2019年阿尔茨海默病十大临床研究进展

1. N Engl J Med—BACE1抑制剂Verubecestat对治疗前驱期阿尔茨海默病无效，甚至会引起认知功能的恶化

英文摘要：

BACKGROUND:

ProdromalAlzheimer's disease offers an opportunity to test the effect of drugs thatmodify the deposition of amyloid in the brain before the onset of dementia.Verubecestat is an orally administered β-site amyloid precursorprotein-cleaving enzyme 1 (BACE-1) inhibitor that blocks production ofamyloid-beta (Aβ). The drug did not prevent clinical progression in a trialinvolving patients with mild-to-moderate dementia due to Alzheimer's disease.

METHODS:

Weconducted a randomized, double-blind, placebo-controlled, 104-week trial toevaluate verubecestat at doses of 12 mg and 40 mg per day, as compared withplacebo, in patients who had memory impairment and elevated brain amyloidlevels but whose condition did not meet the case definition of dementia. The primaryoutcome was the change from baseline to week 104 in the score on the ClinicalDementia Rating Scale-Sum of Boxes (CDR-SB; scores range from 0 to 18, withhigher scores indicating worse cognition and daily function). Secondaryoutcomes included other assessments of cognition and daily function.

RESULTS:

Thetrial was terminated for futility after 1454 patients had been enrolled; 485had been assigned to receive verubecestat at a dose of 12 mg per day (the 12-mggroup), 484 to receive verubecestat at a dose of 40 mg per day (the 40-mggroup), and 485 to receive placebo. A total of 234 patients, 231 patients, and239 patients per group, respectively, completed 104 weeks of the trial regimen.The estimated mean change from baseline to week 104 in the CDR-SB score was1.65 in the 12-mg group, 2.02 in the 40-mg group, and 1.58 in the placebo group(P = 0.67 for the comparison between the 12-mg group and the placebo group andP = 0.01 for the comparison between the 40-mg group and the placebo group),suggesting a worse outcome in the higher-dose group than in the placebo group.The estimated rate of progression to dementia due to Alzheimer's disease was24.5, 25.5, and 19.3 events per 100 patient-years in the 12-mg group, the 40-mggroup, and the placebo group, respectively (hazard ratio for 40 mg vs. placebo,1.38; 97.51% confidence interval, 1.07 to 1.79, not adjusted for multiplecomparisons), favoring placebo. Adverse events were more common in theverubecestat groups than in the placebo group.

CONCLUSIONS:

Verubecestatdid not improve clinical ratings of dementia among patients with prodromalAlzheimer's disease, and some measures suggested that cognition and dailyfunction were worse among patients who received verubecestat than among thosewho received placebo. (Funded by Merck Sharp & Dohme; ClinicalTrials.govnumber, NCT01953601.).

参考文献：

Eganet al (2019). Randomized Trial of Verubecestat for Prodromal Alzheimer'sDisease. N Engl J Med. 2019 Apr 11;380(15):1408-1420.

2. Lancet Neurol—对于高血压患者而言，服用降压药确实可以降低罹患阿尔茨海默病的风险

英文摘要：

BACKGROUND:

Dementiais a major health concern for which prevention and treatment strategies remainelusive. Lowering high blood pressure with specific antihypertensivemedications (AHMs) could reduce the burden of disease. We investigated whetherspecific AHM classes reduced the risk for dementia.

METHODS:

Wedid a meta-analysis of individual participant data from eligible observationalstudies published between Jan 1, 1980, and Jan 1, 2019. Cohorts were eligiblefor inclusion if they prospectively recruited community-dwelling adults;included more than 2000 participants; collected data for dementia events overat least 5 years; had measured blood pressure and verified use of AHMs;included in-person exams, supplemented with additional data, to capturedementia events; and had followed up cases for mortality. We assessed theassociation of incident dementia and clinical Alzheimer's disease with use offive AHM classes, within strata of baseline high (systolic blood pressure [SBP]≥140 mmHg or diastolic blood pressure [DBP] ≥90mm Hg) and normal (SBP <140 mm Hg and DBP <90 mm Hg) blood pressure. Weused a propensity score to control for confounding factors related to theprobability of receiving AHM. Study-specific effect estimates were pooled usingrandom-effects meta-analyses.

RESULTS:

Sixprospective community-based studies (n=31 090 well phenotyped dementia-freeadults older than 55 years) with median follow-ups across cohorts of 7-22 yearswere eligible for analysis. There were 3728 incident cases of dementia and 1741incident Alzheimer's disease diagnoses. In the high blood pressure stratum(n=15 537), those using any AHM had a reduced risk for developing dementia(hazard ratio [HR] 0·88, 95% CI 0·79-0·98; p=0·019) and Alzheimer's disease (HR0·84, 0·73-0·97; p=0·021) compared with those not using AHM. We did not findany significant differences between one drug class versus all others on risk ofdementia. In the normal blood pressure stratum (n=15 553), there was noassociation between AHM use and incident dementia or Alzheimer's disease.

INTERPRETATION:

Overa long period of observation, no evidence was found that a specific AHM drugclass was more effective than others in lowering risk of dementia. Among peoplewith hypertensive levels of blood pressure, use of any AHM with efficacy tolower blood pressure might reduce the risk for dementia. These findings suggestfuture clinical guidelines for hypertension management should also consider thebeneficial effect of AHM on the risk for dementia.

FUNDING:

TheAlzheimer's Drug Discovery Foundation and the National Institute on AgingIntramural Research Program.

参考文献：

Dinget al (2019)—Antihypertensive medications and risk for incident dementiaand Alzheimer's disease: a meta-analysis of individual participant data fromprospective cohort studies. Lancet Neurol. 2020 Jan;19(1):61-70.

3. Nature medicine—纯合子APOE3等位基因可以抵抗常染色体显性阿尔茨海默病的发生

英文摘要：

Weidentified a PSEN1 (presenilin 1) mutation carrier from the world's largestautosomal dominant Alzheimer's disease kindred, who did not develop mildcognitive impairment until her seventies, three decades after the expected ageof clinical onset. The individual had two copies of the APOE3 Christchurch(R136S) mutation, unusually high brain amyloid levels and limited tau andneurodegenerative measurements. Our findings have implications for the role ofAPOE in the pathogenesis, treatment and prevention of Alzheimer's disease.

参考文献：

Arboleda-Velasquez et al (2019). Resistance to autosomaldominant Alzheimer's disease in an APOE3 Christchurch homozygote: a casereport. Nat Med. 2019 Nov;25(11):1680-1683.

4. Lancet Neurol—全球疾病负担研究组发布1990-2016年间全球阿尔茨海默病和其他痴呆的疾病负担数据

英文摘要：

BACKGROUND:

Thenumber of individuals living with dementia is increasing, negatively affectingfamilies, communities, and health-care systems around the world. A successfulresponse to these challenges requires an accurate understanding of the dementiadisease burden. We aimed to present the first detailed analysis of the globalprevalence, mortality, and overall burden of dementia as captured by the GlobalBurden of Diseases, Injuries, and Risk Factors (GBD) Study 2016, and highlightthe most important messages for clinicians and neurologists.

METHODS:

GBD2016 obtained data on dementia from vital registration systems, publishedscientific literature and surveys, and data from health-service encounters ondeaths, excess mortality, prevalence, and incidence from 195 countries andterritories from 1990 to 2016, through systematic review and additionaldata-seeking efforts. To correct for differences in cause of death codingacross time and locations, we modelled mortality due to dementia usingprevalence data and estimates of excess mortality derived from countries thatwere most likely to code deaths to dementia relative to prevalence. Data wereanalysed by standardised methods to estimate deaths, prevalence, years of lifelost (YLLs), years of life lived with disability (YLDs), anddisability-adjusted life-years (DALYs; computed as the sum of YLLs and YLDs),and the fractions of these metrics that were attributable to four risk factorsthat met GBD criteria for assessment (high body-mass index [BMI], high fastingplasma glucose, smoking, and a diet high in sugar-sweetened beverages).

FINDINGS:

In2016, the global number of individuals who lived with dementia was 43·8 million(95% uncertainty interval [UI] 37·8-51·0), increased from 20.2 million(17·4-23·5) in 1990. This increase of 117% (95% UI 114-121) contrasted with aminor increase in age-standardised prevalence of 1·7% (1·0-2·4), from 701 cases(95% UI 602-815) per 100 000 population in 1990 to 712 cases (614-828) per100 000 population in 2016. More women than men had dementia in 2016 (27·0million, 95% UI 23·3-31·4, vs 16.8 million, 14.4-19.6), and dementia was thefifth leading cause of death globally, accounting for 2·4 million (95% UI2·1-2·8) deaths. Overall, 28·8 million (95% UI 24·5-34·0) DALYs were attributedto dementia; 6·4 million (95% UI 3·4-10·5) of these could be attributed to themodifiable GBD risk factors of high BMI, high fasting plasma glucose, smoking,and a high intake of sugar-sweetened beverages.

INTERPRETATION:

Theglobal number of people living with dementia more than doubled from 1990 to2016, mainly due to increases in population ageing and growth. Althoughdifferences in coding for causes of death and the heterogeneity incase-ascertainment methods constitute major challenges to the estimation of theburden of dementia, future analyses should improve on the methods for thecorrection of these biases. Until breakthroughs are made in prevention orcurative treatment, dementia will constitute an increasing challenge tohealth-care systems worldwide.

参考文献：

GBD2016 Dementia Collaborators. Global, regional, and national burden ofAlzheimer's disease and other dementias, 1990-2016: a systematic analysis forthe Global Burden of Disease Study 2016. Lancet Neurol. 2019 Jan;18(1):88-106.

5. Nature medicine和Cell stem cell—今年最大的学术争议之一：阿尔茨海默病中成年海马神经再生是否持续存在？

英文摘要1：

The hippocampus is one of the most affected areas in Alzheimer's disease (AD)¹. Moreover, thisstructure hosts one of the most unique phenomena of the adult mammalian brain,namely, the addition of new neurons throughout life². This process,called adult hippocampal neurogenesis (AHN), confers an unparalleled degree ofplasticity to the entire hippocampal circuitry^3,4. Nonetheless,direct evidence of AHN in humans has remained elusive. Thus, determiningwhether new neurons are continuously incorporated into the human dentate gyrus(DG) during physiological and pathological aging is a crucial question withoutstanding therapeutic potential. By combining human brain samples obtainedunder tightly controlled conditions and state-of-the-art tissue processingmethods, we identified thousands of immature neurons in the DG ofneurologically healthy human subjects up to the ninth decade of life. Theseneurons exhibited variable degrees of maturation along differentiation stagesof AHN. In sharp contrast, the number and maturation of these neuronsprogressively declined as AD advanced. These results demonstrate thepersistence of AHN during both physiological and pathological aging in humansand provide evidence for impaired neurogenesis as a potentially relevantmechanism underlying memory deficits in AD that might be amenable to noveltherapeutic strategies.

英文摘要2：

Whetherhippocampal neurogenesis persists throughout life in the human brain is notfully resolved. Here, we demonstrate that hippocampal neurogenesis ispersistent through the tenth decade of life and is detectable in patients withmild cognitive impairments and Alzheimer's disease.In a cohort of 18 participants with a mean age of 90.6 years, Nestin⁺Sox2⁺neural progenitor cells (NPCs) and DCX⁺ neuroblasts and immatureneurons were detected, but their numbers greatly varied between participants.Nestin⁺ cells localize in the anterior hippocampus, and NPCs,neuroblasts, and immature neurons are evenly distributed along the anterior toposterior axis. The number of DCX⁺PCNA⁺ cells is reducedin mild cognitive impairments, and higher numbers of neuroblasts are associatedwith better cognitive status. The number of DCX⁺PCNA⁺cells correlates with functional interactions between presynaptic SNAREproteins. Our results suggest that hippocampal neurogenesis persists in theaged and diseased human brain and that it is possibly associated withcognition.

参考文献：

1.Moreno-Jiménez et al (2019). Adult hippocampal neurogenesis is abundant inneurologically healthy subjects and drops sharply in patients with Alzheimer'sdisease. Nat Med. 2019 Apr;25(4):554-560.

2.Tobin et al (2019). Human Hippocampal Neurogenesis Persists in Aged Adults andAlzheimer's Disease Patients. Cell Stem Cell. 2019 Jun 6;24(6):974-982.e3.

6. Lancet Neurol—科学家构建了一个可以高效预测MCI进展为痴呆的生物标志物模型

英文摘要：

BACKGROUND:

Biomarker-basedrisk predictions of dementia in people with mild cognitive impairment arehighly relevant for care planning and to select patients for treatment whendisease-modifying drugs become available. We aimed to establish robustprediction models of disease progression in people at risk of dementia.

METHODS:

Inthis modelling study, we included people with mild cognitive impairment (MCI)from single-centre and multicentre cohorts in Europe and North America: theEuropean Medical Information Framework for Alzheimer's Disease (EMIF-AD;n=883), Alzheimer's Disease Neuroimaging Initiative (ADNI; n=829), AmsterdamDementia Cohort (ADC; n=666), and the Swedish BioFINDER study (n=233).Inclusion criteria were a baseline diagnosis of MCI, at least 6 months offollow-up, and availability of a baseline Mini-Mental State Examination (MMSE)and MRI or CSF biomarker assessment. The primary endpoint was clinicalprogression to any type of dementia. We evaluated performance of previouslydeveloped risk prediction models-a demographics model, a hippocampal volumemodel, and a CSF biomarkers model-by evaluating them across cohorts,incorporating different biomarker measurement methods, and determiningprognostic performance with Harrell's C statistic. We then updated the modelsby re-estimating parameters with and without centre-specific effects andevaluated model calibration by comparing observed and expected survival.Finally, we constructed a model combining markers for amyloid deposition,tauopathy, and neurodegeneration (ATN), in accordance with the NationalInstitute on Aging and Alzheimer's Association research framework.

FINDINGS:

Weincluded all 2611 individuals with MCI in the four cohorts, 1007 (39%) of whomprogressed to dementia. The validated demographics model (Harrell's C 0·62, 95%CI 0·59-0·65), validated hippocampal volume model (0·67, 0·62-0·72), andupdated CSF biomarkers model (0·72, 0·68-0·74) had adequate prognosticperformance across cohorts and were well calibrated. The newly constructed ATNmodel had the highest performance (0·74, 0·71-0·76).

INTERPRETATION:

Wegenerated risk models that are robust across cohorts, which adds to theirpotential clinical applicability. The models could aid clinicians in theinterpretation of CSF biomarker and hippocampal volume results in individualswith MCI, and help research and clinical settings to prepare for a future ofprecision medicine in Alzheimer's disease. Future research should focus on theclinical utility of the models, particularly if their use affects participants'understanding, emotional wellbeing, and behaviour.

FUNDING:

ZonMW-Memorabel.

参考文献：

Van et al (2019). Biomarker-based prognosis for peoplewith mild cognitive impairment (ABIDE): a modelling study. Lancet Neurol. 2019Nov;18(11):1034-1044.

7. JAMA—研究发现ATN模型可以有助于预测非痴呆老年人群的记忆力下降

英文摘要：

Importance:

ANational Institute on Aging and Alzheimer's Association workgroup proposed aresearch framework for Alzheimer disease in which biomarker classification ofresearch participants is labeled AT(N) for amyloid, tau, and neurodegenerationbiomarkers.

Objective:

Todetermine the associations between AT(N) biomarker profiles and memory declinein a population-based cohort of individuals without dementia age 60 years orolder, and to determine whether biomarkers provide incremental prognostic valuebeyond more readily available clinical and genetic information.

Design,Setting, and Participants:

Population-basedcohort study of cognitive aging in Olmsted County, Minnesota, that included 480nondemented Mayo Clinic Study of Aging participants who had a clinical evaluationand amyloid positron emission tomography (PET) (A), tau PET (T), and magneticresonance imaging (MRI) cortical thickness (N) measures between April 16, 2015,and November 1, 2017, and at least 1 clinical evaluation follow-up by November12, 2018.

Exposures:

Age,sex, education, cardiovascular and metabolic conditions score, APOE genotype,and AT(N) biomarker profiles. Each of A, T, or (N) can be abnormal (+) ornormal (-), resulting in 8 AT(N) profiles.

MainOutcomes and Measures:

Primaryoutcome was a composite memory score measured longitudinally at 15-monthintervals. Analyses measured the associations between predictor variables andthe memory score, and whether AT(N) biomarker profiles significantly improvedprediction of memory z score rates of change beyond a model with clinical andgenetic variables only.

Results:

Participantswere followed up for a median of 4.8 years (interquartile range [IQR], 3.8-5.1)and 44% were women (211/480). Median (IQR) ages ranged from 67 years (65-73) inthe A-T-(N)- group to 83 years (76-87) in the A+T+(N)+ group. Of theparticipants, 92% (441/480) were cognitively unimpaired but the A+T+(N)+ grouphad the largest proportion of mild cognitive impairment (30%). AT(N) biomarkersimproved the prediction of memory performance over a clinical model from an R2of 0.26 to 0.31 (P < .001). Memory declined fastest in the A+T+(N)+,A+T+(N)-, and A+T-(N)+ groups compared with the other 5 AT(N) groups(P = .002). Estimated rates of decline in the 3 fastest declining groups were-0.13 (95% CI, -0.17 to -0.09), -0.10 (95% CI, -0.16 to -0.05), and -0.10 (95%CI, -0.13 to -0.06) z score units per year, respectively, for an 85-year-oldAPOE ε4 noncarrier.

Conclusionsand Relevance:

Amongolder persons without baseline dementia followed for a median of 4.8 years, aprediction model that included amyloid PET, tau PET, and MRI cortical thicknessresulted in a small but statistically significant improvement in predictingmemory decline over a model with more readily available clinical and geneticvariables. The clinical importance of this difference is uncertain.

参考文献：

Jacket al (2019). Associations of Amyloid, Tau, and Neurodegeneration BiomarkerProfiles With Rates of Memory Decline Among Individuals Without Dementia. JAMA.2019 Jun 18;321(23):2316-2325.

8.       Nature medicine—血清神经丝轻链水平可以预测无症状阿尔次海默病进展为痴呆

英文摘要：

Neurofilamentlight chain (NfL) is a promising fluid biomarker of disease progression forvarious cerebral proteopathies. Here we leverage the unique characteristics ofthe Dominantly Inherited Alzheimer Network and ultrasensitive immunoassaytechnology to demonstrate that NfL levels in the cerebrospinal fluid (n = 187)and serum (n = 405) are correlated with one another and are elevated at thepresymptomatic stages of familial Alzheimer's disease. Longitudinal,within-person analysis of serum NfL dynamics (n = 196) confirmed this elevationand further revealed that the rate of change of serum NfL could discriminatemutation carriers from non-mutation carriers almost a decade earlier thancross-sectional absolute NfL levels (that is, 16.2 versus 6.8 years before theestimated symptom onset). Serum NfL rate of change peaked in participantsconverting from the presymptomatic to the symptomatic stage and was associatedwith cortical thinning assessed by magnetic resonance imaging, but less so withamyloid-β deposition or glucose metabolism (assessed by positron emissiontomography). Serum NfL was predictive for both the rate of cortical thinningand cognitive changes assessed by the Mini-Mental State Examination and LogicalMemory test. Thus, NfL dynamics in serum predict disease progression and brainneurodegeneration at the early presymptomatic stages of familial Alzheimer's disease,which supports its potential utility as a clinically useful biomarker.

参考文献：

Preischeet al (2019). Serum neurofilament dynamics predicts neurodegeneration andclinical progression in presymptomatic Alzheimer's disease. Nat Med. 2019Feb;25(2):277-283.

9.      Lancet Neurol—脆弱程度或许可以用来解释阿尔茨海默病临床和病理不匹配的矛盾

英文摘要：

BACKGROUND:

Somepeople with substantial Alzheimer's disease pathology at autopsy had shown fewcharacteristic clinical symptoms or signs of the disease, whereas others withlittle Alzheimer's disease pathology have been diagnosed with Alzheimer'sdementia. We aimed to examine whether frailty, which is associated with bothage and dementia, moderates the relationship between Alzheimer's diseasepathology and Alzheimer's dementia.

METHODS:

Wedid a cross-sectional analysis of data from participants of the Rush Memory andAging Project, a clinical-pathological cohort study of older adults (older than59 years) without known dementia at baseline, living in Illinois, USA. Participantsin the cohort study underwent annual neuropsychological and clinicalevaluations. In the present cross-sectional analysis, we included thoseparticipants who did not have any form of dementia or who had Alzheimer'sdementia at the time of their last clinical assessment and who had died and forwhom complete autopsy data were available. Alzheimer's disease pathology wasquantified by a summary measure of neurofibrillary tangles and neuritic anddiffuse plaques. Clinical diagnosis of Alzheimer's dementia was based onclinician consensus. Frailty was operationalised retrospectively using healthvariable information obtained at each clincial evaluation using the deficitaccumulation approach (41-item frailty index). Logistic regression andmoderation modelling were used to assess relationships between Alzheimer'sdisease pathology, frailty, and Alzheimer's dementia. All analyses wereadjusted for age, sex, and education.

FINDINGS:

Upto data cutoff (Jan 20, 2017), we included 456 participants (mean age at death89·7 years [SD 6·1]; 316 [69%] women). 242 (53%) had a diagnosis of possible orprobable Alzheimer's dementia at their last clinical assessment. Frailty (oddsratio 1·76, 95% CI 1·54-2·02; p<0·0001) and Alzheimer's disease pathology(4·81, 3·31-7·01; p<0·0001) were independently associated with Alzheimer'sdementia, after adjusting for age, sex, and education. When frailty was addedto the model for the relationship between Alzheimer's disease pathology andAlzheimer's dementia, model fit improved (p<0·0001). There was a significantinteraction between frailty and Alzheimer's disease pathology (odds ratio 0·73,95% CI 0·57-0·94; pinteraction=0·015). People with an increased frailty scorehad a weakened direct link between Alzheimer's disease pathology andAlzheimer's dementia; that is, people with a low amount of frailty were betterable to tolerate Alzheimer's disease pathology, whereas those with higheramounts of frailty were more likely both to have more Alzheimer's diseasepathology and for it to be expressed as dementia.

INTERPRETATION:

Thedegree of frailty among people of the same age modifies the association betweenAlzheimer's disease pathology and Alzheimer's dementia. That frailty is relatedto both odds of Alzheimer's dementia and disease expression has implicationsfor clinical management, since individuals with even a low level of Alzheimer'sdisease pathology might be at risk for dementia if they have high amounts offrailty. Further research should assess how frailty and cognition change overtime to better elucidate this complex relationship.

参考文献：

Wallaceet al (2019). Investigation of frailty as a moderator of the relationshipbetween neuropathology and dementia in Alzheimer's disease: a cross-sectionalanalysis of data from the Rush Memory and Aging Project. Lancet Neurol. 2019Feb;18(2):177-18.

10.   N Engl J Med—穹窿区深部脑刺激可以诱导阿尔茨海默病患者的记忆回想

英文摘要：

In atrial of stimulation of the fornix and subcallosal regions of the hippocampusinvolving 42 patients with Alzheimer’s disease, 20 patients reported vividmemory flashbacks. The robustness and complexity of the memories increased withincreasing voltage applied to the stimulating electrodes.

参考文献：

Deebet al (2019). Fornix-Region Deep Brain Stimulation-Induced Memory Flashbacks inAlzheimer's Disease. N Engl J Med. 2019 Aug 22;381(8):783-785.

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

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

欢迎加入60个“神经科学临床和基础社群”

1、神经科学临床和基础主群（500人）已满；

2、神经科学临床和基础Alzheimer亚群；

3、神经科学临床和基础Parkinson亚群；

4、神经科学临床和基础cerebrovascular亚群；

5、神经科学临床和基础Depression亚群；

6、神经科学临床和基础Movement disorders亚群；

7、神经科学临床和基础Neuroimmunology亚群；

8、神经科学临床和基础Psychiatry亚群；

9、神经科学临床和基础Neuroimaging亚群；

10、神经科学临床和基础Neurogenetics亚群；

11、神经科学临床和基础Neurodegeneration亚群；

12、神经科学临床和基础Epilepsy亚群；

13、神经科学临床和基础Sleep亚群；

14、神经科学临床和基础Neural Development亚群；

15、神经科学临床和基础Electrophysiology亚群；

16、神经科学临床和基础Neural circuits亚群；

17、神经科学临床和基础神经调控和脑机接口亚群；

18、神经科学临床和基础人工智能亚群；

19、神经科学临床和基础重大疾病和疑难病亚群；

20、神经科学临床和基础衰老和永生亚群；

21、神经科学临床和基础周围神经病群；

22、神经科学临床和基础神经肌肉疾病群；

23、神经科学临床和基础视觉系统研究群；

24、神经科学临床和基础疼痛研究群；

25、神经科学临床和基础Emotion研究群；

26、神经科学临床和基础意识研究群；

27、神经科学临床和基础Learning & Memory亚群；

28、神经科学国自然基金申请交流群；

29、神经科学ALS/FTD交流群；

30、神经科学脑外伤和脊髓外伤研究群；

31、神经科学儿科神经病学交流群；

32、神经科学Autism & ADHD研究群；

33、神经科学大数据和组学研究群；

34、神经科学非编码RNA研究群；

35、神经科学schizophrenia研究群；

36、神经科学Non-human primate研究群；

37、神经科学神经损伤与修复研究群；

38、神经科学Epigenetics研究群；

39、神经科学神经介入和静脉溶栓亚群；

40、神经科学计算神经科学亚群；

41、神经科学基因治疗交流群；

42、神经科学细胞治疗交流群；

43、神经科学纳米药物治疗交流群；

44、神经科学中医药治疗交流群；

45、神经科学免疫调节治疗交流群；

46、神经科学类器官和类脑研究交流群；

47、神经科学语言研究交流群；

48、神经科学深度学习和神经网络交流群；

49、神经科学类神经元和类脑器件设计交流群；

50、神经科学半人半机器人交流群；

51、神经科学感染性疾病研究群；

52、神经科学神经系统肿瘤研究群；

53、神经科学星型和小胶质细胞研究群；

54、神经科学神经外科研究群;

55、神经科学系统论和复杂性研究交流群；

56、神经科学脑肠轴和Microbiota交流群；

57、神经科学虚拟现实、增强现实和混合现实交流群；

58、神经科学临床试验和流行病学研究交流群；

59、神经科学单细胞测序研究交流群；

60、神经科学蛋白质解析交流群。

如果想入群，请加我微信（qingyierjing），并回复要加入的群，我会将您拉入群中。

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。