 0.001). Accelerated cognitive decline subsequent to prior-recurrent contact and concussion history is associated with a free radical-mediated suppression of CVR and neuronal injury providing important mechanistic insight that may help better inform clinical management.


Assuntos
Concussão Encefálica/fisiopatologia , Concussão Encefálica/psicologia , Circulação Cerebrovascular , Transtornos Cognitivos/etiologia , Futebol Americano/lesões , Adulto , Biomarcadores/sangue , Velocidade do Fluxo Sanguíneo , Estudos de Casos e Controles , Hemodinâmica , Humanos , Masculino , Artéria Cerebral Média/fisiologia , Óxido Nítrico/sangue , Estresse Oxidativo , Recidiva , Fatores de Risco
7.
Int J Mol Sci ; 22(18)2021 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-34576069

RESUMO

Schizophrenia is a major mental illness characterized by positive and negative symptoms, and by cognitive deficit. Although cognitive impairment is disabling for patients, it has been largely neglected in the treatment of schizophrenia. There are several reasons for this lack of treatments for cognitive deficit, but the complexity of its etiology-in which neuroanatomic, biochemical and genetic factors concur-has contributed to the lack of effective treatments. In the last few years, there have been several attempts to develop novel drugs for the treatment of cognitive impairment in schizophrenia. Despite these efforts, little progress has been made. The latest findings point to the importance of developing personalized treatments for schizophrenia which enhance neuroplasticity, and of combining pharmacological treatments with non-pharmacological measures.


Assuntos
Transtornos Cognitivos/etiologia , Transtornos Cognitivos/terapia , Esquizofrenia/complicações , Antioxidantes/farmacologia , Antioxidantes/uso terapêutico , Ensaios Clínicos como Assunto , Transtornos Cognitivos/genética , Transtornos Cognitivos/fisiopatologia , Humanos , Transmissão Sináptica/fisiologia
8.
Undersea Hyperb Med ; 48(3): 247-253, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34390629

RESUMO

Demyelination throughout the brain stem and spinal cord caused by acute carbon monoxide (CO) poisoning has not been previously reported. Magnetic resonance imaging (MRI) has revealed that acute CO poisoning primarily affects the subcortical white matter of the bilateral cerebral hemispheres and basal ganglia. Here we report the case of a patient with delayed neuropsychological sequelae (DNS) due to acute CO poisoning. A 28-year-old man was admitted to our department following a suicide attempt by acute CO poisoning. After a six-month pseudo-recovery period, he was diagnosed with DNS, with MRI evidence of demyelinating change of the bilateral cerebral peduncles. Demyelination was identified throughout the brain stem, expanding from the bilateral cerebral peduncles to the medulla oblongata, occurring approximately six months after poisoning. One and a half years after acute CO poisoning, demyelination of the cervical and thoracic spine was observed, most notable in the lateral and posterior cords. It is evident that previously published research on this topic is extremely limited. Perhaps in severe cases of acute CO poisoning the fatality rate is higher, leading to fewer surviving cases for possible study. This may be because a more severe case of acute CO poisoning would result in the higher likelihood of secondary demyelination. This research indicates that clinicians should be aware of the risk of secondary demyelination and take increased precautions such as vitamin B supplementation and administration of low-dose corticosteroids for an extended period of time in order to reduce the extent and severity of demyelination.


Assuntos
Encefalopatias/etiologia , Tronco Encefálico , Intoxicação por Monóxido de Carbono/complicações , Doenças Desmielinizantes/etiologia , Doenças da Medula Espinal/etiologia , Adulto , Encefalopatias/diagnóstico por imagem , Encefalopatias/terapia , Tronco Encefálico/diagnóstico por imagem , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/terapia , Doenças Desmielinizantes/diagnóstico por imagem , Doenças Desmielinizantes/terapia , Humanos , Imageamento por Ressonância Magnética , Masculino , Transtornos Mentais/etiologia , Transtornos Mentais/terapia , Doenças da Medula Espinal/diagnóstico por imagem , Doenças da Medula Espinal/terapia , Tentativa de Suicídio , Fatores de Tempo
9.
Nat Metab ; 3(8): 1058-1070, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34417591

RESUMO

Identifying secreted mediators that drive the cognitive benefits of exercise holds great promise for the treatment of cognitive decline in ageing or Alzheimer's disease (AD). Here, we show that irisin, the cleaved and circulating form of the exercise-induced membrane protein FNDC5, is sufficient to confer the benefits of exercise on cognitive function. Genetic deletion of Fndc5/irisin (global Fndc5 knock-out (KO) mice; F5KO) impairs cognitive function in exercise, ageing and AD. Diminished pattern separation in F5KO mice can be rescued by delivering irisin directly into the dentate gyrus, suggesting that irisin is the active moiety. In F5KO mice, adult-born neurons in the dentate gyrus are morphologically, transcriptionally and functionally abnormal. Importantly, elevation of circulating irisin levels by peripheral delivery of irisin via adeno-associated viral overexpression in the liver results in enrichment of central irisin and is sufficient to improve both the cognitive deficit and neuropathology in AD mouse models. Irisin is a crucial regulator of the cognitive benefits of exercise and is a potential therapeutic agent for treating cognitive disorders including AD.


Assuntos
Cognição , Fibronectinas/metabolismo , Hormônios/metabolismo , Condicionamento Físico Animal , Animais , Comportamento Animal , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/metabolismo , Transtornos Cognitivos/psicologia , Modelos Animais de Doenças , Fibronectinas/genética , Deleção de Genes , Expressão Gênica , Camundongos , Camundongos Knockout , Fenótipo
10.
Int J Mol Sci ; 22(16)2021 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-34445708

RESUMO

Brain injury/concussion is a growing epidemic throughout the world. Although evidence supports association between traumatic brain injury (TBI) and disturbance in brain glucose metabolism, the underlying molecular mechanisms are not well established. Previously, we reported the release of cellular prion protein (PrPc) from the brain to circulation following TBI. The PrPc level was also found to be decreased in insulin-resistant rat brains. In the present study, we investigated the molecular link between PrPc and brain insulin resistance in a single and repeated mild TBI-induced mouse model. Mild TBI was induced in mice by dropping a weight (~95 g at 1 m high) on the right side of the head. The procedure was performed once and thrice (once daily) for single (SI) and repeated induction (RI), respectively. Micro PET/CT imaging revealed that RI mice showed significant reduction in cortical, hippocampal and cerebellum glucose uptake compared to SI and control. Mice that received RI also showed significant motor and cognitive deficits. In co-immunoprecipitation, the interaction between PrPc, flotillin and Cbl-associated protein (CAP) observed in the control mice brains was disrupted by RI. Lipid raft isolation showed decreased levels of PrPc, flotillin and CAP in the RI mice brains. Based on observation, it is clear that PrPc has an interaction with CAP and the dislodgment of PrPc from cell membranes may lead to brain insulin resistance in a mild TBI mouse model. The present study generated a new insight into the pathogenesis of brain injury, which may result in the development of novel therapy.


Assuntos
Concussão Encefálica/fisiopatologia , Resistência à Insulina/fisiologia , Animais , Encéfalo/metabolismo , Concussão Encefálica/diagnóstico por imagem , Lesões Encefálicas/complicações , Transtornos Cognitivos/etiologia , Modelos Animais de Doenças , Glucose/metabolismo , Insulina/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Tomografia por Emissão de Pósitrons/métodos , Proteínas Priônicas/metabolismo , Príons/metabolismo , Transdução de Sinais/fisiologia
11.
J Clin Neurosci ; 90: 273-278, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34275563

RESUMO

OBJECTIVES: This study aimed to explore the association of homocysteine (Hcy) with third ventricle (V3) dilatation and mesencephalic area (MA) atrophy as determined by transcranial sonography (TCS) in Parkinson's disease (PD) with cognitive impairment. METHODS: The final statistical analysis included 101 PD patients and 20 age- and sex-matched controls. Using the Movement Disorder Society (MDS) level II criteria for PD with cognitive impairment, we categorized the PD patients into PD with normal cognition group (PD) and PD with cognitive impairment group (PDC). All subjects underwent TCS and laboratory analysis. RESULTS: The V3 width (r = 0.349, P = 0.005) and the MA (r = -0.484, P < 0.001) were significantly correlated with the Hcy concentration in the PDC patients. Binary logistic regression analysis revealed that age (OR [95% CI] = 1.114 [0.991-1.251], P = 0.002), and Hcy level (OR [95% CI] = 0.931 [0.752-1.153], P = 0.411) were independent risk factors for V3 dilatation. Hcy level (OR [95% CI] = 0.557 [0.323-0.967], P = 0.035) were independent risk factors for MA atrophy. After adjustment for confounding factors, the odds ratio of V3 dilatation was 3.50 (95% CI 1.054-11.399, P = 0.031) and the odds ratio of MA atrophy was 4.67 (95% CI 1.395-15.602, P = 0.012) in the patients with higher Hcy level compared with the lower level. CONCLUSIONS: The results revealed a close association between the V3 width, MA and Hcy concentration in PD patients with cognitive impairment. We hypothesized that increased Hcy concentration played a significant role in the development of brain atrophy in PD with cognitive impairment.


Assuntos
Transtornos Cognitivos/etiologia , Homocisteína/sangue , Mesencéfalo/patologia , Doença de Parkinson/sangue , Doença de Parkinson/patologia , Terceiro Ventrículo/patologia , Idoso , Idoso de 80 Anos ou mais , Atrofia , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Mesencéfalo/diagnóstico por imagem , Pessoa de Meia-Idade , Razão de Chances , Doença de Parkinson/psicologia , Fatores de Risco , Terceiro Ventrículo/diagnóstico por imagem , Ultrassonografia Doppler Transcraniana
12.
Nutrients ; 13(6)2021 Jun 20.
Artigo em Inglês | MEDLINE | ID: mdl-34203094

RESUMO

The burden of cognitive disorders is huge and still growing, however the etiology and the degree of cognitive impairment vary considerably. Neurodegenerative and vascular mechanisms were most frequently assessed in patients with dementia. Recent studies have shown the possible involvement of triglycerides levels in cognitive function through putative mechanisms such as brain blood barrier dysfunction or amyloid metabolism imbalance, but not all research in the field found this association. Several clinical studies evaluated the relationship between different forms of cognitive decline and levels of serum triglycerides, independent of other cardiovascular risk factors. This review focuses on the role of triglycerides in cognitive decline, cerebral amyloidosis and vascular impairment. Considering that the management of hypertriglyceridemia benefits from lifestyle modification, diet, and specific drug therapy, future studies are requested to appraise the triglycerides-cognitive impairment relationship.


Assuntos
Disfunção Cognitiva/etiologia , Triglicerídeos/sangue , Adulto , Idoso , Idoso de 80 Anos ou mais , Doença de Alzheimer/sangue , Doença de Alzheimer/diagnóstico , Doença de Alzheimer/etiologia , Amiloidose/diagnóstico , Barreira Hematoencefálica/metabolismo , Encefalopatias/diagnóstico , Transtornos Cerebrovasculares/diagnóstico , Cognição , Transtornos Cognitivos/sangue , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Disfunção Cognitiva/sangue , Disfunção Cognitiva/diagnóstico , Dieta , Feminino , Humanos , Hipertrigliceridemia/terapia , Estilo de Vida , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Triglicerídeos/líquido cefalorraquidiano , Triglicerídeos/metabolismo
13.
Biochemistry (Mosc) ; 86(6): 657-666, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34225589

RESUMO

Ischemic brain injuries are accompanied by the long-term changes in gene expression in the hippocampus, the limbic system structure, involved in the regulation of key aspects of the higher nervous activity, such as cognitive functions and emotions. The altered expression of genes and proteins encoded by them may be related to the development of post-ischemic psycho-emotional and cognitive disturbances. Activation of neuroinflammation following stroke in the hippocampus has been suggested to play an essential role in induction of long-lasting consequences. Identification of changes in the gene expression patterns after ischemia and investigation of the dynamics of these changes in the hippocampus are the necessary first steps toward understanding molecular pathways responsible for the development of post-stroke cognitive impairments and mental pathologies.


Assuntos
Isquemia Encefálica/genética , Transtornos Cognitivos/etiologia , Hipocampo/metabolismo , Transtornos Mentais/etiologia , Acidente Vascular Cerebral/genética , Animais , Lesões Encefálicas , Isquemia Encefálica/complicações , Isquemia Encefálica/metabolismo , Cognição , Depressão/etiologia , Regulação da Expressão Gênica , Humanos , Inflamação , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/metabolismo
14.
Cancer Radiother ; 25(6-7): 713-722, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34274224

RESUMO

Cranial irradiation of primary or metastatic lesions is frequent, historically with 3D-conformal radiation therapy and now with stereotactic radiosurgery and intensity modulation. Evolution of radiotherapy technique is concomitant to systemic treatment evolution permitting long time survival. Thus, physicians have to face underestimated toxicities on long-survivor patients and unknown toxicities from combination of cranial radiotherapy to new therapeutics as targeted therapies and immunotherapies. This article proposes to develop these toxicities, without being exhaustive, to allow a better apprehension of cranial irradiation in current context.


Assuntos
Irradiação Craniana/efeitos adversos , Alopecia/etiologia , Sobreviventes de Câncer , Catarata/etiologia , Transtornos Cognitivos/etiologia , Irradiação Craniana/métodos , Distúrbios do Sono por Sonolência Excessiva/etiologia , Síndromes do Olho Seco/etiologia , Epilepsia/etiologia , Humanos , Doenças Hipotalâmicas/etiologia , Sistema Hipotálamo-Hipofisário/efeitos da radiação , Imunoterapia/efeitos adversos , Carcinomatose Meníngea/etiologia , Transtornos de Enxaqueca/etiologia , Terapia de Alvo Molecular/efeitos adversos , Transtornos do Olfato/etiologia , Radiocirurgia/métodos , Radioterapia Conformacional/tendências , Radioterapia de Intensidade Modulada/tendências , Síndrome , Distúrbios do Paladar , Xerostomia/etiologia
16.
Ann Intern Med ; 174(7): ITC97-ITC112, 2021 07.
Artigo em Inglês | MEDLINE | ID: mdl-34251902

RESUMO

This review focuses on the diagnosis and management of menopause, highlighting both hormonal and nonhormonal treatment options. In particular, the article focuses on recent data on the risks and benefits of hormone therapy to help clinicians better counsel their patients about decision making with regard to understanding and treating menopause symptoms.


Assuntos
Menopausa/fisiologia , Neoplasias da Mama/etiologia , Doenças Cardiovasculares/prevenção & controle , Transtornos Cognitivos/etiologia , Contraindicações de Medicamentos , Terapia de Reposição de Estrogênios/efeitos adversos , Feminino , Estilo de Vida Saudável , Fogachos/tratamento farmacológico , Fogachos/terapia , Humanos , Menopausa/sangue , Menopausa/psicologia , Osteoporose Pós-Menopausa/prevenção & controle , Educação de Pacientes como Assunto , Medição de Risco , Inibidores de Captação de Serotonina/uso terapêutico , Sudorese/fisiologia , Vagina/fisiologia , Sistema Vasomotor/fisiologia
17.
Int J Mol Sci ; 22(11)2021 May 31.
Artigo em Inglês | MEDLINE | ID: mdl-34072743

RESUMO

Alzheimer's disease (AD) is a neurodegenerative disease with a high incidence rate. The main pathological features of AD are ß-amyloid plaques (APs), which are formed by ß-amyloid protein (Aß) deposition, and neurofibrillary tangles (NFTs), which are formed by the excessive phosphorylation of the tau protein. Although a series of studies have shown that the accumulation of metal ions, including calcium ions (Ca2+), can promote the formation of APs and NFTs, there is no systematic review of the mechanisms by which Ca2+ affects the development and progression of AD. In view of this, the current review summarizes the mechanisms by which Ca2+ is transported into and out of cells and organelles, such as the cell, endoplasmic reticulum, mitochondrial and lysosomal membranes to affect the balance of intracellular Ca2+ levels. In addition, dyshomeostasis of Ca2+ plays an important role in modulating the pathogenesis of AD by influencing the production and aggregation of Aß peptides and tau protein phosphorylation and the ways that disrupting the metabolic balance of Ca2+ can affect the learning ability and memory of people with AD. In addition, the effects of these mechanisms on the synaptic plasticity are also discussed. Finally, the molecular network through which Ca2+ regulates the pathogenesis of AD is introduced, providing a theoretical basis for improving the clinical treatment of AD.


Assuntos
Doença de Alzheimer/metabolismo , Peptídeos beta-Amiloides/metabolismo , Cálcio/metabolismo , Íons/metabolismo , Agregação Patológica de Proteínas/metabolismo , Proteínas tau/metabolismo , Doença de Alzheimer/etiologia , Doença de Alzheimer/patologia , Animais , Transporte Biológico , Membrana Celular/metabolismo , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/metabolismo , Transtornos Cognitivos/patologia , Modelos Animais de Doenças , Progressão da Doença , Suscetibilidade a Doenças , Retículo Endoplasmático/metabolismo , Humanos , Lisossomos/metabolismo , Memória , Mitocôndrias/metabolismo , Plasticidade Neuronal , Neurônios/metabolismo , Fosforilação
18.
J Psychiatr Res ; 140: 545-550, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34182240

RESUMO

The impact of the Neurofibromatosis type 1 (NF1) on cognition have been subject to much clinical investigation, but environmental modifiers of disease expression have not yet been systematically investigated. The aim of this paper is to determine the role of demographic and environmental factors such as age, sex, socioeconomic status, parental NF1 status and neurological complications on the cognitive, behavioural and academic outcomes in NF1. Participants included 206 children aged 4-18 years seen within the Manchester clinical research NF1 service. Multiple linear regression models were used to study the effect of the hypothesized predictor variables on cognitive, behavioural and academic outcomes. Relative to population norms, 80% of the NF1 sample demonstrated significantly lower scores in at least one cognitive, behavioural or academic domains. Family history of NF1 and lower SES were independently associated with poorer cognitive, behavioural and academic outcomes. Neurological problems such as epilepsy and hydrocephalus were associated with lower IQ and academic skills. Cognitive and behavioural phenotypes emerge commonly via a complex interplay between genes and environmental factors, and this is true also of a monogenic condition such as NF1. Early interventions and remedial education may be targeted to risk groups such those with familial NF1, families with lower SES and those with associated neurological comorbidities.


Assuntos
Transtornos Cognitivos , Neurofibromatose 1 , Criança , Cognição , Transtornos Cognitivos/epidemiologia , Transtornos Cognitivos/etiologia , Intervenção Educacional Precoce , Humanos , Neurofibromatose 1/complicações , Neurofibromatose 1/epidemiologia , Pais
19.
Psychiatry Res ; 302: 113971, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34182311

RESUMO

Different dimensions of formal thought disorder (FTD) are distinguished by different patterns of cognitive dysfunction in patients with schizophrenia; however, inconsistent findings may relate to patient-related confounds. To avoid these confounds, we examined relationships between FTD dimensions and cognitive domains in a non-clinical sample with attenuated schizophrenia-like traits, or schizotypal traits, on the Schizotypal Personality Questionnaire (N = 91). To our knowledge, no study has done this. FTD dimension scores were derived following principal component analysis of the Scale for the Assessment of Thought, Language and Communication (TLC dimensions: Disorganisation, Verbosity, Emptiness) and the Thought and Language Index (TLI dimensions: Negative, Idiosyncratic). The sample completed a comprehensive neuropsychological battery. Findings indicate that higher-order reasoning, executive function (set shift and generative ability) and language/semantic functioning are the primary drivers of FTD in our non-clinical sample with elevated schizotypal traits, in line with schizophrenia research. FTD may have shared aetiology along the schizophrenia spectrum.


Assuntos
Transtornos Cognitivos , Esquizofrenia , Cognição , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Função Executiva , Humanos , Esquizofrenia/complicações , Pensamento
20.
Am Soc Clin Oncol Educ Book ; 41: e90-e99, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34061562

RESUMO

Cognitive symptoms occur in almost all patients with brain tumors at varying points in the disease course. Deficits in neurocognitive function may be caused by the tumor itself, treatment (surgery, radiation, or chemotherapy), or other complicating factors (e.g., seizures, fatigue, mood disturbance) and can have a profound effect on functional independence and quality of life. Assessment of neurocognitive function is an important part of comprehensive care of patients with brain tumors. In the neuro-oncology clinic, assessment may include cognitive screening tools and inquiry into subjective cognitive function. Neuropsychological assessment is an important adjunct to identify cognitive symptoms and can be used as an opportunity to intervene through transformative feedback and treatment planning. Preventative measures can be taken to reduce cognitive side effects of treatment, such as awake craniotomies with intraoperative mapping during neurosurgery or prophylactic measures during radiation therapy (e.g., hippocampal avoidance, neuroprotectant treatment with memantine). Rehabilitative therapies, including cognitive rehabilitation and computerized cognitive exercise, are options for managing cognitive problems in an individualized manner. Pharmacotherapy, including use of stimulant medications and acetylcholinesterase inhibitors, has shown benefits for patients with brain tumors when tailored to an individual's cognitive profile. Identification and management of co-occurring issues, such as sleep disturbance, fatigue, and depression, can also improve neurocognitive function. There are promising therapies under development that may provide new options for treatment in the future. Integrating careful assessment and treatment of cognition throughout the disease course for patients with brain tumors can improve functional outcomes and quality of life.


Assuntos
Neoplasias Encefálicas , Transtornos Cognitivos , Neoplasias Encefálicas/complicações , Neoplasias Encefálicas/diagnóstico , Neoplasias Encefálicas/terapia , Cognição , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/terapia , Fadiga/diagnóstico , Fadiga/epidemiologia , Fadiga/etiologia , Humanos , Qualidade de Vida
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