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The concept of the glial-vascular unit (GVU) was raised recently to emphasize the close associations between brain cells and cerebral vessels, and their coordinated reactions to diverse neurological insults from a "glio-centric" view. GVU is a multicellular structure composed of glial cells, perivascular cells, and perivascular space. Each component is closely linked, collectively forming the GVU. The central roles of glial and perivascular cells and their multi-level interconnections in the GVU under normal conditions and in central nervous system (CNS) disorders have not been elucidated in detail. Here, we comprehensively review the intensive interactions between glial cells and perivascular cells in the niche of perivascular space, which take part in the modulation of cerebral blood flow and angiogenesis, formation of the blood-brain barrier, and clearance of neurotoxic wastes. Next, we discuss dysfunctions of the GVU in various neurological diseases, including ischemic stroke, spinal cord injury, Alzheimer's disease, and major depression disorder. In addition, we highlight the possible therapies targeting the GVU, which may have potential clinical applications.
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Humans , Neuroglia , Nervous System Diseases , Blood-Brain Barrier , Alzheimer Disease , Glymphatic SystemABSTRACT
The purpose of this study is to describe the principles in selection and application of antidepressants in patients with depression complicating glaucoma or at high risk of glaucoma. With the aim of providing a partial reference for relevant issues， this paper elaborated a case of major depression after glaucoma surgery receiving 6 weeks of treatment with escitalopram oxalate and sulpiride achieved significant improvement in depressive and psychotic symptoms without triggering or exacerbating glaucoma.
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Major depression disorder (MDD) is a serious mental illness with high disability rate and high recurrence rate, accompanied by cognitive impairment including language processing. This article reviews neurophysiological evidences of abnormal semantic processing in MDD patients in recent years. Electrophysiological data indicates that abnormal semantic processing in the patients begins in the early stages of perceptual processing and persists in subsequent cognitive processing stages with hemispheric lateralization. Brain imaging studies show that the patients have abnormal activation levels in the medial prefrontal cortex and inferior frontal gyrus. The current research paradigms cannot separate semantic processing from other cognitive processes, and more research is needed.
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In recent years,the research direction of the pathogenesis of depression has gradually ex-panded from classical neurotransmitter disorders and neuroendocrine disorders theory to the related fields of immuno-inflammatory response and researchers believe that depression is a psycho-neuro-immune disorder disease. Because many patients with chronic inflammation,cancer and autoimmune diseases are easy to suffer depression,it confirms that the occurrence of depression may be related to the adverse effects of immune in-flammation in the brain. A large number of clinical and experimental studies have shown that the role of im-mune inflammation in depression is mainly due to the release of inflammatory factors from immune cells through the blood-brain barrier,activation or intensification of brain immune cell response,or changes in the structure and function of neuroendocrine axis,neurotransmitters,emotional regulation-related brain regions, leading to the occurrence and development of depression. The purpose of this review is to summarize the pos-sible mechanisms and links of immune inflammation in depression in recent years,and to provide ideas and methods for the research and treatment of depression.
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Objective To explore the psychological process of cognitive impairment in patients with recurrent major depression disorder (MDD). Methods Patients with first-episode (n=30) and recurrent MDD (n=68) in the outpatient department of the First Affiliated Hospital of Zhengzhou University from Sep-tember 2016 to December 2017 were collected and healthy controls(n=30) were collected at the same time. According to HAMD-24 score,the group with recurrent attacks was further divided into recurrent attacks-on-set period (n=35) and recurrent attacks-remission period (n=33). All subjects were tested for cognitive function by MATRICS Consensus Cognitive Battery( MCCB). Results (1) In terms of cognitive function assessment,the scores of information processing speed ( 41. 27 ± 8. 44, 37. 00 ± 11. 68), working memory (40. 53±10. 33,41. 26±9. 37),attention/alertness ( 40. 50± 7. 25,39. 58± 8. 23),word learning ( 38. 83± 8. 39,38. 84±9. 57),visual memory(39. 30±14. 03,37. 57±10. 42),reasoning and problem solving(37. 80± 9. 55,38. 78±8. 66),and social cognition (34. 63± 9. 66) in the first-episode group and the recurrent group were lower than those in the control group ( information processing speed ( 48. 23±7. 63),working memory (50. 57±7. 84),attention/alertness (51. 63±7. 41),word learning (45. 57±9. 55),visual memory (50. 57± 8. 42),reasoning and problem solving (50. 03±9. 87) and social cognition (47. 90±19. 01)) (F=12. 818, 12. 173,26. 166,6. 004,15. 085,18. 331,10. 218,P<0. 05); (2) In working memory and social cognition, the difference was statistically significant in the first-episode group,repeated attacks-episodes(working mem-ory:37. 89±9. 15,social cognition:28. 48± 8. 35) and recurrent group-remission( working memory:44. 85± 8. 32,social cognition:40. 44 ± 11. 36, P=0. 010,0. 001). Further comparisons revealed that the score of working memory in repeated attacks-episodes was lower than that in recurrent group-remission (P=0. 003). the score of social cognition in the first-episode group was higher than that in the recurrent-attack period group (P=0. 038). The score of social cognition in the recurrent group-remission was higher than that in re-current-attack period group (P<0. 01). Conclusion There is cognitive impairment in the first episode and the recurrence MDD. The impairment in the recurrent episode is more serious than that in the first episode of depression. The impairment of social cognitive in the recurrent attacks-episodes is more serious than that in the first-episode of depression.
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Major depression disorder (MDD) is a common but serious affective disorder in modern society. Suicide idea and suicide behaviour induced by MDD during its later stage put a heavy burden on society and family. Anti-depression drugs lack efficiency in treating a portion of MDD patients. This is referred to as treatment resistant depression (TRD). A study reported the rapid onset and long lasting anti-depression effect of ketamine, which also come into effect in TRD patients. △9-Tetrahydrocannabinol is the active substance of marijuana, which also exerts rapid anti-depression effect via targeting at brain cannabinoid receptors. The two central nerve system stimulants belonging to the tightly controlled psychoactive substances have obvious adverse effects. This article summarizes the action of ketamine and endocannabinoid system in rapid anti-depression therapy in recent researches.
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Major depression disorder (MDD) is a common but serious affective disorder in modern society. Suicide idea and suicide behaviour induced by MDD during its later stage put a heavy burden on society and family. Anti-depression drugs lack efficiency in treating a portion of MDD patients. This is referred to as treatment resistant depression (TRD). A study reported the rapid onset and long lasting anti-depression effect of ketamine, which also come into effect in TRD patients. Δ9-Tetrahydrocannabinol is the active substance of marijuana, which also exerts rapid anti-depression effect via targeting at brain cannabinoid receptors. The two central nerve system stimulants belonging to the tightly controlled psychoactive substances have obvious adverse effects. This article summarizes the action of ketamine and endocannabinoid system in rapid anti-depression therapy in recent researches.
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Abstract Introduction Few studies have evaluated positive measures for therapeutic response. Thus, the objective of this study was to assess the effects of resilience on severity of depressive and anxious symptoms after brief cognitive psychotherapy for depression. Methods This was a clinical follow-up study nested in a randomized clinical trial of cognitive therapies. The Resilience Scale was applied at baseline. The Hamilton Anxiety Rating Scale (HARS) and the Hamilton Depression Rating Scale (HDRS) were used at baseline, post-intervention, and at six-month follow-up. Results Sixty-one patients were assessed at baseline, post-intervention and at six-month follow-up. Resilience scores were significantly different between baseline and post-intervention assessments (p<0.001), as well as at baseline and at six-month follow-up (p<0.001). We observed a weak negative correlation between baseline resilience scores and HDRS scores at post-intervention (r=-0.295, p=0.015) and at six-month follow-up (r=-0.354, p=0.005). Furthermore, we observed a weak negative correlation between resilience scores and HARS scores at post-intervention (r=-0.292, p=0.016). Conclusion Subjects with higher resilience scores at baseline showed a lower severity of symptoms at post-intervention and at six-month follow-up.
Resumo Introdução Poucos estudos têm avaliado medidas positivas de resposta terapêutica. Assim, o objetivo deste estudo foi verificar os efeitos da resiliência na severidade dos sintomas depressivos e ansiosos após psicoterapia cognitiva breve para depressão. Métodos Trata-se de um estudo de intervenção clínica aninhado a um ensaio clínico com dois diferentes modelos de terapia cognitiva. A Resilience Scale foi aplicada no baseline, enquanto que a Hamilton Anxiety Rating Scale e a Hamilton Depression Rating Scale foram utilizadas no baseline, após a intervenção e no acompanhamento de seis meses. Resultados Sessenta e um pacientes foram avaliados no baseline, no pós-intervenção e no acompanhamento de seis meses. Os escores de resiliência foram significativamente diferentes entre as avaliações de baseline e pós-intervenção (p<0,001), bem como no baseline vs. acompanhamento de seis meses (p<0,001). Observamos uma correlação negativa fraca entre os escores de resiliência no baseline e os escores de sintomas depressivos no pós-intervenção (r=-0,295; p=0,015) e em seis meses de acompanhamento (r=-0,354; p=0,005). Além disso, observamos uma correlação negativa fraca entre os escores de resiliência e sintomas ansiosos no pós-intervenção (r=-0,292; p=0,016). Conclusão Indivíduos com maiores escores de resiliência na avaliação pré-tratamento apresentaram uma menor severidade de sintomas no pós-intervenção e no acompanhamento de seis meses.
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Humans , Male , Female , Adolescent , Adult , Young Adult , Depressive Disorder, Major/psychology , Depressive Disorder, Major/therapy , Resilience, Psychological , Psychiatric Status Rating Scales , Cognitive Behavioral Therapy/methods , Double-Blind Method , Follow-Up Studies , Depression/psychology , Depression/therapyABSTRACT
The dysfunction in the serotoninergic neurotransmission has been classically associated with major depressive disorder (MDD); however, other pathways and processes seem to have a role in this illness, such as neurogenesis and related molecules: the Brain-Derived Neurotrophic Factor (BDNF) and the Apolipoprotein E (APOE). There are many reports that indicate an association between certain polymorphism in these genes and MDD. The aim of our study was to analyze the possible association between MDD and polymorphisms in HTR2A (5-hydroxytryptamine receptor 2A), BDNF and APOE genes in a sample of the Argentinean population previously studied for 2 polymorphisms in SLC6A4 (Solute Carrier Family 6 Member 4) gene. Five polymorphisms were studied (rs6311 and rs6313 in HTR2A; rs429358 and rs7412 in APOE, and rs6265 in BDNF) in 95 MDD patients and 107 non-related controls. No statistically significant differences were observed between groups when analyzing the association with a single marker using logistic regression; however, when a possible combinatory effect of the polymorphisms (including previously studied polymorphisms in SLC6A4 gene) was analyzed using a dominant model for the risk alleles, the genotypes L/S_10/12_G/A (OR=3.57(95%CI=1.43-8.93); p=0.004, adjusted p-value=0.01) in SLC6A4 and BDNF genes and L/S_10/12_T/C_3/3_G/A in SLC6A4, HTR2A, APOE and BDNF genes (OR=5.99(95%CI=1.66-21.56); p=0.002, adjusted p-value=0.07), were more prevalent in patients than in controls (20%vs.6% and 15%vs.3%, respectively). Even though it is necessary to replicate these findings in a larger population, our results suggest a possible interaction between molecules involved in neurogenesis (BDNF and APOE), serotoninergic neurotransmission (SLC6A4 and HTR2A) and the pathogenesis of MDD. (AU)
La disfunción en la neurotransmisión serotoninérgica ha sido clásicamente asociada con el trastorno depresivo mayor (TDM); sin embargo, otras vías y procesos parecerían tener un rol en esta enfermedad, como la neurogénesis y moléculas asociadas: el factor neurotrófico derivado del cerebro (BDNF) y la apoliproteína E (APOE). Existen reportes en los que se establecen asociaciones entre polimorfismos en estos genes y el TDM. El objetivo de nuestro trabajo fue analizar la posible asociación entre el TDM y polimorfismos en los genes HTR2A (receptor 5-hidroxitriptamina 2A), BDNF y APOE en una muestra de la población argentina previamente estudiada para 2 polimorfismos en el gen SLC6A4 (transportador soluble familia 6 miembro 4). Se estudiaron 5 polimorfismos (rs6311 y rs6313 en HTR2A; rs429358 y rs7412 en APOE; rs6265 en BDNF) en 95 pacientes con TDM y 107 controles no relacionados. No se observaron diferencias significativas entre grupos al analizar la asociación por regresión logística con un único marcador; cuando se analizó el posible efecto combinatorio de polimorfismos (incluyendo los previamente estudiados para el gen SCL6A4) usando un modelo dominante para los alelos de riesgo, los genotipos L/S_10/12_G/A (OR=3,57(95%CI=1,43-8,93); p=0,004, valor-p-ajustado=0,01) en SLC6A4 y BDNF y L/S_10/12_T/C_3/3_G/A en SLC6A4, HTR2A, APOE y BDNF (OR=5,99(95%CI=1,66-21,56); p=0,002, valor-p-ajustado=0,07), fueron más prevalentes en pacientes que controles (20%vs.6% y 15%vs.3% respectivamente). Si bien es necesario replicar estos hallazgos en una población más grande, nuestros resultados sugieren una posible interacción entre moléculas involucradas en la neurogénesis (BDNF y APOE), la neurotransmisión serotoninérgica (SLC6A4 y HTR2A) y la patogenia de la depresión mayor. (AU)
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Young Adult , Apolipoproteins E/deficiency , Polymorphism, Genetic , Brain-Derived Neurotrophic Factor/deficiency , Receptors, Serotonin, 5-HT2/deficiency , Depressive Disorder, Major/genetics , Serotonin Plasma Membrane Transport Proteins/deficiency , Apolipoproteins E/genetics , Argentina/epidemiology , Brain-Derived Neurotrophic Factor/genetics , Receptors, Serotonin, 5-HT2/genetics , Depressive Disorder, Major/pathology , Serotonin Plasma Membrane Transport Proteins/geneticsABSTRACT
Objective To study the characteristics and differences of the amplitude of low-frequency fluctuation (ALFF) and the fractional ALFF (fALFF) of the major disorder depression (MDD) and their first-degree relatives in the resting state by functional magnetic resonance imaging (fMRI),to understand the early brain function in patients with MDD.Methods 3.0T fMRI in the resting state was performed in 10 patients with MDD (the depression group),10 first-degree relatives of MDD (the first-degree relatives group) and 10 healthy volunteers (the control group).A statistics analysis of ALFF and fALFF were performed subsequently.Results The ALFF and fALFF values measured in left cerebellum, left precuneus and left medial prefrontal cortex of MDD group were significantly lower than those of the first-degree relatives group (P<0.05).The ALFF values measured in right posterior cingulate cortex and right superior parietal lobule of MDD group were significantly lower than those of the first-degree relatives group (P<0.05).The ALFF and fALFF values measured in left cerebellum, left precuneus and left superior parietal lobule of MDD group were significantly lower than those of the control group (P<0.05).The ALFF values measured in right cingulate cortex and medial prefrontal cortex of MDD group were significantly lower than those of the control group (P<0.05).There was no significance difference found in ALFF values between the first-degree relatives group and the control group,the fALFF values measured in left superior parietallobule of the first-degree relatives group were significantly lower than those of the control group (P<0.05).Conclusion As the widespread ALFF, fALFF abnormalities of brain in MDD and first-degree relatives of MDD,a hypothesis can be get that these abnormal brain region may be associated with cognitive network disorders and emotional distress in MDD.
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Objective To examine the reliability,validity and sensitivity of Montgomery-Asberg Depression Rating Scale (MADRS) for patients with current major depression disorder (MDD). Methods One hundred and twenty-two current MDD (DSM-Ⅳ) patients were administered with MADRS, Hamilton Rating Scale for Depression-17 item version (HAMD) and Clinical Global Impression of Severity (CGI-S) at baseline, 12 patients were selected to complete rater agreement test,and 47 patients receiving antidepressant treatment were followed up at 2,4,6 and 8 week and administered with MADRS and HAMD. Correlation analysis, reliability analysis and effect size (ES) calculation were used to determine the reliability,validity and sensitivity to changes during drug treatment. Results Intra rater reliability for MADRS was 0. 954. Baseline item-total score correlations were between 0. 445 and 0. 770 (P ＜ 0. 01 ), and the average correlation was 0. 629. The Cronbach α coefficient was 0. 847. The criterion related validity with HAMD and CGI-S was 0. 853 and 0. 672 (P＜0.01) ,respectively. The re-test reliability for MADRS at 2,4,6 and 8 week was 0. 737 ,0. 651,0. 543 and 0. 524 (P＜0. 01 ) ,respectively.MADRS had higher ES than HAMD when taken as clinical endpoint outcome measurement (0.41 vs 0.40,0.87 vs 0. 72,1.14 vs 0. 88,1.20 vs 0. 96 for 2nd,4th,6th and 8th week, respectively). Conclusion MADRS has good reliability and validity for patients with MDD. It is more sensitive to assess drug effect than HAMD.