​1. Nature—eIF4E介导氯胺酮的抗抑郁效果

Abstract

Effective pharmacotherapy for majordepressive disorder remains a major challenge, as more than 30% of patients areresistant to the first line of treatment (selective serotonin reuptake inhibitors)1.Sub-anaesthetic doses of ketamine, a non-competitive N-methyl-D-aspartatereceptor antagonist2,3, provide rapid and long-lasting antidepressant effectsin these patients4-6, but the molecular mechanism of these effects remainsunclear7,8. Ketamine has been proposed to exert its antidepressant effectsthrough its metabolite (2R,6R)-hydroxynorketamine ((2R,6R)-HNK)9. Theantidepressant effects of ketamine and (2R,6R)-HNK in rodents requireactivation of the mTORC1 kinase10,11. mTORC1 controls various neuronalfunctions12, particularly through cap-dependent initiation of mRNA translationvia the phosphorylation and inactivation of eukaryotic initiation factor4E-binding proteins (4E-BPs)13. Here we show that 4E-BP1 and 4E-BP2 are keyeffectors of the antidepressant activity of ketamine and (2R,6R)-HNK, and thatketamine-induced hippocampal synaptic plasticity depends on 4E-BP2 and, to alesser extent, 4E-BP1. It has been hypothesized that ketamine activatesmTORC1-4E-BP signalling in pyramidal excitatory cells of the cortex8,14. Totest this hypothesis, we studied the behavioural response to ketamine and(2R,6R)-HNK in mice lacking 4E-BPs in either excitatory or inhibitory neurons.The antidepressant activity of the drugs is mediated by 4E-BP2 in excitatoryneurons, and 4E-BP1 and 4E-BP2 in inhibitory neurons. Notably, genetic deletionof 4E-BP2 in inhibitory neurons induced a reduction in baseline immobility inthe forced swim test, mimicking an antidepressant effect. Deletion of 4E-BP2specifically in inhibitory neurons also prevented the ketamine-induced increasein hippocampal excitatory neurotransmission, and this effect concurred with theinability of ketamine to induce a long-lasting decrease in inhibitoryneurotransmission. Overall, our data show that 4E-BPs are central to theantidepressant activity of ketamine.

参考文献：Antidepressant actions of ketamineengage cell-specific translation via eIF4E. Nature. 2020 Dec 16.

2. Nature genetics—抑郁症GWAS研究中，抑郁症的定义应依据于最新临床诊断标准，而非患者自我病史陈述

Abstract

Minimal phenotyping refers to thereliance on the use of a small number of self-reported items for disease caseidentification, increasingly used in genome-wide association studies (GWAS).Here we report differences in genetic architecture between depression definedby minimal phenotyping and strictly defined major depressive disorder (MDD):the former has a lower genotype-derived heritability that cannot be explainedby inclusion of milder cases and a higher proportion of the genome contributingto this shared genetic liability with other conditions than for strictlydefined MDD. GWAS based on minimal phenotyping definitions preferentiallyidentifies loci that are not specific to MDD, and, although it generates highlypredictive polygenic risk scores, the predictive power can be explainedentirely by large sample sizes rather than by specificity for MDD. Our resultsshow that reliance on results from minimal phenotyping may bias views of thegenetic architecture of MDD and impede the ability to identify pathwaysspecific to MDD.

参考文献：Minimal phenotyping yieldsgenome-wide association signals of low specificity for major depression. NatGenet. 2020 Apr;52(4):437-447.

3. Nature biotechnology—科学家利用机器学习方法构建了一个可以预测抑郁症治疗效果的脑电图特征模型

Abstract

Antidepressants are widelyprescribed, but their efficacy relative to placebo is modest, in part becausethe clinical diagnosis of major depression encompasses biologicallyheterogeneous conditions. Here, we sought to identify a neurobiological signatureof response to antidepressant treatment as compared to placebo. We designed alatent-space machine-learning algorithm tailored for resting-stateelectroencephalography (EEG) and applied it to data from the largestimaging-coupled, placebo-controlled antidepressant study (n = 309). Symptomimprovement was robustly predicted in a manner both specific for theantidepressant sertraline (versus placebo) and generalizable across differentstudy sites and EEG equipment. This sertraline-predictive EEG signaturegeneralized to two depression samples, wherein it reflected generalantidepressant medication responsivity and related differentially to arepetitive transcranial magnetic stimulation treatment outcome. Furthermore, wefound that the sertraline resting-state EEG signature indexed prefrontal neuralresponsivity, as measured by concurrent transcranial magnetic stimulation andEEG. Our findings advance the neurobiological understanding of antidepressanttreatment through an EEG-tailored computational model and provide a clinicalavenue for personalized treatment of depression.

参考文献：An electroencephalographic signature predicts antidepressant response in major depression. Nat Biotechnol. 2020Apr;38(4):439-447.

4. Lancet—香港暴乱增加港人抑郁症和创伤后应激障碍综合征的发生（高于11%）

Abstract

Background: Hong Kong has beenembroiled in increasingly violent social unrest since June, 2019. We examinedthe associated population mental health burden, risk factors, and health-careneeds.

Methods: In a population-basedprospective cohort, adult participants aged 18 years or older were assessed atnine timepoints from 2009. Probable depression was measured using the PatientHealth Questionnaire-9 (score ≥10) and suspected post-traumatic stress disorder (PTSD) bythe PTSD Checklist-Civilian Version (score ≥14), plus direct exposure totraumatic events related to the ongoing social unrest. We used multivariablelogistic regression to identify factors associated with both outcomes,adjusting for doctor-diagnosed depression or anxiety disorders before theunrest. On the basis of routine service statistics and respondents' intentionto seek professional care, we projected the number of additional ambulatoryspecialist psychiatric visits required.

Findings: After the two baselinesurveys, we followed up random subsets of 1213-1736 adults at eachtimepoint. Probable depression was reported by 11·2% (95% CI 9·8-12·7) ofparticipants in 2019, compared with 1·9% (1·6-2·1) during 2009-14 and 6·5%(5·3-7·6) in 2017 after the Occupy Central Movement and before the currentunrest. Prevalence of suspected PTSD in 2019 was estimated to be 12·8%(11·2-14·4). Age, sex, educational attainment, or household income were notassociated with either outcome, whereas heavy social media use (≥2 h per day) was associated withboth. Political attitude or protest participation was not associated withprobable depression, but neutrality towards the extradition bill approximatelyhalved the risk of suspected PTSD. Family support mitigated against probabledepression. We estimated that the mental health burden identified wouldtranslate into roughly an excess 12% service requirement to the public sectorqueue or equivalent.

Interpretation: We have identified amajor mental health burden during the social unrest in Hong Kong, which willrequire substantial increases in service surge capacity. Health-care and socialcare professionals should be vigilant in recognising possible mental healthsequelae. In a world of increasing unrest, our findings might have implicationsfor service planning to better protect population mental health globally.

参考文献：Depression and post-traumatic stress during major social unrest in Hong Kong: a 10-year prospective cohort study. Lancet.2020 Jan 25;395(10220):273-284.

5. JAMA—抑郁症状显著增加心血管疾病的发生风险

Abstract

Importance: It is uncertain whetherdepressive symptoms are independently associated with subsequent risk ofcardiovascular diseases (CVDs).

Objective: To characterize theassociation between depressive symptoms and CVD incidence across the spectrumof lower mood.

Design, setting, and participants: Apooled analysis of individual-participant data from the Emerging Risk FactorsCollaboration (ERFC; 162 036 participants; 21 cohorts; baseline surveys,1960-2008; latest follow-up, March 2020) and the UK Biobank (401 219participants; baseline surveys, 2006-2010; latest follow-up, March 2020).Eligible participants had information about self-reported depressive symptomsand no CVD history at baseline.

Exposures: Depressive symptoms wererecorded using validated instruments. ERFC scores were harmonized acrossstudies to a scale representative of the Center for Epidemiological StudiesDepression (CES-D) scale (range, 0-60; ≥16 indicates possible depressivedisorder). The UK Biobank recorded the 2-item Patient Health Questionnaire 2(PHQ-2; range, 0-6; ≥3 indicates possible depressive disorder).

Main outcomes and measures: Primaryoutcomes were incident fatal or nonfatal coronary heart disease (CHD), stroke,and CVD (composite of the 2). Hazard ratios (HRs) per 1-SD higher log CES-D orPHQ-2 adjusted for age, sex, smoking, and diabetes were reported.

Results: Among 162 036 participantsfrom the ERFC (73%, women; mean age at baseline, 63 years [SD, 9 years]), 5078CHD and 3932 stroke events were recorded (median follow-up, 9.5 years).Associations with CHD, stroke, and CVD were log linear. The HR per 1-SD higherdepression score for CHD was 1.07 (95% CI, 1.03-1.11); stroke, 1.05 (95% CI,1.01-1.10); and CVD, 1.06 (95% CI, 1.04-1.08). The corresponding incidencerates per 10 000 person-years of follow-up in the highest vs the lowestquintile of CES-D score (geometric mean CES-D score, 19 vs 1) were 36.3 vs 29.0for CHD events, 28.0 vs 24.7 for stroke events, and 62.8 vs 53.5 for CVDevents. Among 401 219 participants from the UK Biobank (55% were women, meanage at baseline, 56 years [SD, 8 years]), 4607 CHD and 3253 stroke events wererecorded (median follow-up, 8.1 years). The HR per 1-SD higher depression scorefor CHD was 1.11 (95% CI, 1.08-1.14); stroke, 1.10 (95% CI, 1.06-1.14); andCVD, 1.10 (95% CI, 1.08-1.13). The corresponding incidence rates per 10 000person-years of follow-up among individuals with PHQ-2 scores of 4 or higher vs0 were 20.9 vs 14.2 for CHD events, 15.3 vs 10.2 for stroke events, and 36.2 vs24.5 for CVD events. The magnitude and statistical significance of the HRs werenot materially changed after adjustment for additional risk factors.

Conclusions and relevance: In apooled analysis of 563 255 participants in 22 cohorts, baseline depressivesymptoms were associated with CVD incidence, including at symptom levels lowerthan the threshold indicative of a depressive disorder. However, the magnitudeof associations was modest.

参考文献：Association Between DepressiveSymptoms and Incident Cardiovascular Diseases. JAMA. 2020 Dec15;324(23):2396-2405.

6. JAMA—补充维生素D3并不能预防抑郁症！！

Abstract

Importance: Low levels of25-hydroxyvitamin D have been associated with higher risk for depression laterin life, but there have been few long-term, high-dose large-scale trials.

Objective: To test the effects ofvitamin D3 supplementation on late-life depression risk and mood scores.

Design, setting, and participants:There were 18 353 men and women aged 50 years or older in the VITAL-DEP(Vitamin D and Omega-3 Trial-Depression Endpoint Prevention) ancillary study toVITAL, a randomized clinical trial of cardiovascular disease and cancerprevention among 25 871 adults in the US. There were 16 657 at risk forincident depression (ie, no depression history) and 1696 at risk for recurrentdepression (ie, depression history but no treatment for depression within thepast 2 years). Randomization occurred from November 2011 through March 2014;randomized treatment ended on December 31, 2017, and this was the final date offollow-up.

Intervention: Randomized assignmentin a 2 × 2 factorial design to vitamin D3 (2000 IU/d of cholecalciferol) andfish oil or placebo; 9181 were randomized to vitamin D3 and 9172 wererandomized to matching placebo.

Main outcomes and measures: Theprimary outcomes were the risk of depression or clinically relevant depressivesymptoms (total of incident and recurrent cases) and the mean difference inmood scores (8-item Patient Health Questionnaire depression scale [PHQ-8];score range, 0 points [least symptoms] to 24 points [most symptoms]; theminimal clinically important difference for change in scores was 0.5 points).

Results: Among the 18 353 randomizedparticipants (mean age, 67.5 [SD, 7.1] years; 49.2% women), the mediantreatment duration was 5.3 years and 90.5% completed the trial (93.5% amongthose alive at the end of the trial). Risk of depression or clinicallyrelevant depressive symptoms was not significantly different between thevitamin D3 group (609 depression or clinically relevant depressive symptomevents; 12.9/1000 person-years) and the placebo group (625 depression orclinically relevant depressive symptom events; 13.3/1000 person-years) (hazardratio, 0.97 [95% CI, 0.87 to 1.09]; P = .62); there were no significantdifferences between groups in depression incidence or recurrence. Nosignificant differences were observed between treatment groups for change inmood scores over time; mean change in PHQ-8 score was not significantlydifferent from zero (mean difference for change in mood scores, 0.01 points[95% CI, -0.04 to 0.05 points]).

Conclusions and relevance: Amongadults aged 50 years or older without clinically relevant depressive symptomsat baseline, treatment with vitamin D3 compared with placebo did not result ina statistically significant difference in the incidence and recurrence ofdepression or clinically relevant depressive symptoms or for change in mood scoresover a median follow-up of 5.3 years. These findings do not support the use ofvitamin D3 in adults to prevent depression.

参考文献：Effect of Long-term Vitamin D3Supplementation vs Placebo on Risk of Depression or Clinically RelevantDepressive Symptoms and on Change in Mood Scores: A Randomized Clinical Trial. JAMA.2020 Aug 4;324(5):471-480. doi: 10.1001/jama.2020.10224.

7. JAMA —如何高效诊断抑郁症？PHQ-2联合PHQ-9诊断抑郁症优于PHQ-9

Abstract

Importance: The Patient HealthQuestionnaire depression module (PHQ-9) is a 9-item self-administeredinstrument used for detecting depression and assessing severity of depression.The Patient Health Questionnaire-2 (PHQ-2) consists of the first 2 items of thePHQ-9 (which assess the frequency of depressed mood and anhedonia) and can beused as a first step to identify patients for evaluation with the full PHQ-9.

Objective: To estimate PHQ-2 accuracyalone and combined with the PHQ-9 for detecting major depression.

Data sources: MEDLINE, MEDLINEIn-Process & Other Non-Indexed Citations, PsycINFO, and Web of Science(January 2000-May 2018).

Study selection: Eligible data setscompared PHQ-2 scores with major depression diagnoses from a validateddiagnostic interview.

Data extraction and synthesis:Individual participant data were synthesized with bivariate random-effects meta-analysisto estimate pooled sensitivity and specificity of the PHQ-2 alone among studiesusing semistructured, fully structured, or Mini International NeuropsychiatricInterview (MINI) diagnostic interviews separately and in combination with thePHQ-9 vs the PHQ-9 alone for studies that used semistructured interviews. ThePHQ-2 score ranges from 0 to 6, and the PHQ-9 score ranges from 0 to 27.

Results: Individual participant datawere obtained from 100 of 136 eligible studies (44 318 participants; 4572 withmajor depression [10%]; mean [SD] age, 49 [17] years; 59% female). Amongstudies that used semistructured interviews, PHQ-2 sensitivity and specificity(95% CI) were 0.91 (0.88-0.94) and 0.67 (0.64-0.71) for cutoff scores of 2 orgreater and 0.72 (0.67-0.77) and 0.85 (0.83-0.87) for cutoff scores of 3 orgreater. Sensitivity was significantly greater for semistructured vs fullystructured interviews. Specificity was not significantly different across thetypes of interviews. The area under the receiver operating characteristic curvewas 0.88 (0.86-0.89) for semistructured interviews, 0.82 (0.81-0.84) for fullystructured interviews, and 0.87 (0.85-0.88) for the MINI. There were nosignificant subgroup differences. For semistructured interviews, sensitivityfor PHQ-2 scores of 2 or greater followed by PHQ-9 scores of 10 or greater(0.82 [0.76-0.86]) was not significantly different than PHQ-9 scores of 10 orgreater alone (0.86 [0.80-0.90]); specificity for the combination wassignificantly but minimally higher (0.87 [0.84-0.89] vs 0.85 [0.82-0.87]). Thearea under the curve was 0.90 (0.89-0.91). The combination was estimated toreduce the number of participants needing to complete the full PHQ-9 by 57%(56%-58%).

Conclusions and relevance: In anindividual participant data meta-analysis of studies that compared PHQ scoreswith major depression diagnoses, the combination of PHQ-2 (with cutoff ≥2) followed by PHQ-9 (with cutoff ≥10) had similar sensitivity buthigher specificity compared with PHQ-9 cutoff scores of 10 or greater alone.Further research is needed to understand the clinical and research value ofthis combined approach to screening.

参考文献：Accuracy of the PHQ-2 Alone and inCombination With the PHQ-9 for Screening to Detect Major Depression: SystematicReview and Meta-analysis. JAMA. 2020 Jun 9;323(22):2290-2300.

8. Nat Neurosci—夜里太多光照为啥引发抑郁？ipRGC→dpHb→NAc通路介导了夜间光照诱导的抑郁样行为表型

Abstract

Besides generating vision, lightmodulates various physiological functions, including mood. While light therapyapplied in the daytime is known to have anti-depressive properties, excessivelight exposure at night has been reportedly associated with depressivesymptoms. The neural mechanisms underlying this day-night difference in theeffects of light are unknown. Using a light-at-night (LAN) paradigm in mice, weshowed that LAN induced depressive-like behaviors without disturbing thecircadian rhythm. This effect was mediated by a neural pathway from retinalmelanopsin-expressing ganglion cells to the dorsal perihabenular nucleus (dpHb)to the nucleus accumbens (NAc). Importantly, the dpHb was gated by thecircadian rhythm, being more excitable at night than during the day. Thisindicates that the ipRGC→dpHb→NAc pathway preferentially conducts light signals at night,thereby mediating LAN-induced depressive-like behaviors. These findings may berelevant when considering the mental health effects of the prevalent nighttimeillumination in the industrial world.

参考文献：A circadian rhythm-gated subcorticalpathway for nighttime-light-induced depressive-like behaviors in mice. NatNeurosci. 2020 Jul;23(7):869-880.

9. Nat Neurosci—单细胞组学应用广泛！！单细胞转录组学揭示少突胶质前体细胞和兴奋性神经元是抑郁症的重要驱动细胞（Nature neurosci—科学家发现前额叶少突胶质细胞前体细胞和兴奋性神经元的转录组改变是抑郁症患者的重要神经生物学特征）

Abstract

Major depressive disorder (MDD) hasan enormous impact on global disease burden, affecting millions of peopleworldwide and ranking as a leading cause of disability for almost threedecades. Past molecular studies of MDD employed bulk homogenates of postmortembrain tissue, which obscures gene expression changes within individual celltypes. Here we used single-nucleus transcriptomics to examine ~80,000 nucleifrom the dorsolateral prefrontal cortex of male individuals with MDD (n = 17)and of healthy controls (n = 17). We identified 26 cellular clusters, and over60% of these showed differential gene expression between groups. We found thatthe greatest dysregulation occurred in deep layer excitatory neurons andimmature oligodendrocyte precursor cells (OPCs), and these contributed almosthalf (47%) of all changes in gene expression. These results highlight theimportance of dissecting cell-type-specific contributions to the disease andoffer opportunities to identify new avenues of research and novel targets fortreatment.

参考文献：Single-nucleus transcriptomics of theprefrontal cortex in major depressive disorder implicates oligodendrocyteprecursor cells and excitatory neurons. Nat Neurosci. 2020 Jun;23(6):771-781.

10. Neuron—长非编码RNA研究变火！！长非编码RNA LINC00473下调可能是女性抑郁症的特异性驱动因素（Neuron—重视长非编码RNA在大脑疾病中的作用！！LncRNA LINC00473是女性抑郁症的抵抗因子）

Abstract

Depression is a common disorder thataffects women at twice the rate of men. Here, we report that long non-codingRNAs (lncRNAs), a recently discovered class of regulatory transcripts,represent about one-third of the differentially expressed genes in the brainsof depressed humans and display complex region- and sex-specific patterns ofregulation. We identified the primate-specific, neuronal-enriched geneLINC00473 as downregulated in prefrontal cortex (PFC) of depressed females butnot males. Using viral-mediated gene transfer to express LINC00473 in adultmouse PFC neurons, we mirrored the human sex-specific phenotype by inducingstress resilience solely in female mice. This sex-specific phenotype was accompaniedby changes in synaptic function and gene expression selectively in female miceand, along with studies of human neuron-like cells in culture, implicatesLINC00473 as a CREB effector. Together, our studies identify LINC00473 as afemale-specific driver of stress resilience that is aberrant in femaledepression.

参考文献：Sex-Specific Role for the LongNon-coding RNA LINC00473 in Depression. Neuron. 2020 Jun 17;106(6):912-926.e5.

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2020年十大研究进展名录

2019年十大研究进展名录

1. 年终盘点：2019年帕金森病十大基础研究进展

2. 年终盘点：2019年帕金森病十大临床研究进展

3. 年终盘点：2019年阿尔茨海默病十大基础研究进展

4. 年终盘点：2019年阿尔茨海默病十大临床研究进展

5. 年终盘点：2019年神经科学领域十大基础研究进展

6. 年终盘点：2019年抑郁症领域十大基础研究进展（一半来自中国）

7. 年终盘点：2019年脑血管病领域十大基础研究进展

8. 年终盘点：2019年神经炎症领域十大基础研究进展

9. 年终盘点：2019年神经活动记录十大基础研究进展

10. 年终盘点：2019年ALS/FTD十大基础研究进展

11. 年终盘点：2019年医学和生物学领域深度学习和神经网络十大基础研究进展

12. 年终盘点：2019年神经内科十大临床研究突破

13. 年终盘点：2019年疼痛防治和痛觉机制十大研究突破

14. 年终盘点：2019年睡眠和失眠领域十大研究突破

15.年终盘点：2019年神经发育及成年神经再生十大研究突破

16. 年终盘点：2019年大脑学习和记忆的十大研究突破

17. 年终盘点：2019年衰老和长寿十大研究突破

18. 年终盘点：2019年自闭症十大研究突破

2018年十大研究进展名录

1.盘点2018年阿尔茨海默病十大研究突破

2.盘点2018年帕金森病十大研究突破

3. 盘点2018年神经科学二十大研究突破

4. 盘点2018年渐冻症（ALS）十大研究进展

5. 盘点2018年全球脑卒中十大研究进展

6. 盘点2018年神经影像十大研究进展

7. 盘点2018年神经炎症领域的十大研究突破

8. 盘点2018年神经变性痴呆十大研究突破

9. 2018年神经科学“学习和记忆”领域十大研究进展

10. 2018年抑郁症领域的十大研究突破

11. 2018年痛觉和疼痛领域的十大研究突破

12. 2018年的神经干细胞研究十大研究进展

13. 2018年的神经干细胞研究十大研究进展

14. 2018年的十大睡眠研究突破

15. 2018年“衰老和长生不老”领域的十大研究突破

16. 2018年自闭症领域的十大研究突破

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20个神经科学领域的突破可能获得诺贝尔奖

1. 意识研究：意识的本质、组成、运行机制及其物质载体；不同意识层次的操控和干预，意识障碍性疾病的治疗。

2. 学习和记忆的机制及其调控：记忆的形成和消退机制，记忆的人为移植和记忆的人为消除等；

3. 痴呆研究：阿尔茨海默病的机制和治疗研究，血管性痴呆、额颞叶痴呆、路易体痴呆的机制研究和治疗。

4. 睡眠和睡眠障碍的机制和干预研究。

5. 情绪研究：喜、怒、哀、恐等基本情绪的机制和相关疾病的治疗。

6. 计算和逻辑推理的神经科学基础研究。

7. 语言的神经科学基础研究。

8. 视觉图像形成和运用的神经科学基础研究。

9. 创造力、想象力和艺术文学创造的神经基础研究。

10. 痛觉的神经科学基础及其干预研究

11. 性行为研究：性行为的神经科学基础研究和性行为的调控和干预。

12. 脑和脊髓损伤的机制及其干预研究，包括脑卒中、脊髓损伤机制研究，神经干细胞移植研究，新型神经修复技术，神经康复技术。

13. 精神类疾病的机制和干预研究：自闭症、精分、抑郁症、智能障碍、药物成瘾等；

14. 运动神经元病等神经变性病机制研究及其干预。

15. 衰老的机制和永生研究，包括大脑衰老的机制和寿命延长研究。

16. 神经系统遗传病的机制研究及基因治疗。

17. 神经操纵和调控技术：光遗传技术、药物遗传技术、基因编辑技术、经颅磁刺激、深部脑刺激和电刺激等。

18. 脑组织兼容性电子微芯片及脑机互动装置研究，包括脑机接口、神经刺激芯片、记忆存储芯片，意识存储芯片，人脑非语言互动装置等。

19. 半人半机器人的设计、完善和修复技术：包括任何机械肢体的人类移植，大脑移植入机器体内等。

20. 新型大脑成像和神经元活动记录技术：高分辨率成像技术、大型电极微阵列技术等。

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