落實好各部門在規劃實施中的主體責任。2019年阿爾茨海默病十大臨床研究進展1. N Engl J Med─BACE1抑制劑Verubecestat對治療前驅期阿爾茨海默病無效，甚至會引起認知功能的惡化英文摘要：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錛 double-blind錛 placebo-controlled錛 104-week trial toevaluate verubecestat at doses of 12 mg and 40 mg per day錛 as compared withplacebo錛 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錛 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)錛 484 to receive verubecestat at a dose of 40 mg per day (the 40-mggroup)錛 and 485 to receive placebo. A total of 234 patients錛 231 patients錛 and239 patients per group錛 respectively錛 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錛 2.02 in the 40-mg group錛 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)錛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錛 25.5錛 and 19.3 events per 100 patient-years in the 12-mg group錛 the 40-mggroup錛 and the placebo group錛 respectively (hazard ratio for 40 mg vs. placebo錛1.38; 97.51% confidence interval錛 1.07 to 1.79錛 not adjusted for multiplecomparisons)錛 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錛 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錛 NCT01953601.).參考文獻：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─對于高血壓患者而言，
服用降壓藥確實可以降低罹患阿爾茨海默病的風險英文摘要：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錛 1980錛 and Jan 1錛 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錛 supplemented with additional data錛 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錛 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)錛 those using any AHM had a reduced risk for developing dementia(hazard ratio [HR] 0·88錛 95% CI 0·79-0·98; p=0·019) and Alzheimer's disease (HR0·84錛 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)錛 there was noassociation between AHM use and incident dementia or Alzheimer's disease.INTERPRETATION:Overa long period of observation錛 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錛 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.參考文獻：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─純合子APOE3等位基因可以抵抗常染色體顯性阿爾茨海默病的發生英文摘要：Weidentified a PSEN1 (presenilin 1) mutation carrier from the world's largestautosomal dominant Alzheimer's disease kindred錛 who did not develop mildcognitive impairment until her seventies錛 three decades after the expected ageof clinical onset. The individual had two copies of the APOE3 Christchurch(R136S) mutation錛 unusually high brain amyloid levels and limited tau andneurodegenerative measurements. Our findings have implications for the role ofAPOE in the pathogenesis錛 treatment and prevention of Alzheimer's disease.參考文獻：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─全球疾病負擔研究組發布1990-2016年間全球阿爾茨海默病和其他癡呆的疾病負擔數據英文摘要：BACKGROUND:Thenumber of individuals living with dementia is increasing錛 negatively affectingfamilies錛 communities錛 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錛 mortality錛 and overall burden of dementia as captured by the GlobalBurden of Diseases錛 Injuries錛 and Risk Factors (GBD) Study 2016錛 and highlightthe most important messages for clinicians and neurologists.METHODS:GBD2016 obtained data on dementia from vital registration systems錛 publishedscientific literature and surveys錛 and data from health-service encounters ondeaths錛 excess mortality錛 prevalence錛 and incidence from 195 countries andterritories from 1990 to 2016錛 through systematic review and additionaldata-seeking efforts. To correct for differences in cause of death codingacross time and locations錛 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錛 prevalence錛 years of lifelost (YLLs)錛 years of life lived with disability (YLDs)錛 anddisability-adjusted life-years (DALYs; computed as the sum of YLLs and YLDs)錛and the fractions of these metrics that were attributable to four risk factorsthat met GBD criteria for assessment (high body-mass index [BMI]錛 high fastingplasma glucose錛 smoking錛 and a diet high in sugar-sweetened beverages).FINDINGS:In2016錛 the global number of individuals who lived with dementia was 43·8 million(95% uncertainty interval [UI] 37·8-51·0)錛 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)錛 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錛 95% UI 23·3-31·4錛 vs 16.8 million錛 14.4-19.6)錛 and dementia was thefifth leading cause of death globally錛 accounting for 2·4 million (95% UI2·1-2·8) deaths. Overall錛 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錛 high fasting plasma glucose錛 smoking錛and a high intake of sugar-sweetened beverages.INTERPRETATION:Theglobal number of people living with dementia more than doubled from 1990 to2016錛 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錛 future analyses should improve on the methods for thecorrection of these biases. Until breakthroughs are made in prevention orcurative treatment錛 dementia will constitute an increasing challenge tohealth-care systems worldwide.參考文獻：GBD2016 Dementia Collaborators. Global錛 regional錛 and national burden ofAlzheimer's disease and other dementias錛 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─今年最大的學術爭議之一：阿爾茨海默病中成年海馬神經再生是否持續存在？英文摘要1：The hippocampus is one of the most affected areas in Alzheimer's disease (AD)1. Moreover錛 thisstructure hosts one of the most unique phenomena of the adult mammalian brain錛namely錛 the addition of new neurons throughout life2. This process錛called adult hippocampal neurogenesis (AHN)錛 confers an unparalleled degree ofplasticity to the entire hippocampal circuitry3錛4. Nonetheless錛direct evidence of AHN in humans has remained elusive. Thus錛 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錛 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錛 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錛 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錛 Nestin+Sox2+neural progenitor cells (NPCs) and DCX+ neuroblasts and immatureneurons were detected錛 but their numbers greatly varied between participants.Nestin+ cells localize in the anterior hippocampus錛 and NPCs錛neuroblasts錛 and immature neurons are evenly distributed along the anterior toposterior axis. The number of DCX+PCNA+ cells is reducedin mild cognitive impairments錛 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.參考文獻：1.Moreno-Jim□nez 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─科學家構建了一個可以高效預測MCI進展為癡呆的生物標志物模型英文摘要：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錛 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)錛 Alzheimer's Disease Neuroimaging Initiative (ADNI; n=829)錛 AmsterdamDementia Cohort (ADC; n=666)錛 and the Swedish BioFINDER study (n=233).Inclusion criteria were a baseline diagnosis of MCI錛 at least 6 months offollow-up錛 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錛 a hippocampal volumemodel錛 and a CSF biomarkers model-by evaluating them across cohorts錛incorporating different biomarker measurement methods錛 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錛 we constructed a model combining markers for amyloid deposition錛tauopathy錛 and neurodegeneration (ATN)錛 in accordance with the NationalInstitute on Aging and Alzheimer's Association research framework.FINDINGS:Weincluded all 2611 individuals with MCI in the four cohorts錛 1007 (39%) of whomprogressed to dementia. The validated demographics model (Harrell's C 0·62錛 95%CI 0·59-0·65)錛 validated hippocampal volume model (0·67錛 0·62-0·72)錛 andupdated CSF biomarkers model (0·72錛 0·68-0·74) had adequate prognosticperformance across cohorts and were well calibrated. The newly constructed ATNmodel had the highest performance (0·74錛 0·71-0·76).INTERPRETATION:Wegenerated risk models that are robust across cohorts錛 which adds to theirpotential clinical applicability. The models could aid clinicians in theinterpretation of CSF biomarker and hippocampal volume results in individualswith MCI錛 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錛 particularly if their use affects participants'understanding錛 emotional wellbeing錛 and behaviour.FUNDING:ZonMW-Memorabel.參考文獻：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─研究發現ATN模型可以有助于預測非癡呆老年人群的記憶力下降英文摘要：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錛 tau錛 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錛 and to determine whether biomarkers provide incremental prognostic valuebeyond more readily available clinical and genetic information.Design錛Setting錛 and Participants:Population-basedcohort study of cognitive aging in Olmsted County錛 Minnesota錛 that included 480nondemented Mayo Clinic Study of Aging participants who had a clinical evaluationand amyloid positron emission tomography (PET) (A)錛 tau PET (T)錛 and magneticresonance imaging (MRI) cortical thickness (N) measures between April 16錛 2015錛and November 1錛 2017錛 and at least 1 clinical evaluation follow-up by November12錛 2018.Exposures:Age錛sex錛 education錛 cardiovascular and metabolic conditions score錛 APOE genotype錛and AT(N) biomarker profiles. Each of A錛 T錛 or (N) can be abnormal (+) ornormal (-)錛 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錛 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]錛 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錛 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)+錛A+T+(N)-錛 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錛 -0.17 to -0.09)錛 -0.10 (95% CI錛 -0.16 to -0.05)錛 and -0.10 (95%CI錛 -0.13 to -0.06) z score units per year錛 respectively錛 for an 85-year-oldAPOE ε4 noncarrier.Conclusionsand Relevance:Amongolder persons without baseline dementia followed for a median of 4.8 years錛 aprediction model that included amyloid PET錛 tau PET錛 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.參考文獻：Jacket al (2019). Associations of Amyloid錛 Tau錛 and Neurodegeneration BiomarkerProfiles With Rates of Memory Decline Among Individuals Without Dementia. JAMA.2019 Jun 18;321(23):2316-2325. 8. Nature medicine─血清神經絲輕鏈水平可以預測無症狀阿爾次海默病進展為癡呆英文摘要：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錛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錛 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錛 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錛 NfL dynamics in serum predict disease progression and brainneurodegeneration at the early presymptomatic stages of familial Alzheimer's disease錛which supports its potential utility as a clinically useful biomarker.參考文獻：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─脆弱程度或許可以用來解釋阿爾茨海默病臨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錛 whereas others withlittle Alzheimer's disease pathology have been diagnosed with Alzheimer'sdementia. We aimed to examine whether frailty錛 which is associated with bothage and dementia錛 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錛 a clinical-pathological cohort study of older adults (older than59 years) without known dementia at baseline錛 living in Illinois錛 USA. Participantsin the cohort study underwent annual neuropsychological and clinicalevaluations. In the present cross-sectional analysis錛 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錛 frailty錛 and Alzheimer's dementia. All analyses wereadjusted for age錛 sex錛 and education.FINDINGS:Upto data cutoff (Jan 20錛 2017)錛 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錛 95% CI 1·54-2·02; p0·0001) and Alzheimer's disease pathology(4·81錛 3·31-7·01; p0·0001) were independently associated with Alzheimer'sdementia錛 after adjusting for age錛 sex錛 and education. When frailty was addedto the model for the relationship between Alzheimer's disease pathology andAlzheimer's dementia錛 model fit improved (p0·0001). There was a significantinteraction between frailty and Alzheimer's disease pathology (odds ratio 0·73錛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錛 people with a low amount of frailty were betterable to tolerate Alzheimer's disease pathology錛 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錛 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.參考文獻：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─穹窿區深部腦刺激可以誘導阿爾茨海默病患者的記憶回想英文摘要：In atrial of stimulation of the fornix and subcallosal regions of the hippocampusinvolving 42 patients with Alzheimer’s disease錛 20 patients reported vividmemory flashbacks. The robustness and complexity of the memories increased withincreasing voltage applied to the stimulating electrodes.參考文獻：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年十大研究進展名錄1. 年終盤點：2019年帕金森病十大基礎研究進展2. 年終盤點：2019年帕金森病十大臨床研究進展3. 年終盤點：2019年阿爾茨海默病十大基礎研究進展2018年十大研究進展名錄1.盤點2018年阿爾茨海默病十大研究突破2.盤點2018年帕金森病十大研究突破3. 盤點2018年神經科學二十大研究突破4. 盤點2018年漸凍症（ALS）十大研究進展5. 盤點2018年全球腦卒中十大研究進展6. 盤點2018年神經影像十大研究進展7. 盤點2018年神經炎症領域的十大研究突破8. 盤點2018年神經變性癡呆十大研究突破9. 2018年神經科學“學習和記憶”領域十大研究進展10. 2018年抑鬱症領域的十大研究突破11. 2018年痛覺和疼痛領域的十大研究突破12. 2018年的神經幹細胞研究十大研究進展13. 2018年的神經幹細胞研究十大研究進展14. 2018年的十大睡眠研究突破15. 2018年“衰老和長生不老”領域的十大研究突破16. 2018年自閉症領域的十大研究突破歡迎加入60個“神經科學臨床和基礎社群”1、神經科學臨床和基礎主群（500人）已滿；2、神經科學臨床和基礎Alzheimer亞群；3、神經科學臨床和基礎Parkinson亞群；4、神經科學臨床和基礎cerebrovascular亞群；5、神經科學臨床和基礎Depression亞群；6、神經科學臨床和基礎Movement disorders亞群；7、神經科學臨床和基礎Neuroimmunology亞群；8、神經科學臨床和基礎Psychiatry亞群；9、神經科學臨床和基礎Neuroimaging亞群；10、神經科學臨床和基礎Neurogenetics亞群；11、神經科學臨床和基礎Neurodegeneration亞群；12、神經科學臨床和基礎Epilepsy亞群；13、神經科學臨床和基礎Sleep亞群；14、神經科學臨床和基礎Neural Development亞群；15、神經科學臨床和基礎Electrophysiology亞群；16、神經科學臨床和基礎Neural circuits亞群；17、神經科學臨床和基礎神經調控和腦機接口亞群；18、神經科學臨床和基礎人工智能亞群；19、神經科學臨床和基礎重大疾病和疑難病亞群；20、神經科學臨床和基礎衰老和永生亞群；21、神經科學臨床和基礎週圍神經病群；22、神經科學臨床和基礎神經肌肉疾病群；23、神經科學臨床和基礎視覺系統研究群；24、神經科學臨床和基礎疼痛研究群；25、神經科學臨床和基礎Emotion研究群；26、神經科學臨床和基礎意識研究群；27、神經科學臨床和基礎Learning & Memory亞群；28、神經科學國自然基金申請交流群；29、神經科學ALS/FTD交流群；30、神經科學腦外傷和脊髓外傷研究群；31、神經科學兒科神經病學交流群；32、神經科學Autism & ADHD研究群；33、神經科學大數據和組學研究群；34、神經科學非編碼RNA研究群；35、神經科學schizophrenia研究群；36、神經科學Non-human primate研究群；37、神經科學神經損傷與修復研究群；38、神經科學Epigenetics研究群；39、神經科學神經介入和靜脈溶栓亞群；40、神經科學計算神經科學亞群；41、神經科學基因治療交流群；42、神經科學細胞治療交流群；43、神經科學納米藥物治療交流群；44、神經科學中醫藥治療交流群；45、神經科學免疫調節治療交流群；46、神經科學類器官和類腦研究交流群；47、神經科學語言研究交流群；48、神經科學深度學習和神經網絡交流群；49、神經科學類神經元和類腦器件設計交流群；50、神經科學半人半機器人交流群；51、神經科學感染性疾病研究群；52、神經科學神經系統腫瘤研究群；53、神經科學星型和小膠質細胞研究群；54、神經科學神經外科研究群;55、神經科學系統論和復雜性研究交流群；56、神經科學腦腸軸和Microbiota交流群；57、神經科學虛擬現實、增強現實和混合現實交流群；58、神經科學臨床試驗和流行病學研究交流群；59、神經科學單細胞測序研究交流群；60、神經科學蛋白質解析交流群。如果想入群，請加我微信（qingyierjing），並回復要加入的群，我會將您拉入群中。20個神經科學領域的突破可能獲得諾貝爾獎1. 意識研究：意識的本質、組成、運行機制及其物質載體；不同意識層次的操控和幹預，意識障礙性疾病的治療。2. 學習和記憶的機制及其調控：記憶的形成和消退機制，記憶的人為移植和記憶的人為消除等；3. 癡呆研究：阿爾茨海默病的機制和治療研究，血管性癡呆、額顳葉癡呆、路易體癡呆的機制研究和治療。4. 睡眠和睡眠障礙的機制和幹預研究。5. 情緒研究：喜、怒、哀、恐等基本情緒的機制和相關疾病的治療。6. 計算和邏輯推理的神經科學基礎研究。7. 語言的神經科學基礎研究。8. 視覺圖像形成和運用的神經科學基礎研究。9. 創造力、想象力和藝術文學創造的神經基礎研究。10. 痛覺的神經科學基礎及其幹預研究11. 性行為研究：性行為的神經科學基礎研究和性行為的調控和幹預。12. 腦和脊髓損傷的機制及其幹預研究，包括腦卒中、脊髓損傷機制研究，
