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2.
Neuron ; 2020 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-33171117

RESUMO

Light exerts profound effects on cognitive functions across species, including humans. However, the neuronal mechanisms underlying the effects of light on cognitive functions are poorly understood. In this study, we show that long-term exposure to bright-light treatment promotes spatial memory through a di-synaptic visual circuit related to the nucleus reuniens (Re). Specifically, a subset of SMI-32-expressing ON-type retinal ganglion cells (RGCs) innervate CaMKIIα neurons in the thalamic ventral lateral geniculate nucleus and intergeniculate leaflet (vLGN/IGL), which in turn activate CaMKIIα neurons in the Re. Specific activation of vLGN/IGL-projecting RGCs, activation of Re-projecting vLGN/IGL neurons, or activation of postsynaptic Re neurons is sufficient to promote spatial memory. Furthermore, we demonstrate that the spatial-memory-promoting effects of light treatment are dependent on the activation of vLGN/IGL-projecting RGCs, Re-projecting vLGN/IGL neurons, and Re neurons. Our results reveal a dedicated subcortical visual circuit that mediates the spatial-memory-promoting effects of light treatment.

3.
Int J Mol Sci ; 21(19)2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-33019767

RESUMO

Age-related macular degeneration (AMD) is a leading cause of severe visual loss among the elderly. AMD patients are tormented by progressive central blurring/loss of vision and have limited therapeutic options to date. Drusen accumulation causing retinal pigment epithelial (RPE) cell damage is the hallmark of AMD pathogenesis, in which oxidative stress and inflammation are the well-known molecular mechanisms. However, the underlying mechanisms of how RPE responds when exposed to drusen are still poorly understood. Programmed cell death (PCD) plays an important role in cellular responses to stress and the regulation of homeostasis and diseases. Apart from the classical apoptosis, recent studies also discovered novel PCD pathways such as pyroptosis, necroptosis, and ferroptosis, which may contribute to RPE cell death in AMD. This evidence may yield new treatment targets for AMD. In this review, we summarized and analyzed recent advances on the association between novel PCD and AMD, proposing PCD's role as a therapeutic new target for future AMD treatment.

4.
Neuroscience ; 448: 172-190, 2020 Nov 10.
Artigo em Inglês | MEDLINE | ID: mdl-32976986

RESUMO

Caveolin-1 (Cav-1) is an important modulator for adult neurogenesis in post stroke brain repair but its underlying mechanisms are largely unknown. In the present study, we report that endothelial Cav-1 inhibits neuronal differentiation of neural stem/progenitor cells (NSCs/NPCs) in post ischemic brain via regulating vascular endothelial growth factor (VEGF) and NeuroD1 signaling pathway. We first investigated the dynamic change of Cav-1 and its impact on neuronal differentiation in rat and mouse models of 2 h transient middle cerebral artery occlusion (MCAO) plus 1, 7, 14, 21 and 28 day of reperfusion. We then studied the roles of endothelial Cav-1 in modulating the neuronal differentiation of NPCs which were co-cultured with brain microvascular endothelial cells (BMVECs) under 2 h oxygen-glucose deprivation plus 5 days reoxygenation (OGD/R). The major discoveries include: (1) Cav-1 expression in the hippocampal dentate gyrus (DG) was down-regulated on day 1 after 2 h cerebral ischemia, and gradually recovered with reperfusion time, accompanied with transient increased but gradually reduced neuronal differentiation of NPCs marked by doublecortin (DCX). (2) Cav-1 knockout mice exhibited the increased DCX and VEGF at the granular cell layers of hippocampal DG in post-ischemic brains. (3) Co-cultured with BMVECs, NPCs had remarkably decreased neuronal differentiation under OGD/R. Knockdown of Cav-1 in the BMVECs increased VEGF secretion into the medium and NeuroD1+ cells, and rescued the neuronal differentiation of NPCs without affecting astroglial and oligodendroglial differentiation. (4) Cav-1 exosomes released from BMVECs inhibited neuronal differentiation of NPCs via decreasing the expression of VEGF, p44/42MAPK phosphorylation and NeuronD1 upon OGD/R insults. Taken together, endothelial Cav-1 serves as a niche regulator to inhibit neuronal differentiation via negatively modulating VEGF, p44/42MAPK phosphorylation and NeuronD1 signaling pathway.

5.
J Affect Disord ; 277: 443-449, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32871530

RESUMO

BACKGROUND: Light therapy has been successfully used to treat seasonal and non-seasonal depression, but there is limited evidence for its efficacy in subthreshold depression. This study examines the efficacy of light therapy for symptoms of depression and anxiety in non-seasonal subthreshold depression. METHODS: College students with non-seasonal subthreshold depression were recruited. The participants were randomly allocated to one of the three conditions: high- (LT-5000 lux) and low-intensity (LT-500 lux) light therapy conditions and a waiting-list control condition (WLC). The primary outcome was Hamilton Depression Rating Scale (HAMD), and secondary outcomes were Beck Depression Inventory-II (BDI-II) and state anxiety inventory (SAI), which were assessed at baseline (Week 0), during the trial (Week 4), and after completion of the light therapy (Week 8). RESULTS: A total of 142 participants completed the trial. The LT-5000 (effect size [d] = 1.56, 95% CI: 1.15 to 1.98) and LT-500 conditions (d = 0.84, 95% CI: 0.43 to 1.26) were significantly superior to the WLC condition. For the LT-5000, LT-500, and WLC conditions by the end of the 8-week trial, a response on the HAMD was achieved by 70.0%, 42.0% and 19.0% of the participants, and remission was achieved by 76.0%, 54.0%, and 19.0%, respectively. LIMITATIONS: The subjects were not followed up regularly after completion of the trial. CONCLUSION: Light therapy, both at high- and low-intensity, was efficacious in the treatment of college students with non-seasonal subthreshold depression. High-intensity light therapy was superior to low-intensity light therapy by the end of an 8-week trial.

6.
Int J Mol Sci ; 21(13)2020 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-32629957

RESUMO

Age-related macular degeneration (AMD) is a sight-threatening disease with limited treatment options. We investigated whether amyloid ß1-40 (Aß1-40) could cause pyroptosis and evaluated the effects of Lycium barbarum polysaccharides (LBP) on Aß1-40 oligomers-induced retinal pigment epithelium 19 (ARPE-19) damage, which is an in vitro AMD model. Aß1-40 oligomers verified by Western blot were added to ARPE-19 cells with or without 24 h LBP treatment. Aß1-40 oligomers significantly decreased ARPE-19 cell viability with obvious morphological changes under light microscopy. SEM revealed swollen cells with a bubbling appearance and ruptured cell membrane, which are morphological characteristics of pyroptosis. ELISA results showed increased expression of IL-1ß and IL-18, which are the final products of pyroptosis. LBP administration for 24 h had no toxic effects on ARPE-19 cells and improved cell viability and morphology while disrupting Aß1-40 oligomerization in a dose-dependent manner. Furthermore, Aß1-40 oligomers up-regulated the cellular immunoreactivity of pyroptosis markers including NOD-like receptors protein 3 (NLRP3), caspase-1, and membrane N-terminal cleavage product of GSDMD (GSDMD-N), which could be reversed by LBP treatment. Taken together, this study showed that LBP effectively protects the Aß1-40 oligomers-induced pyroptotic ARPE-19 cell damages by its anti-Aß1-40 oligomerization properties and its anti-pyroptotic effects.

7.
Neuroscience ; 441: 217-225, 2020 08 10.
Artigo em Inglês | MEDLINE | ID: mdl-32512137

RESUMO

The dorsal raphe nucleus (DRN) participates in stress responses and in mood regulation via its ascending release of serotonin (5-HT) onto neural circuits within the forebrain. Although the 5-HT DRN region is easily defined via 5-HT-expressing DRN neurons, the neuroarchitecture and microcircuitry that confer its multifunctionality have remained incompletely understood and have required further investigation. In this present study, neurochemical interactions within different subregions of the rat DRN were precisely analyzed. We found that 97.5% of GABAergic neurons in the DRN expressed ionotropic 5-HT3A receptors (5-HT3ARs), whereas there were only rare parvalbumin (PV)-positive or somatostatin (SOM)-positive GABAergic neurons. Furthermore, corticosterone administration into male rats as a rodent model of depression induced significantly higher c-Fos expression in 5-HT3AR-positive GABAergic neurons compared to that in 5-HT neurons within the DRN. Taken together, our findings suggest that 5-HT3AR-positive GABAergic neurons in the DRN participate in responses to stress hormones in a rat model of depression.

8.
PLoS One ; 15(5): e0232932, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32413063

RESUMO

Childhood sexual abuse (CSA) has been shown to predict the coupling of depression and inflammation in adulthood. Trust within intimate relationships, a core element in marital relations, has been shown to predict positive physical and mental health outcomes, but the mediating role of trust in partners in the association between CSA and inflammation in adulthood requires further study. The present study aimed to examine the impact of CSA on inflammatory biomarkers (IL-6 and IL-1ß) in adults with depression and the mediating role of trust. A cross-sectional survey data set of adults presenting with mood and sleep disturbance was used in the analysis. CSA demonstrated a significant negative correlation with IL-6 level (r = -0.28, p<0. 01) in adults with clinically significant depression, while trust showed a significant positive correlation with IL-6 level (r = 0.36, p < .01). Sobel test and bootstrapping revealed a significant mediating role for trust between CSA and IL-6 level. CSA and trust in partners were revealed to have significant associations with IL-6 level in adulthood. Counterintuitively, the directions of association were not those expected. Trust played a mediating role between CSA and adulthood levels of IL-6. Plausible explanations for these counterintuitive findings are discussed.


Assuntos
Sobreviventes Adultos de Maus-Tratos Infantis/psicologia , Interleucina-6/imunologia , Confiança/psicologia , Adulto , Criança , Abuso Sexual na Infância/psicologia , Estudos Transversais , Depressão/metabolismo , Feminino , Humanos , Inflamação/imunologia , Interleucina-1beta/análise , Interleucina-1beta/sangue , Interleucina-6/análise , Interleucina-6/sangue , Relações Interpessoais , Masculino , Casamento/psicologia , Transtornos Mentais/psicologia , Pessoa de Meia-Idade , Fatores de Risco , Parceiros Sexuais/psicologia
9.
ACS Appl Mater Interfaces ; 12(15): 17207-17219, 2020 Apr 15.
Artigo em Inglês | MEDLINE | ID: mdl-32207300

RESUMO

The formation of a fluid-filled cystic cavity after spinal cord injury (SCI) is a major obstacle for neural regeneration. In this study, the post-SCI cavity was bridged by a functional self-assembling peptide (F-SAP) nanofiber hydrogel coupled with growth factor "cocktail". A sustained release of growth factors was achieved by carefully tailoring the physical hindrances and charge-induced interactions between the growth factors and the peptide nanofibers. Such an engineering microenvironment elicited axon regeneration, as determined by tracing of the descending pathway in the dorsal columns and immunochemical detection of regenerating axons beyond the lesion. Furthermore, the dynamic spatiotemporal activation line of endogenous NSCs (eNSCs) after severe SCI was thoroughly investigated. The results indicated that the growth factor-coupled F-SAP greatly facilitated eNSC proliferation, neuronal differentiation, maturation, myelination, and more importantly, the formation of interconnection with severed descending corticospinal tracts. The robust endogenous neurogenesis essentially led to the recovery of locomotion and electrophysiological properties. In conclusion, the growth factor-coupled F-SAP nanofiber hydrogel elucidated the therapeutic effect of eliciting endogenous neurogenesis by locally reassembling an extracellular matrix.

10.
Cell Mol Gastroenterol Hepatol ; 9(1): 145-160, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31562937

RESUMO

BACKGROUND & AIMS: Toll-like receptor 2 (TLR2) and TLR3 regulate hepatic immunity under pathological conditions, but their functions and potential drug targets in alcoholic liver disease (ALD) remain poorly understood. METHODS: ALD-associated liver injury were induced in TLR2 knockout (TLR2-/-), TLR3-/-, TLR2-/- bone marrow transplanted (BMT), TLR3-/- BMT, IL-10-/- mice, and their wild-type littermates through ethanol challenge with or without co-administered epigallocatechin-3-gallate (EGCG). Moreover, Kupffer cells were depleted by GdCl3 injection to evaluate their pathogenic roles in ALD. RESULTS: We identified that deficiency of TLR2 and TLR3 significantly alleviated and aggravated ALD-induced liver injury, respectively. Mechanistically, Kupffer cell inactivation, M1 to M2 polarization, and IL-10 production via STAT3 activation contributed to hepatic protection mediated by concurrent TLR2 inhibition and TLR3 agonism. These findings were further confirmed in TLR2 and TLR3 BMT mice. We also identified a novel ALD-protective agent EGCG which directly interacted with Kupffer cell TLR2/3 to induce IL-10 production. Deficiency of IL-10 aggravated ALD injury and blunted EGCG-mediated hepatoprotection while depletion of Kupffer cells partially recovered liver injury but abolished EGCG's actions. CONCLUSIONS: Altogether, our results illustrate the divergent roles of Kupffer cells TLR2/3 in ALD progression via anti-inflammatory cytokine IL-10 production.

11.
J Ethnopharmacol ; 248: 112357, 2020 Feb 10.
Artigo em Inglês | MEDLINE | ID: mdl-31693919

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Gogi berry is a traditional food supplement and medical herbal which has been widely used in Eastern Asian countries. Lycium barbarum polysaccharides (LBP) are the major active components of Gogi berry and have been proved to possess a lot of biological activities. AIM OF THE STUDY: We aimed to delineate the protective effect and mechanism of LBP on hepatic encephalopathy (HE). MATERIALS AND METHODS: We investigated the protective mechanism of LBP in a thioacetamide (TAA, intraperitoneally injected, 400 mg/kg) induced acute HE mice model. Key phenotypes of clinical HE were phenocopied in the mice model, including high mortality, severe hepatic histology injury, increased hepatic oxidative stress, apoptosis, enhanced circulating levels of pro-inflammatory cytokines and ammonia, suppressed tryptophan hydroxylase activity, and deficits in locomotor activity. RESULTS: The pathological alterations were effectively ameliorated by the oral administration with LBP (5 mg/kg, oral gavage, everyday), which were mediated by regulating MAPK pathways in both the liver and brain. Knockout of pro-inflammatory cytokines TNF-α or IL-6 effectively ameliorated impaired mice locomotor activity and MAPK activation in the brain. In an in vitro TNF-α-, IL-6-, or ammonia-induced microglia damaged cell model, cell injuries were evidently protected by the co-administration with LBP (50 µg/ml). CONCLUSION: LBP ameliorated the hepatic/brain injuries and impaired locomotor activities in a HE mice model. Pro-inflammatory cytokines may serve as communicating molecules linking the liver and brain for the HE pathogenesis, partly through MAPK regulation.


Assuntos
Encéfalo/efeitos dos fármacos , Citocinas/metabolismo , Encefalopatia Hepática/prevenção & controle , Mediadores da Inflamação/metabolismo , Fígado/efeitos dos fármacos , Lycium , Extratos Vegetais/farmacologia , Polissacarídeos/farmacologia , Animais , Encéfalo/metabolismo , Encéfalo/patologia , Linhagem Celular , Citocinas/deficiência , Citocinas/genética , Modelos Animais de Doenças , Frutas , Encefalopatia Hepática/induzido quimicamente , Encefalopatia Hepática/metabolismo , Encefalopatia Hepática/patologia , Interleucina-6/metabolismo , Fígado/metabolismo , Fígado/patologia , Locomoção/efeitos dos fármacos , Lycium/química , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Extratos Vegetais/isolamento & purificação , Polissacarídeos/isolamento & purificação , Transdução de Sinais , Tioacetamida , Fator de Necrose Tumoral alfa/metabolismo
12.
Brain Behav Immun ; 83: 192-199, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31614176

RESUMO

Neuro-inflammation might impact on clinical manifestations and cognition function via changing the volumes of key brain structures such as the anterior cingulate cortex (ACC) in bipolar disorder (BD). In this study, we investigated the interrelations among interleukin (IL)-6 cytokine level, grey matter (GM) volume of the anterior cingulated cortex (ACC), and attention function among offspring of parents diagnosed with BD. The offspring were categorized as being either asymptomatic or symptomatic based on whether they manifested pre-defined sub-threshold mood symptoms. We found that the symptomatic offspring showed significantly higher serum levels of IL-6 than the asymptomatic offspring (F(1, 59) = 67.65, p < 0.001). On the brain level, we obtained significant interactive effect of group and IL6 level on the ACC GM (PFWE = 0.017). Specifically, the GM volume of the rostral ACC was negatively associated with the levels of IL-6 in the asymptomatic offspring (PFWE = 0.021), but not the symptomatic offspring (PFWE > 0.05). Mediation analyses revealed that the GM volume of the rostral ACC significantly mediated the negative association between the IL-6 levels and attention performance in the asymptomatic offspring (bootstrapping Confidence Interval (CI) = -6.0432 to -0.0731) but not the symptomatic offspring (bootstrapping CI = -0.3197 to 1.3423). Our data suggest that the asymptomatic and symptomatic bipolar offspring may exhibit different neurocognitive-inflammatory profiles, which could be further validated as viable biosignatures for BD risk and resilience.

13.
Restor Neurol Neurosci ; 37(6): 571-581, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31796710

RESUMO

Many ocular diseases (such as glaucoma, diabetic retinopathy, age-related macular degeneration, and traumatic eye injuries) can result in the degeneration of retinal cells and the subsequent loss of vision. Some kinds of treatments, such as drugs, stem cell transplantation and surgery are reported to be effective in certain patients. However, no confirmatively effective, convenient and low-price intervention has been available so far. Physical exercise has been reported to exert neuroprotective effects on several neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease. Studies investigating the potential impacts of exercise on retinal diseases are rapidly emerging. Here we review these up-to-date findings from both human and animal studies, and discuss the possible mechanisms underlying exercise-elicited protection on retina.

14.
Invest Ophthalmol Vis Sci ; 60(14): 4606-4618, 2019 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-31756254

RESUMO

Purpose: To investigate the neuroprotective effects of Lycium barbarum polysaccharides (LBP) against chronic ocular hypertension (OHT) in rats and to consider if effects differed when treatment was applied before (pretreatment) or during (posttreatment) chronic IOP elevation. Methods: Sprague-Dawley rats (10-weeks old) underwent suture implantation around the limbus for 15 weeks (OHT) or 1 day (sham). Four experimental groups were studied, three OHT groups (n = 8 each) treated either with vehicle (PBS), LBP pretreatment or posttreatment, and a sham control (n = 5) received no treatment. LBP (1 mg/kg) pre- and posttreatment were commenced at 1 week before and 4 weeks after OHT induction, respectively. Treatments continued up through week 15. IOP was monitored twice weekly for 15 weeks. Optical coherence tomography and ERG were measured at baseline, week 4, 8, 12, and 15. Eyes were collected for ganglion cell layer (GCL) histologic analysis at week 15. Results: Suture implantation successfully induced approximately 50% IOP elevation and the cumulative IOP was similar between the three OHT groups. When compared with vehicle control (week 4: -23 ± 5%, P = 0.03), LBP pretreatment delayed the onset of retinal nerve fiber layer (RNFL) thinning (week 4, 8: -2 ± 7%, -11 ± 3%, P > 0.05) and arrested further reduction up through week 15 (-10 ± 4%, P > 0.05). LBP posttreatment intervention showed no significant change in rate of loss (week 4, 15: -25 ± 4.1%, -28 ± 3%). However, both LBP treatments preserved the retinal ganglion cells (RGC) and retinal functions up to week 15, which were significantly reduced in vehicle control. Conclusions: LBP posttreatment arrested the subsequent neuronal degeneration after treatment commencement and preserved RGC density and retinal functions in a chronic OHT model, which was comparable with pretreatment outcomes.


Assuntos
Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/uso terapêutico , Degeneração Neural/prevenção & controle , Fármacos Neuroprotetores/uso terapêutico , Hipertensão Ocular/tratamento farmacológico , Animais , Doença Crônica , Eletrorretinografia , Feminino , Pressão Intraocular/fisiologia , Degeneração Neural/metabolismo , Degeneração Neural/fisiopatologia , Fibras Nervosas/patologia , Hipertensão Ocular/metabolismo , Hipertensão Ocular/fisiopatologia , Ratos , Ratos Sprague-Dawley , Retina/fisiopatologia , Células Ganglionares da Retina/patologia , Tomografia de Coerência Óptica
15.
Int Rev Neurobiol ; 147: 199-217, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31607355

RESUMO

Body-weight-supported locomotor training is an activity-based therapy used frequently to train individuals with spinal cord injury (SCI) for restoring walking ability. Locomotor training after SCI is developed on the basic scientific findings of activity-dependent neuroplasticity. Based on the research from animal SCI models, there exists a spinal neural networks for locomotion which can be reactivated by intense repetitive locomotor training. Notably, the effectiveness of locomotor training depends largely on the severity of injury and time after injury. Locomotor training, using body-weight-supported walking overground or on a treadmill, with assistance manually or robotically, with a variety of training intensity and training programs, has been shown to elicit improvements in locomotor function for incomplete SCI individuals. For chronic and motor complete SCI, other interventions with proven effectiveness such as epidural stimulation might be applied in addition to locomotor training to improve the chance of locomotor recovery. In this chapter, we review the factors that influence the functional outcomes of locomotor training. We also summarize the circuitry, cellular and molecular levels of mechanisms underlying the positive role of locomotor training in inducing neuroplasticity and functional recovery following SCI.


Assuntos
Locomoção/fisiologia , Recuperação de Função Fisiológica/fisiologia , Traumatismos da Medula Espinal/fisiopatologia , Traumatismos da Medula Espinal/terapia , Medula Espinal/fisiologia , Animais , Humanos
16.
Int Rev Neurobiol ; 147: 281-294, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31607358

RESUMO

Adiponectin, one kind of adipokines, has been shown to be neuroprotective in different neurodegenerative diseases. Adiponectin exerts its role through combination with its receptors and activates downstream molecular pathways. In the retinas, the expression of adiponectin can be detected and adiponectin receptors (AdipoRs) locate in different retinal cells. Adiponectin is mainly produced by adipose tissue, enters the circulation and passes through blood-brain barrier (BBB) without injury. It can also be produced locally in the brains as well as in the retinas. Therefore, it is possible that adiponectin from blood as well as that produced locally in the retinas take part in defense of different eye diseases. Here we have summarized the published data about the protective effects of adiponectin in eye diseases. Because exercise can increase the production of adiponectin systemically in the whole body and locally in the brain although no evidence has shown that exercise can increase the production of adiponectin in the eyes until now, we hypothesize that exercise will have a potential protective effect for the eyes via increasing the levels of adiponectin which needs further investigation.


Assuntos
Adiponectina/metabolismo , Adiponectina/uso terapêutico , Terapia por Exercício , Oftalmopatias/prevenção & controle , Receptores de Adiponectina/metabolismo , Retina/metabolismo , Animais , Humanos , Fármacos Neuroprotetores/uso terapêutico
17.
Int Rev Neurobiol ; 147: 323-360, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31607360

RESUMO

Exercise training improves mental and cognitive functions by enhancing neurogenesis and neuroprotection. Recent studies suggest the facilitation of spinogenesis across different brain regions including hippocampus and cerebral cortex by physical activity. In this article we will summarize major findings for exercise effects on synaptogenesis and spinogenesis, in order to provide mechanisms for exercise intervention of both psychiatric diseases and neurodegenerative disorders. We will also revisit major findings for molecular mechanism governing exercise-related spinogenesis, and will discuss the screening for novel factors, or exerkines, whose levels are correlated with endurance training and affect neural plasticity. We believe that further studies focusing on the molecular mechanism of exercise-mediate spinogenesis should benefit the optimization of exercise therapy in clinics and the evaluation of treatment efficiency using specific biomarkers.


Assuntos
Encéfalo/fisiologia , Cognição/fisiologia , Terapia por Exercício , Exercício Físico/fisiologia , Exercício Físico/psicologia , Neurogênese/fisiologia , Condicionamento Físico Animal/fisiologia , Animais , Encefalopatias/fisiopatologia , Encefalopatias/terapia , Humanos , Transtornos Mentais/fisiopatologia , Transtornos Mentais/terapia
19.
Brain Behav Immun ; 82: 178-187, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31437533

RESUMO

Minimal hepatic encephalopathy (MHE) is characterized as cognitive deficits including memory and learning dysfunctions after liver injuries or hepatic diseases. Our understandings of neurological mechanisms of MHE-associated cognitive syndromes, however, are far from complete. In the current study we generated a mouse MHE model by repetitive administrations of thioacetamide (TAA), which induced hyperammonemia plus elevated proinflammatory cytokines in both the general circulation and motor cortex. MHE mice presented prominent motor learning deficits, which were associated with excess dendritic spine pruning in the motor cortex under 2-photon in vivo microscopy. The pharmaceutical blockade of glucocorticoid receptor or suppression of its biosynthesis further rescued motor learning deficits and synaptic protein loss. Moreover, MHE mice presented microglial activation, which can be alleviated after glucocorticoid pathway inhibition. In sum, our data demonstrates corticosterone-induced microglial activation, synaptic over-pruning and motor learning impairments in MHE, providing new insights for MHE pathogenesis and potential targets of clinical interventions.

20.
Neural Regen Res ; 14(11): 1845-1850, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31290433

RESUMO

Glaucoma is a chronic, progressive optic neuropathy characterized by the loss of peripheral vision first and then central vision. Clinically, normal tension glaucoma is considered a special subtype of glaucoma, in which the patient's intraocular pressure is within the normal range, but the patient experiences typical glaucomatous changes. However, increasing evidence has challenged the traditional pathophysiological view of normal tension glaucoma, which is based only on intraocular pressure, and breakthroughs in central nervous system imaging may now greatly increase our knowledge about the mechanisms underlying normal tension glaucoma. In this article, we review the latest progress in understanding the pathogenesis of normal tension glaucoma and in developing imaging techniques to detect it, to strengthen the appreciation for the connection between normal tension glaucoma and the brain.

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