阿尔茨海默病研究与治疗是阿尔茨海默病转化研究的主要论坛，也是该领域领先的开放获取期刊。它隶属于阿尔茨海默病国际 (ADI)，出版以转化为重点的开放获取基础研究，以及临床试验、药物发现和开发研究以及流行病学研究。该杂志还提供评论、观点、评论和辩论和报告。虽然主要关注的是阿尔茨海默氏症，但范围包括对其他神经退行性疾病的转化研究。

Alzheimer's Research and Therapy is a leading open-access journal and a major forum for translational research on Alzheimer's disease. It is affiliated with the Alzheimer's Disease International (ADI) and publishes open-access research focused on translational studies, including basic research, clinical trials, drug discovery and development, as well as epidemiological studies. The journal also features reviews, opinions, debates, and reports. While primarily focused on Alzheimer's disease, it also encompasses translational research on other neurodegenerative diseases.

《Alzheimer's Research and Therapy》是阿尔茨海默病转化研究的主要论坛，也是该领域领先的开放获取期刊。该期刊隶属于阿尔茨海默病国际（ADI），专注于转化研究，涵盖基础研究、临床试验、药物发现与开发研究以及流行病学研究。此外，期刊还提供评论、观点、辩论和报告等内容。虽然主要关注阿尔茨海默病，但也包括其他神经退行性疾病的转化研究。

Alzheimer's Research and Therapy

Abstract Background Predicting future Alzheimer’s disease (AD)-related cognitive decline among individuals with subjective cognitive decline (SCD) or mild cognitive impairment (MCI) is an important task for healthcare. Structural brain imaging as measured by magnetic resonance imaging (MRI) could potentially contribute when making such predictions. It is unclear if the predictive performance of MRI can be improved using entire brain images in deep learning (DL) models compared to using pre-defined brain regions. Methods A cohort of 332 individuals with SCD/MCI were included from the Swedish BioFINDER-1 study. The goal was to predict longitudinal SCD/MCI-to-AD dementia progression and change in Mini-Mental State Examination (MMSE) over four years. Four models were evaluated using different predictors: (1) clinical data only, including demographics, cognitive tests and APOE ε4 status, (2) clinical data plus hippocampal volume, (3) clinical data plus all regional MRI gray matter volumes ( N = 68) extracted using FreeSurfer software, (4) a DL model trained using multi-task learning with MRI images, Jacobian determinant images and baseline cognition as input. A double cross-validation scheme, with five test folds and for each of those ten validation folds, was used. External evaluation was performed on part of the ADNI dataset, including 108 patients. Mann-Whitney U-test was used to determine statistically significant differences in performance, with p -values less than 0.05 considered significant. Results In the BioFINDER cohort, 109 patients (33%) progressed to AD dementia. The performance of the clinical data model for prediction of progression to AD dementia was area under the curve (AUC) = 0.85 and four-year cognitive decline was R 2 = 0.14. The performance was improved for both outcomes when adding hippocampal volume (AUC = 0.86, R 2 = 0.16). Adding FreeSurfer brain regions improved prediction of four-year cognitive decline but not progression to AD (AUC = 0.83, R 2 = 0.17), while the DL model worsened the performance for both outcomes (AUC = 0.84, R 2 = 0.08). A sensitivity analysis showed that the Jacobian determinant image was more informative than the MRI image, but that performance was maximized when both were included. In the external evaluation cohort from ADNI, 23 patients (21%) progressed to AD dementia. The results for predicted progression to AD dementia were similar to the results for the BioFINDER test data, while the performance for the cognitive decline was deteriorated. Conclusions The DL model did not significantly improve the prediction of clinical disease progression in AD, compared to regression models with a single pre-defined brain region.

Ida Arvidsson

Olof Strandberg

Sebastian Palmqvist

Erik Stomrud

Nicholas Cullen

Shorena Janelidze

Pontus Tideman

Anders Heyden

Karl Åström

Oskar Hansson

Niklas Mattsson-Carlgren

Alzheimer s Research & Therapy

Comparing a pre-defined versus deep learning approach for extracting brain atrophy patterns to predict cognitive decline due to Alzheimer’s disease in patients with mild cognitive symptoms

The pathological hallmarks of Alzheimer's disease (AD) involve alterations in the expression of numerous genes associated with transcriptional levels, which are determined by chromatin accessibility. Here, the landscape of chromatin accessibility was studied to understand the outline of the transcription and expression of AD-associated metabolism genes in an AD mouse model.The assay for transposase-accessible chromatin by sequencing (ATAC-seq) was used to investigate the AD-associated chromatin reshaping in the APPswe/PS1dE9 (APP/PS1) mouse model. ATAC-seq data in the hippocampus of 8-month-old APP/PS1 mice were generated, and the relationship between chromatin accessibility and gene expression was analyzed in combination with RNA sequencing. Gene ontology (GO) analysis was applied to elucidate biological processes and signaling pathways altered in APP/PS1 mice. Critical transcription factors were identified; alterations in chromatin accessibility were further confirmed using chromatin immunoprecipitation assays.We identified 1690 increased AD-associated chromatin-accessible regions in the hippocampal tissues of APP/PS1 mice. These regions were enriched in genes related to diverse signaling pathways, including the PI3K-Akt, Hippo, TGF-β, and Jak-Stat signaling pathways, which play essential roles in regulating cell proliferation, apoptosis, and inflammatory responses. A total of 1003 decreased chromatin-accessible regions were considered to be related with declined AD-associated biological processes including cellular response to hyperoxia and insulin stimulus, synaptic transmission, and positive regulation of autophagy. In the APP/PS1 hippocampus, 1090 genes were found to be upregulated and 1081 downregulated. Interestingly, enhanced ATAC-seq signal was found in approximately 740 genes, with 43 exhibiting upregulated mRNA levels. Several genes involved in AD development were found to have a significantly increased expression in APP/PS1 mice compared to controls, including Sele, Clec7a, Cst7, and Ccr6. The signatures of numerous transcription factors, including Olig2, NeuroD1, TCF4, and NeuroG2, were found enriched in the AD-associated accessible chromatin regions. The transcription-activating marks of H3K4me3 and H3K27ac were also found increased in the promoters of these genes. These results indicate that the mechanism for the upregulation of genes could be attributed to the enrichment of open chromatin regions with transcription factors motifs and the histone marks H3K4me3 and H3K27ac.Our study reveals that alterations in chromatin accessibility may be an initial mechanism in AD pathogenesis.

Yaqi Wang

Xiaomin Zhang

Qiao Song

Yuli Hou

Jing Liu

Yu Sun

Peichang Wang

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model

阿尔茨海默病（AD）小鼠模型中染色质可及性的表征

Mild cognitive impairment (MCI) is a precursor to Alzheimer's disease (AD), but not all MCI patients develop AD. Biomarkers for early detection of individuals at high risk for MCI-to-AD conversion are urgently required.We used blood-based microRNA expression profiles and genomic data of 197 Japanese MCI patients to construct a prognosis prediction model based on a Cox proportional hazard model. We examined the biological significance of our findings with single nucleotide polymorphism-microRNA pairs (miR-eQTLs) by focusing on the target genes of the miRNAs. We investigated functional modules from the target genes with the occurrence of hub genes though a large-scale protein-protein interaction network analysis. We further examined the expression of the genes in 610 blood samples (271 ADs, 248 MCIs, and 91 cognitively normal elderly subjects [CNs]).The final prediction model, composed of 24 miR-eQTLs and three clinical factors (age, sex, and APOE4 alleles), successfully classified MCI patients into low and high risk of MCI-to-AD conversion (log-rank test P = 3.44 × 10-4 and achieved a concordance index of 0.702 on an independent test set. Four important hub genes associated with AD pathogenesis (SHC1, FOXO1, GSK3B, and PTEN) were identified in a network-based meta-analysis of miR-eQTL target genes. RNA-seq data from 610 blood samples showed statistically significant differences in PTEN expression between MCI and AD and in SHC1 expression between CN and AD (PTEN, P = 0.023; SHC1, P = 0.049).Our proposed model was demonstrated to be effective in MCI-to-AD conversion prediction. A network-based meta-analysis of miR-eQTL target genes identified important hub genes associated with AD pathogenesis. Accurate prediction of MCI-to-AD conversion would enable earlier intervention for MCI patients at high risk, potentially reducing conversion to AD.

Daichi Shigemizu

Shintaro Akiyama

Sayuri Higaki

Taiki Sugimoto

Takashi Sakurai

Keith A. Boroevich

Alok Sharma

Tatsuhiko Tsunoda

Takahiro Ochiya

Shumpei Niida

Kouichi Ozaki

Prognosis prediction model for conversion from mild cognitive impairment to Alzheimer’s disease created by integrative analysis of multi-omics data

基于多组学数据整合分析构建的轻度认知障碍向阿尔茨海默病转化的预后预测模型

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder for which no effective therapy is currently available. Given that various attempts to target beta-amyloid (Aβ) have been unsuccessful in clinical trials, other potential pathogenic factors such as brain energy metabolism (EM) have attracted increasing attention. Traditional Chinese medicines, including danggui-shaoyao-san (DSS), play a notable role in AD. However, it remains unclear whether DSS exerts therapeutic effects on AD through EM regulation. In this study, we conducted behavioural tests, Nissl staining, haematoxylin and eosin staining, and thioflavin S staining, in APP/PS1 mice to assess the pharmacodynamic effect of DSS on AD. Subsequently, we integrated the drug target network of herbal ingredients in DSS and evaluated their absorption, distribution, metabolism, excretion, and toxicity properties to identify the core ingredients. We used proteomic and metabolomic approaches to explore the potential mechanisms of action of DSS against AD. Consequently, we verified the mechanism underlying EM using qPCR, western blotting, and ELISA. In vivo experimental results revealed that DSS ameliorated cognitive impairment in APP/PS1 mice, attenuated neuronal apoptosis, and reduced Aβ burden. Furthermore, the drug-target network comprised 6,514 drug-target interactions involving 1,118 herbal ingredients and 218 AD genes, of which 253 were identified as the core ingredients in DSS. The proteomic results implied that DSS could act on EM to alleviate AD, and targeted energy metabolomics suggested that DSS regulated 47 metabolites associated with EM. Mechanistically, we found that DSS could regulate the GSK3β/PGC1α signalling pathway to improve brain glucose uptake and mitigate mitochondrial dysfunction and oxidative stress, ultimately promoting EM to treat AD. Our study is the first to integrate multi-omics approaches to reveal that DSS could regulate the GSK3β/PGC1α signalling pathway to exert therapeutic effects in AD through the promotion of EM, thereby providing new insights into the mechanism of action of DSS against AD.

Qihui Wu

Wei Wang

Zhuangzi Huang

Xianghao Lin

Maozhong Yao

Chuipu Cai

Guohu Weng

Yong Gu

Hongying Li

Jinman Liu

Jiansong Fang

Weirong Li

Unveiling the molecular mechanisms of Danggui-Shaoyao-San against Alzheimer’s disease in APP/PS1 mice via integrating proteomic and metabolomic approaches

揭示当归芍药散通过整合蛋白质组学和代谢组学方法对抗APP/PS1小鼠阿尔茨海默病的分子机制

Electroencephalogram (EEG) has emerged as a non-invasive tool to detect the aberrant neuronal activity related to different stages of Alzheimer’s disease (AD). However, the effectiveness of EEG in the precise diagnosis and assessment of AD and its preclinical stage, amnestic mild cognitive impairment (MCI), has yet to be fully elucidated. In this study, we aimed to identify key EEG biomarkers that are effective in distinguishing patients at the early stage of AD and monitoring the progression of AD.
A total of 890 participants, including 189 patients with MCI, 330 patients with AD, 125 patients with other dementias (frontotemporal dementia, dementia with Lewy bodies, and vascular cognitive impairment), and 246 healthy controls (HC) were enrolled. Biomarkers were extracted from resting-state EEG recordings for a three-level classification of HC, MCI, and AD. The optimal EEG biomarkers were then identified based on the classification performance. Random forest regression was used to train a series of models by combining participants’ EEG biomarkers, demographic information (i.e., sex, age), CSF biomarkers, andAPOEphenotype for assessing the disease progression and individual’s cognitive function.
The identified EEG biomarkers achieved over 70% accuracy in the three-level classification of HC, MCI, and AD. Among all six groups, the most prominent effects of AD-linked neurodegeneration on EEG metrics were localized at parieto-occipital regions. In the cross-validation predictive analyses, the optimal EEG features were more effective than the CSF +APOEbiomarkers in predicting the age of onset and disease course, whereas the combination of EEG + CSF +APOEmeasures achieved the best performance for all targets of prediction.
Our study indicates that EEG can be used as a useful screening tool for the diagnosis and disease progression evaluation of MCI and AD.

Bin Jiao

Rihui Li

Hui Zhou

Kunqiang Qing

Hui Liu

Hefu Pan

Yanqin Lei

Wenjin Fu

Xiaoan Wang

Xuewen Xiao

Xixi Liu

Qijie Yang

Xinxin Liao

Yafang Zhou

Liangjuan Fang

Yanbin Dong

Yuanhao Yang

Haiyan Jiang

Sha Huang

Lu Shen

Alzheimer's Research &amp; Therapy

Alz Res Therapy

Neural biomarker diagnosis and prediction to mild cognitive impairment and Alzheimer’s disease using EEG technology

使用脑电图技术对轻度认知障碍和阿尔茨海默病的神经生物标志物诊断与预测

Recent research has postulated that the activation of cGAS-STING-interferon signalling pathways could be implicated in the pathogenesis of Alzheimer's disease (AD). However, the precise types of interferons and related cytokines, both from the brain and periphery, responsible for cognitive impairment in patients with AD remain unclear. A total of 131 participants (78 [59.5%] female and 53 [40.5%] male; mean [SD] age, 61.5 [7.6] years) with normal cognition and cognitive impairment from the China Aging and Neurodegenerative Initiative cohort were included. CSF and serum IFNα-2a, IFN-β, IFN-γ, TNF-α, IL-6, IL-10, MCP-1and CXCL-10 were tested. The correlation between these interferons and related cytokines with AD core biomarkers in the CSF and plasma, cognition performance, and brain MRI measures were analysed. We found that only CSF IFN-β levels were significantly elevated in Alzheimer's disease compared to normal cognition. Furthermore, CSF IFN-β levels were significantly associated with AD core biomarkers (CSF P-tau and Aβ42/Aβ40 ratio) and cognitive performance (MMSE and CDR score). Additionally, the CSF IFN-β levels were significantly correlated with the typical pattern of brain atrophy in AD (such as hippocampus, amygdala, and precuneus). In contrast, CSF IL-6 levels were significantly elevated in non-AD cognitively impaired patients compared to other groups. Moreover, CSF IL-6 levels were significantly associated with cognitive performance in non-AD individuals and correlated with the vascular cognitive impairment-related MRI markers (such as white matter hyperintensity). Our findings demonstrate that distinct inflammatory molecules are associated with different cognitive disorders. Notably, CSF IFN-β levels are significantly linked to the pathology and cognitive performance of AD, identifying this interferon as a potential target for AD therapy.

Qiong Wang

Shufen Yuan

Chenxi Wang

Duntao Huang

Mengguo Zhang

Yaxi Zhan

Feng Gao

Jiong Shi

Allan I. Levey

Yong Shen

Brain derived β-interferon is a potential player in Alzheimer’s disease pathogenesis and cognitive impairment

脑源性β-干扰素在阿尔茨海默病发病机制和认知障碍中具有潜在作用

Alzheimer's disease neuropathologic change (ADNC) and Lewy pathology (LP) often coexist in cognitively impaired individuals. These pathologies' relative distribution and severity may modify these individuals' clinical presentation, cognitive profile, and prognosis. Therefore, we examined the contributions of LP and concomitant ADNC to disease survival and profiles of cognitive decline in preclinical and clinical stages in a large neuropathologically diagnosed group. We evaluated 597 participants with LP and 491 participants with intermediate/high ADNC in the absence of LP from the National Alzheimer Coordinating Center (NACC) database. At baseline, 237 participants were cognitively normal (CN), 255 were diagnosed with mild cognitive impairment (MCI), and 596 with dementia. Cognition was assessed using three cognitive domain scores (i.e., Memory, Executive, and Language) from the NACC Uniform Dataset (UDS) neuropsychological test battery, MMSE, and Clinical Dementia Rating (CDR). Multivariate adaptive regression splines were used to evaluate associations between baseline cognitive scores and mean annual rate of change over two years. The likelihood of progression to MCI or dementia was assessed using Cox hazard models. Neocortical LP, independent of the clinical diagnosis, was associated with lower Executive and higher Language and Memory scores at baseline, whereas Braak V-VI neurofibrillary tangle pathology was associated with lower Memory and Language scores. Similarly, neocortical LP was associated with faster Executive decline, whereas Braak V-VI neurofibrillary tangle pathology was associated with faster Memory and Language decline. A clinical diagnosis of Lewy Body Dementia (i.e., a strong LP phenotype) was associated with the LP cognitive profile and shorter disease duration. Progression to incident MCI or dementia was primarily associated with the degree of tau pathology; neocortical LP or a diagnosis of Lewy Body Dementia only predicted progression when those with intermediate/high ADNC were excluded. LP and ADNC differentially affected cross-sectional and longitudinal cognitive profiles in a large autopsy sample. Concomitant Braak V-VI neurofibrillary tangle pathology had a strong impact on clinical progression in those with LP, regardless of the initial stage. Thus, LB and ADNC co-pathology interact to affect cognitive domains that may be used to track Lewy Body disease longitudinally and as outcome measures in therapeutic trials.

Jon B. Toledo

David P. Salmon

Melissa J. Armstrong

Douglas Galasko

Cognitive decline profiles associated with lewy pathology in the context of Alzheimer’s disease neuropathologic change

阿尔茨海默病神经病理改变背景下与路易体病理相关的认知衰退特征

Accumulation of critically short telomeres (CST) is implicated in decreased tissular regenerative capacity and increased susceptibility to degenerative diseases such as Alzheimer's disease (AD). Telomere shortening has also been associated with age-related brain changes. However, it remains unclear whether CST accumulation is directly associated with AD markers or instead amplifies age-related effects, potentially increasing susceptibility of developing AD in cognitively healthy older adults. This cross-sectional study used baseline data of 129 community-dwelling cognitively healthy older adults from the Age-Well trial (NCT02977819), aged 65 years and older enrolled between 2016 and 2018, in France. Using linear regressions, we analyzed the relationship between an innovative marker of telomere shortening, the percentage of CST (%CST), structural, functional and molecular neuroimaging outcomes, and multiple blood-based biomarkers related to AD pathophysiology. The effect of apolipoprotein E ε4 genotype (APOE4) was assessed on these relationships using interaction analysis. A higher %CST was associated with lower global kurtosis fractional anisotropy (β = -.230; P = .010), particularly in frontal and temporal regions. A higher %CST was also related to higher plasma levels of Neurofilament light chain (β = .195; P = .020) and a lower subiculum volume (β = -.206; P = .020), although these associations did not meet the threshold for multiple comparisons. %CST was not associated with AD-related neuroimaging markers, including the AD-sensitive gray matter pattern (β = -.060; P = .441), glucose metabolism pattern (β = -.099; P = .372), brain perfusion pattern (β = -.106; P = .694) or hippocampus volume (β = -.106; P = .194). In APOE4 carriers, higher %CST was associated with lower subiculum (β = -.423; P = 0.003), DG (β = -.410; P = 0.018) and CA1 volumes (β = -.373; P = 0.024), even though associations with DG and CA1 volumes did not survive multiple comparison. Although an increase in %CST does not appear to be directly linked to the pathophysiology of AD in cognitively healthy older adults, it could heighten the susceptibility of APOE4 carriers to develop AD plausibly due to greater vulnerability to age-related effects. However, longitudinal studies would be necessary to determine whether %CST influences the development and progression of AD later in life.

Asrar Lehodey

Perla Kaliman

Cassandre Palix

Robin de Florès

Edelweiss Touron

Anne-Laure Turpin

Séverine Fauvel

Florence Mézenge

Brigitte Landeau

Anne Chocat

Agathe Vrillon

Claire Paquet

Denis Vivien

Vincent de La Sayette

Gaël Chételat

Géraldine Poisnel

Claire André

Eider M. Arenaza-Urquijo

Pierre Champetier

Fabienne Colette

Robin De Flores

Marion Delarue

Francesca Felisatti

Egantine Ferrand Devouge

Antoine Garnier-Crussard

Julie Gonneaud

Marc Heidmann

Frank Jessen

Olga Klimecki

Elizabeth Kuhn

Gwendoline Le Du

Valérie Lefranc

Antoine Lutz

Natalie Marchant

Florence Mezenge

Inès Moulinet

Valentin Ourry

Léo Paly

Stefano Poletti

Anne Quillard

Géraldine Rauchs

Stéphane Rehel

Eric Salmon

Siya Sherif

Matthieu Vanhoutte

Patrik Vuilleumier

Caitliin Ware

Miranka Wirth

Association of critically short telomeres with brain and blood markers of ageing and Alzheimer’s disease in older adults

关键性端粒缩短与老年人脑部和血液中衰老及阿尔茨海默病标志物的关联

The advent of Alzheimer's disease-modifying drugs requires accurate biological diagnosis to identify candidates for these therapies. So far, the most promising single plasma biomarker is phosphorylated tau at threonine 217 (p-tau217). To understand its biological features, it is essential to know its longitudinal trajectory and factors influencing it in cognitively unimpaired subjects with no brain pathology. We analyzed longitudinal plasma p-tau217 values (mean follow-up time = 768.3 days) in a cohort of 209 healthy volunteers. We have studied factors associated with plasma p-tau217 changes by using different linear mixed-effects models. In amyloid-negative cognitively healthy subjects (n = 151) carriers of ApoE ε4 allele had significantly higher p-tau217 values than non-carriers (0.85 pg/mL; p-value < 0.001) and also a greater rate of change (0.01 pg/mL/year; p-value < 0.001). In the overall sample, including subjects with amyloid and tau pathology we have seen that amyloid positive subjects had higher predicted baseline plasma p-tau217 values than amyloid negative subjects (0.16 pg/mL; p-value < 0.001) and a greater rate of change (0.00004 pg/mL/day; p-value < 0.001). Subjects considered tau positive also showed a greater rate of change of p-tau217 with respect to tau negative (0.00005 pg/mL/day; p-value < 0.001). A + T + N + participants showed a higher baseline p-tau217 levels than A-T-N- subjects (0.2 pg/mL; p-value < 0.001) and also a greater rate of change (0.00006 pg/mL/day; p-value = 0.002). ApoE ε4 carriers had a greater rate of change than non-carriers (0.00003 pg/mL/day; p-value = 0.03). In amyloid-negative cognitively unimpaired subjects, ApoE4 status influenced both baseline levels and rate of change of plasma p-tau217. Other factors such as age, sex or glomerular filtration rate have not shown significant influence on plasma p-tau217 levels in this group.

Francisco Martínez-Dubarbie

Armando Guerra-Ruiz

Sara López-García

Carmen Lage

Marta Fernández-Matarrubia

Ana Pozueta-Cantudo

María García-Martínez

Andrea Corrales-Pardo

María Bravo

Marcos López-Hoyos

Juan Irure-Ventura

Enrique Marco de Lucas

Marta Drake-Pérez

María Teresa García-Unzueta

Pascual Sánchez-Juan

Eloy Rodríguez-Rodríguez

Longitudinal trajectory of plasma p-tau217 in cognitively unimpaired subjects

认知正常受试者血浆p-tau217的纵向轨迹

Abstract Background Although there is growing evidence of the association between gender and early diagnosis of preclinical Alzheimer's disease, little attention has been given to the enrolment ratio of men and women in clinical trials and data reporting. Methods This study aims to analyze gender differences in sociodemographic factors associated with the willingness to participate in clinical trials and undergo specific procedures in the context of an Alzheimer's disease prevention research cohort. 2544 cognitively unimpaired participants from the ALFA parent cohort (age 45–75 years) of the Barcelonaβeta Brain Research Center were contacted through a structured phone call to determine their willingness to participate in Alzheimer's disease clinical trials and undergo trial-related procedures (magnetic resonance imaging, lumbar puncture, positron emission tomography, and cognitive assessment). Sociodemographic data on education, occupational attainment, civil and caregiver status were gathered. Stepwise logistic regression models were performed in order to study the interaction between gender and sociodemographic factors in the willingness to participate in clinical trials and to undergo clinical trial-related procedures. Results 1,606 out of the 2,544 participants were women (63.1%). Women were significantly younger and had lower educational attainment compared with men. In addition, women were more likely to be caregivers, single and unemployed. Women showed a significantly lower willingness than men to participate in a clinical trial ( p = 0.003) and to undergo a lumbar puncture ( p &lt; 0.001). Single women were less willing to participate in clinical trials than single men ( p = 0.041). Regarding clinical trial-related procedures, women with higher years of education were significantly less willing to undergo a lumbar puncture ( p = 0.031). Conclusion We found gender differences regarding the sociodemographic factors that predict the willingness to participate in clinical trials and to undergo clinical trial-related procedures. Our results highlight the urgent need to design recruitment strategies accounting for gender-related factors, particularly those related to marital status and education.

Lidia Canals-Gispert

Alba Cañas-Martínez

Gema Huesa

Marc Suárez-Calvet Alomà

Marta Milà-Alomà

Eider Arenaza-Urquijo

Davide Cirillo

Annemarie Schumacher Dimech

Maria Florencia Iulita

Julie Novakova Martinkova

Maria Carmela Tartaglia

Frances-Catherine Quevenco

Antonella Santuccione Chadha

Gonzalo Sánchez-Benavides

Carolina Minguillón

Maria Teresa Ferretti

Karine Fauria

Anna Brugulat-Serrat

Jordi Freixa

Juan Domingo Gispert

Oriol Grau-Rivera

Xavier Gotsens

Xavier Meléndez

Tania Menchón

José Luis Molinuevo

Pau Sánchez

Montserrat Vilà

Impact of gender on the willingness to participate in clinical trials and undergo related procedures in individuals from an Alzheimer’s prevention research cohort

性别对阿尔茨海默病预防研究队列中个体参与临床试验及相关程序意愿的影响

Abbreviation	Alz Res Therapy
Journal Impact	8.07
Quartiles(Global)	NEUROSCIENCES(Q1)

ISSN	1758-9193
h-index	97
Top Journals	Yes

Publication Information	Publisher: BioMed Central Ltd，Publishing cycle: ，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 2010，Proportion of original research papers: 91.15%，Self Citation Rate:2.50%， Gold OA Rate: 100.00%
Journal Fees	$3990Details
Average review cycle	网友分享经验：>12周，或约稿

Alzheimer's Research and Therapy

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