一句话贡献（摘要首句摘录）：The basal forebrain (BF) provides the principal cholinergic innervation to the cortex and the hippocampus and is among the earliest regions affected by neurodegenerative processes.

核心要点（正文原句摘录）：
① [Results] Normative modelling of basal forebrain cholinergic subnuclei across mid-to-late adulthood We first constructed normative reference models for the two principal compartments of the basal forebrain cholinergic system — Ch1–3 (medial septum and vertical/horizontal limbs of the diagonal band) and Ch4 (NbM) — in participants across mid-to-late life between the ages of 45 and 87 years.
② [Discussion] These dissociable profiles are supported by a previous study in healthy adults aged 20–94 years, showing the most pronounced linear age-related decline in the Ch419.
③ [（全文补选）] In AD, early post-mortem work reported profound (>75%) neuronal loss in Ch4, while later stereological analyses indicate that neuronal shrinkage and marker downregulation contribute to this7,8, while in vivo MRI studies showed Ch4 volume loss already at prodromal stages9,10.
④ [（全文补选）] In LBD, Ch4 degeneration and cortical cholinergic denervation have been related to, and shown to predict, cognitive decline and dementia11–13.
⑤ [（全文补选）] While previous works provided evidence that Ch4 and Ch1–3 may behave differently in AD and LBD8,14–17, whether the two compartments are indeed differentially affected across diseases, and if so, how, still remains to be established, with recent reviews explicitly highlighting the need for disease-related, subregional-resolved analysis and for a clearer temporal staging of BF vulnerability16,18.

数据速览（正文抽取）：75% · 10 · 13 · 14 · 17 · 18

保留意见/局限（原文摘录）：① While previous works provided evidence that Ch4 and Ch1–3 may behave differently in AD and LBD8,14–17, whether the two compartments are indeed differentially affected across diseases, and if so, how, still remains to be established, with recent reviews explicitly highlighting the need for disease-related, subregional-resolved analysis and for a clearer temporal staging of BF vulnerability16,18.
② Furthermore, it remains unclear whether BF vulnerability is specific to neurodegenerative aetiology or reflects a broader susceptibility shared across neuropsychiatric disorders20.

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一句话贡献（摘要首句摘录）：Abstract C9orf72 encodes a protein that is important for both typical neurodevelopment and homeostatic processes across the lifespan.

核心要点（正文原句摘录）：
① [Results] Participant demographics Young adult C9orf72 repeat expansion carriers (n=72) and non-carriers (n=48) from the FPI did not differ in age (range 18-30 years), sex, and total intracranial volume (Table 1).
② [Discussion] Extending prior findings from older asymptomatic C9orf72 repeat expansion carriers with a mean age of 43.9±11.7 years19 to the present results in young adulthood, this sample of young adult carriers aged 18-30 years demonstrated smaller volumes in the pulvinar (bilateral PuM, PuA, and PuI), mediodorsal (bilateral MDl and MDm), and lateral (left LD and LP) thalamic nuclei.
③ [（全文补选）] ## Introduction Frontotemporal lobar degeneration (FTLD) is a neurodegenerative dementia that demonstrates heterogeneous age of onset, clinical symptomology, and neuropathology.1 Around 10-15% of all FTLD cases are caused by autosomal dominant variants, with 13-50% caused by hexanucleotide repeat expansions in C9orf72.2,3 Both fundamental research on C9orf724 and preclinical models of C9orf72-associated FTD/amyotrophic lateral sclerosis in neurodevelopmental contexts5–7 have shown that C9orf72 is important for typical neurodevelopmental processes, including regulating cortical and thalamic volume development, neural stem cell proliferation, self-renewal, and maintenance, neuronal survival, synaptogenesis, and axonogenesis.
④ [（全文补选）] The question of whether C9orf72 repeat expansions may affect neurodevelopment in FTLD is thus being increasingly explored,8–14 with efforts underway to test this hypothesis in human youth carriers of genetic FTLD variants.15,16 In asymptomatic young adult carriers of pathogenic C9orf72 repeat expansions aged 18-30 years, arguably the last window of neurodevelopment where synaptic pruning, myelination, and maturation processes remain prominent,17 clinical neuroimaging studies have consistently observed smaller thalamic volumes at the group level.8,10,11 The earliest average age at which smaller thalamic volumes have been detected in young adult expansion carriers compared to non-carriers was 26 years old.10 Longitudinal modelling of cortical and subcortical volumes in young adult C9orf72 expansion carriers across two international FTLD cohorts extended these findings, and did not find an interaction with with age across 18 to 30 years old, supporting the hypothesis that thalamic volume differences may have neurodevelopmental origins.8 Studies of slightly older asymptomatic C9orf72 expansion carriers (aged 39.8±11.1 years) found differences in average gray matter volumes, white matter integrity, and neuropsychological test scores,18 as well as smaller volumes at the level of specific thalamic nuclei, with earliest differences affecting the laterodorsal, lateral geniculate, and pulvinar nuclei in carriers aged 43.9±11.7 years.19 A natural hypothesis arising from both preclinical and clinical neuroimaging literature, then, is that if volume differences within specific thalamic nuclei are present in young adult C9orf72 expansion carriers, the potential underlying cellular and molecular mechanisms could reflect neurodevelopmental and/or FTLD-related neurodegenerative processes.
⑤ [（全文补选）] As the thalamus is reliably the earliest region where volumetric differences are observed in C9orf72-associated FTLD,8,10,11 understanding its early developmental characteristics may provide a framework for investigating mechanisms contributing to C9orf72-associated FTLD vulnerability and resilience.

数据速览（正文抽取）：10 · 15% · 13 · 50% · 14 · 15

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：Stroke, dementia, and late-life depression share overlapping vascular pathophysiology, yet simple markers of shared neurological vulnerability across these conditions remain limited.

核心要点（正文原句摘录）：
① [RESULTS] 3.1 Sample Characteristics The larger sample comprised 2,308 participants (mean age 61.5±9.2 years; 54% women), and the dementia sample comprised 1,148 participants (mean age 68.6±5.8 years; 53% women).
② [DISCUSSION] 4.1 Quick versus Usual Walking Speed for Incident Dementia Slower QWS was associated with higher 10-year dementia risk, consistent with earlier work in this cohort linking quick-pace walking to incident dementia (12).
③ [Conclusions] QWS was also associated with incident dementia over 10 years, whereas the UWS association did not reach statistical significance.
④ [（全文补选）] 1 Dementia, stroke, and late-life depression collectively account for a substantial and growing share of age-related disability worldwide, contributing to more than 200 million disability-adjusted life years globally (1).
⑤ [（全文补选）] These conditions arise in part from shared vascular and cerebral small vessel pathology and cluster within individuals, and estimates attribute at least 60% of strokes, 40% of dementia cases, and 35% of late-life depression cases to modifiable risk factors (1, 2).

数据速览（正文抽取）：200 · 60% · 40% · 35% · 10 · 11

保留意见/局限（原文摘录）：① Evaluating both paces within the same cohort allowed a direct comparison unavailable to studies recording usual pace alone.
② Examining five outcomes in one cohort allowed cross-outcome comparisons, and rigorous surveillance supported high-confidence ascertainment of incident dementia and stroke.

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一句话贡献（摘要首句摘录）：and Aims: Dilated cardiomyopathy (DCM) is a genetically heterogeneous cause of heart failure and sudden cardiac death.

核心要点（正文原句摘录）：
① [（全文补选）] medrxivMEDRXIVeurheartjmedRxivmedRxiv3067-2007Cold Spring Harbor Laboratory PressMEDRXIV/2026/36178010.64898/2026.09.02.26361780medrxiv;2026.09.02.26361780v2medrxiv;2026.09.02.263617802026.09.02.263617802026.09.02.263617802026.09.02.263617802.1Genetic and Genomic Medicine 1 National Heart and Lung Institute, Imperial College London, London, United Kingdom; Royal Brompton and Harefield Hospitals, Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; 2 Garvan Institute of Medical Research and University of New South Wales, Sydney, NSW, Australia; School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, NSW, Australia; 3 MRC Laboratory of Medical Sciences, Imperial College London, London, United Kingdom; 4 National Heart and Lung Institute, Imperial College London, London, United Kingdom; 5 National Heart and Lung Institute, Imperial College London, London, United Kingdom; MRC Laboratory of Medical Sciences, Imperial College London, London, United Kingdom; 6 Leeds Clinical Genomics Service, Leeds Teaching Hospitals NHS Trust, Leeds, United Kingdom; 7 Garvan Institute of Medical Research and University of New South Wales, Sydney, NSW, Australia; 8 Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, United Kingdom; 9 New York Genome Center, New York, NY, USA; 10 Department of Genomic Medicine, Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Medicine, University of Melbourne, Melbourne, VIC, Australia; Familial Cancer Centre, Peter MacCallum Cancer Centre, Melbourne VIC, Australia; 11 Department of Genomic Medicine, Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Medicine, University of Melbourne, Melbourne, VIC, Australia; 12 Department of Genomic Medicine, Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Medicine, University of Melbourne, Melbourne, VIC, Australia; Department of Cardiology, Royal Melbourne Hospital, Melbourne, VIC, Australia; 13 Institute of Health Informatics, University College London, London, United Kingdom; 14 National Heart and Lung Institute, Imperial College London, London, United Kingdom; Royal Brompton and Harefield Hospitals, Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; MRC Laboratory of Medical Sciences, Imperial College London, Lon; 15 Charite-Universitatsmedizin Berlin and Max Delbruck Center for Molecular Medicine, Berlin, Germany; DZHK, Berlin, Germany; 16 Royal Brompton and Harefield Hospitals, Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom; 17 National Heart and Lung Institute, Imperial College London, London, United Kingdom; Great Ormond Street Hospital NHS Foundation Trust, London, United Kingdom * Corresponding author; email: c.smithdiaz@garvan.org.au http://orcid.org/0000-0001-7688-615XJosephsKatherine S.1http://orcid.org/0000-0002-3334-7495Smith-DiazCarlos C.218c.smithdiaz@garvan.org.auWoodsAngela3PrinceClaire4ZhengSean L.5http://orcid.org/0000-0003-2490-9289BuchanRachel1http://orcid.org/0009-0007-3087-4736CavanaghEsme1http://orcid.org/0009-0004-4219-3215ElahiShezan1http://orcid.org/0009-0006-0397-2800JenningsEmma1ProcterHenry6McTaggartJames S.6JananRiyad4http://orcid.org/0000-0001-8718-230XTheotokisPantazis4BakerAmy7http://orcid.org/0009-0006-6756-6190HendenNatasha7http://orcid.org/0000-0002-5445-6906McGurkKathryn A.5PrescottKatrina6Newcastle Clinical Genetics Team8http://orcid.org/0000-0003-0962-7873JobanputraVaidehi9JamesPaul10http://orcid.org/0000-0002-9405-6595ThompsonTina11http://orcid.org/0000-0003-0437-1581ZentnerDominica12TayalUpasana1http://orcid.org/0000-0002-5876-1748HallidayBrian P.1PrasadSanjay K.1O'ReganDeclan P.3http://orcid.org/0000-0002-9077-4741LumbersR.
② [（全文补选）] Thomas13http://orcid.org/0000-0002-1165-7767BartonPaul J.
③ [（全文补选）] F.1HartillVerity L.6PageStephen P.6RobertsAngharad M.17http://orcid.org/0000-0002-2316-1830CarlingDavid3http://orcid.org/0000-0002-4846-7676InglesJodie2http://orcid.org/0000-0002-6110-5880WareJames S.14GoDCM Consortium2026 692026 15102026 692026 2026.09.02.26361780 0292026 14102026 15102026 © 2026, Posted by openRxiv2026This pre-print is available under a Creative Commons License (Attribution 4.0 International), CC BY 4.0, as described at http://creativecommons.org/licenses/by/4.0/ Background and Aims: Dilated cardiomyopathy (DCM) is a genetically heterogeneous cause of heart failure and sudden cardiac death.
④ [（全文补选）] Results: In 117 paediatric cardiomyopathy trios from the 100,000 Genomes Project, two probands harboured rare de novo MAP3K7 missense variants, significantly more than expected (Bonferroni-adjusted p=0.036).
⑤ [（全文补选）] Rare damaging non-truncating variants were enriched in DCM versus INTERVAL (OR 22, p=0.007) and gnomAD controls (OR 14, p=6.2x10-4), while truncating variants were associated with DCM in Genomics England and increased left ventricular volumes in UK Biobank.

数据速览（正文抽取）：2026 · 36178010 · 64898 · 09 · 02 · 263617802026

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：Background.

核心要点（正文原句摘录）：
① [（全文补选）] All 36 pairs were analysed in both directions using inverse-variance weighted (IVW), MR-Egger, weighted-median and weighted-mode estimators, with Cochran's Q, I2, leave-one-out and single-variant diagnostics, a pre-specified analysis excluding HLA-region instruments, and iterative Q-based outlier removal.
② [（全文补选）] One of 36 forward pairs survived correction.
③ [（全文补选）] Longer telomeres reduced ILD risk: outlier-robust IVW odds ratio (OR) 0.59 per standard deviation (SD), 95% CI 0.49-0.71, p = 2.7 x 10^-8, on 77 instruments, with no residual heterogeneity (I2 = 6%) and concordance across estimators.
④ [（全文补选）] Four pleiotropic instruments - in TERT, TERC, APOE and ATM - inflated the unfiltered estimate to OR 0.46 (0.37-0.57) and accounted for all of its heterogeneity.
⑤ [（全文补选）] The effect was reproduced in 5,159 clinician-diagnosed European IPF cases (OR 0.18, 0.12-0.25, p = 5.0 x 10^-23) and in 1,210 East Asian cases (OR 0.54, 0.35-0.83, p = 0.005).

数据速览（正文抽取）：36 · 59 · 95% · 49 · 71 · x 10^-8

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：Background: Blood-based biomarkers (BBMs) may facilitate early detection of Alzheimers disease (AD), yet data in Latino populations remain limited.

核心要点（正文原句摘录）：
① [（全文补选）] medrxivMEDRXIVmedRxivmedRxiv3067-2007Cold Spring Harbor Laboratory PressMEDRXIV/2026/36530410.64898/2026.10.13.26365304medrxiv;2026.10.13.26365304v1medrxiv;2026.10.13.263653042026.10.13.263653042026.10.13.263653042026.10.13.263653041.1Neurology 1 Boston University; 2 Massachusetts General Hospital * Corresponding author; email: yquiroz@bu.edu Tristao-PereiraCatarina1SilvaGeorge1LopezKelly2KuVivian1GonzalezAmanda1MartinezJairo E.1GiudicessiAveri1RoweMeredith1GarciaSandry M.1Gonzalez CatalanMarta2SaldanaDaniel2GatchelJennifer R.2Ramirez GomezLiliana2http://orcid.org/0000-0001-9714-8244QuirozYakeel T.13yquiroz@bu.edu2026 15102026 15102026 2026.10.13.26365304 13102026 13102026 15102026 © 2026, Posted by openRxiv2026This pre-print is available under a Creative Commons License (Attribution-NonCommercial-NoDerivs 4.0 International), CC BY-NC-ND 4.0, as described at http://creativecommons.org/licenses/by-nc-nd/4.0/ Background: Blood-based biomarkers (BBMs) may facilitate early detection of Alzheimers disease (AD), yet data in Latino populations remain limited.
② [（全文补选）] Methods: Baseline data from 122 older adults without dementia were analyzed.
③ [（全文补选）] Plasma AB42/40, brain-derived phosphorylated tau (p-tau) 217, neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) were measured using NULISA.
④ [（全文补选）] AB42/40 showed no significant associations.
⑤ [（全文补选）] Quirozcitation_submitter_emailyquiroz@bu.educitation_submitter_id83306citation_submitter_institutionBoston Universitycitation_submitter_orcid0000-0001-9714-8244Competing Interest Statement Dr.

数据速览（正文抽取）：2026 · 36530410 · 64898 · 10 · 13 · 263653042026

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：Despite recent evidence of the ability of systemic and organ-specific proteomic aging clocks to predict a large range of age-related diseases, their utility in cancer research remains largely underexplored.

核心要点（正文原句摘录）：
① [（全文补选）] In this study, we evaluated the predictive ability of systemic and organ-specific proteomic aging clocks for (i) all-cause mortality, (ii) cancer-related mortality, and (iii) cancer incidence in a sample of Finnish twins (N = 401, mean age at baseline 62.3 years) with Olink proteomic data.
② [（全文补选）] Participants were followed for a mean of 10.6 years (SD +- 1.6), with estimates from four systemic and 18 organ-specific proteomic aging clocks calculated at baseline.
③ [（全文补选）] Cox proportional hazards regression models adjusted for sex and age at baseline identified 15 proteomic aging clocks as significant predictors of all-cause mortality (Ncases = 28) after multiple testing correction (FDR < 0.05), with 11 remaining significant after lifestyle adjustment (Ncases = 27).
④ [（全文补选）] In predicting cancer-related deaths among participants without a prior cancer diagnosis at baseline (Ncases = 9), only the Immune clock showed a significant positive association after multiple testing correction in basic (HR = 2.94, 95% CI: 1.88-4.59) and lifestyle-adjusted models (HR = 3.31, 95% CI: 1.78-6.17).
⑤ [（全文补选）] No associations with cancer incidence (Ncases = 34 basic, Ncases = 31 adjusted) survived multiple testing correction, although several nominal associations were observed.

数据速览（正文抽取）：N = 401 · 62.3 years · 10.6 years · 18 · 15 · 28

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：Summary Background No known treatments prevent Parkinson's disease (PD) onset or delay its progression.

核心要点（正文原句摘录）：
① [（全文补选）] medrxivMEDRXIVmedRxivmedRxiv3067-2007Cold Spring Harbor Laboratory PressMEDRXIV/2025/32794310.1101/2025.05.20.25327943medrxiv;2025.05.20.25327943v2medrxiv;2025.05.20.253279432025.05.20.253279432025.05.20.253279432025.05.20.253279432.1Neurology 1 Stephen & Denise Adams Center for Parkinson's Disease Research of Yale School of Medicine, New Haven, CT 06510, USA; 2 Department of Biomedical Informatics and Data Science, Yale School of Medicine, New Haven, CT 06510, USA; 3 Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; 4 Milton Academy, Milton, MA 02186, USA; 5 Department of Neurology, Yale School of Medicine, New Haven, CT 06510, USA * Corresponding author; email: xianjun.dong@yale.edu http://orcid.org/0000-0003-2931-2991HuYuxuan1http://orcid.org/0000-0002-2429-8791LiuWeiqiang1ZhouYujia2WaitsMiles3http://orcid.org/0000-0002-5823-2926ZhaoYiyong1http://orcid.org/0000-0002-2799-7336Olivero-AcostaMaria I.1ShengKatherine4http://orcid.org/0000-0002-4860-831XZhangLe5XuHua2http://orcid.org/0000-0002-0567-9193ScherzerClemens R.1http://orcid.org/0000-0002-8052-9320DongXianjun16xianjun.dong@yale.edu2026 2152025 15102026 2152025 2025.05.20.25327943 2052025 15102026 15102026 © 2026, Posted by openRxiv2026This pre-print is available under a Creative Commons License (Attribution 4.0 International), CC BY 4.0, as described at http://creativecommons.org/licenses/by/4.0/ Summary Background No known treatments prevent Parkinson's disease (PD) onset or delay its progression.
② [（全文补选）] The target trial emulation included 269,617 individuals with primary hypertension (25,965 ARB initiators; 36,873 CCB initiators; and 206,779 initiators of other first-line antihypertensives).
③ [（全文补选）] ARB initiation was associated with a lower hazard of incident PD than initiation of other first-line antihypertensives (adjusted HR [aHR] 0.70, 95% CI 0.59-0.83); the corresponding association for CCB initiation was smaller (aHR 0.88, 95% CI 0.77-0.99).
④ [（全文补选）] ARB initiation was also associated with a lower PD risk than ACE inhibitor initiation (aHR 0.81, 95% CI 0.67-0.97).
⑤ [（全文补选）] Aligning Science Across Parkinson's https://ror.org/03zj4c476ASAP-000301ASAP-028376Exploration World Program from China Pharmaceutical University citation_submitter_nameYuxuan Hucitation_submitter_emailyuxuan.hu@yale.educitation_submitter_id153818citation_submitter_institutionStephen & Denise Adams Center for Parkinson's Disease Research of Yale School of Medicine, New Haven, CT 06510, USAcitation_submitter_orcid0000-0003-2931-2991 has-earlier-version yes Competing Interest Statement The authors have declared no competing interest.

数据速览（正文抽取）：2025 · 32794310 · 1101 · 05 · 20 · 253279432025

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：Genetic regulation of neurodevelopmental disorders that impair brain development and social interaction is complex and poorly understood.

核心要点（正文原句摘录）：
① [（全文补选）] medrxivMEDRXIVmedRxivmedRxiv3067-2007Cold Spring Harbor Laboratory PressMEDRXIV/2026/36518210.64898/2026.10.13.26365182medrxiv;2026.10.13.26365182v1medrxiv;2026.10.13.263651822026.10.13.263651822026.10.13.263651822026.10.13.263651821.1Neurology 1 Department of Cell and Developmental Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; 2 Stanley Manne Childrens Research Institute, Ann & Robert H.
② [（全文补选）] Lurie Childrens Hospital of Chicago, Chicago, IL 60611, USA; 3 Department of Translational Genomics, Center for Genomic Medicine, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia; 4 Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA; 5 Division of Neonatology, Ann & Robert H.
③ [（全文补选）] Lurie Children's Hospital of Chicago, Chicago IL 60611; 6 Edwards Family Division of Genetics & Rare Diseases, Ann & Robert H.
④ [（全文补选）] Lurie Childrens Hospital of Chicago, Chicago, IL 60611, USA; 7 Edwards Family Division of Genetics & Rare Diseases, Ann & Robert H.
⑤ [（全文补选）] Lurie Children's Hospital of Chicago, Chicago, IL 60611, USA; 8 Department of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; 9 Departments of Neuroscience and Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; 10 Genomic Medicine Center of Excellence (GMCoE), King Faisal Specialist Hospital and Research Center, Riyadh 11211, Saudi Arabia; 11 Lifera Omics and Department of Human Genetics, College of Medicine, Alfaisal University, Riyadh, Saudi Arabia; 12 Stanley Manne Children's Research Institute, Ann & Robert H.

数据速览（正文抽取）：2026 · 36518210 · 64898 · 10 · 13 · 263651822026

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

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一句话贡献（摘要首句摘录）：INTRODUCTION: This study examined the extent to which educational attainment, Alzheimer's disease (AD) knowledge, and research attitudes are associated with willingness to participate in AD research, and whether AD knowledge and research attitudes mediate associations between educational attainme….

核心要点（正文原句摘录）：
① [（全文补选）] medrxivMEDRXIVmedRxivmedRxiv3067-2007Cold Spring Harbor Laboratory PressMEDRXIV/2026/36509510.64898/2026.10.13.26365095medrxiv;2026.10.13.26365095v1medrxiv;2026.10.13.263650952026.10.13.263650952026.10.13.263650952026.10.13.263650951.1Neurology 1 Department of Psychology, University of Michigan; 2 Department of Psychology, The Ohio State University; 3 University of Maryland School of Graduate Studies; 4 Center for Autism Spectrum Disorders, Nationwide Childrens Hospital; 5 Office of Health Equity, The Ohio State University Wexner Medical Center; 6 The James Cancer Hospital, The Ohio State University Wexner Medical Center; 7 Urban Aging Residents Coalition; 8 Alzheimers Association, Central Ohio Chapter; 9 African American Alzheimers & Wellness Association; 10 St.
② [（全文补选）] Pauls AME Church; 11 Church of Christ of the Apostolic Faith; 12 Tabernacle Baptist Church; 13 Eta Nu Nu Chapter, Omega Psi Phi Fraternity; 14 American Heart Association; 15 African American Male Wellness Agency * Corresponding author; email: grant.866@osu.edu http://orcid.org/0009-0009-8409-0691BontaKyra M1http://orcid.org/0009-0000-3965-1845CorbettEmma2http://orcid.org/0009-0004-1994-0358AlemuMeseret K2http://orcid.org/0000-0002-4112-1509DargeBeniam D3HIlderbrandLauren K2RichardsonKaytlin A2OgonuweStephanie S2http://orcid.org/0009-0008-1253-1227BlumIsabella M2http://orcid.org/0009-0001-5525-6877ShenKevin2http://orcid.org/0009-0009-3924-3708McGuireMadison K2http://orcid.org/0009-0002-2802-2909PandhiDiya H2http://orcid.org/0009-0005-8857-3966GallagherLewis W2http://orcid.org/0009-0001-4964-2413HunterJennifer M2http://orcid.org/0009-0005-7039-7271GrantFredrica4SimmonsWyEsha5DavisLoletia6ShieldsPamela7CooperSue7RouseMissy8Wilson-LawsonKimberly S9Hughes-CulpCarlotta10HowardMary11MonroeMertice12ColemanMatthew13LeathDeleah14ButschJackiethia5DavisNeale5HenryJimmy15GregoryPamela15http://orcid.org/0000-0002-5344-2430GrantJeremy G216grant.866@osu.edu2026 15102026 15102026 2026.10.13.26365095 13102026 13102026 15102026 © 2026, Posted by openRxiv2026This pre-print is available under a Creative Commons License (Attribution-NonCommercial-NoDerivs 4.0 International), CC BY-NC-ND 4.0, as described at http://creativecommons.org/licenses/by-nc-nd/4.0/ INTRODUCTION: This study examined the extent to which educational attainment, Alzheimer's disease (AD) knowledge, and research attitudes are associated with willingness to participate in AD research, and whether AD knowledge and research attitudes mediate associations between educational attainment and willingness to participate.
③ [（全文补选）] METHODS: 201 older adults completed self-report measures of AD knowledge, research attitudes, prior research participation, and willingness to participate in diagnostic procedures (neuropsychological assessment, blood draw, brain MRI) and non-pharmacological intervention research (tracking physical activity, aerobic exercise).
④ [（全文补选）] Alzheimer's Association https://ror.org/0375f4d26AARFD-24-1309508citation_submitter_nameJeremy G Grantcitation_submitter_emailgrant.866@osu.educitation_submitter_id207668citation_submitter_institutionDepartment of Psychology, The Ohio State Universitycitation_submitter_orcid0000-0002-5344-2430Competing Interest Statement The authors have declared no competing interest.

数据速览（正文抽取）：2026 · 36509510 · 64898 · 10 · 13 · 263650952026

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

对本栏价值（自动评估）：★★☆

一句话贡献（摘要首句摘录）：Background: Dopamine replacement reshapes subthalamic activity in Parkinson's disease, but whether this response reflects anatomically organized network reconfiguration remains unclear.

核心要点（正文原句摘录）：
① [（全文补选）] medrxivMEDRXIVmedRxivmedRxiv3067-2007Cold Spring Harbor Laboratory PressMEDRXIV/2026/36525910.64898/2026.10.13.26365259medrxiv;2026.10.13.26365259v1medrxiv;2026.10.13.263652592026.10.13.263652592026.10.13.263652592026.10.13.263652591.1Neurology 1 Case Western Reserve University; 2 Case Western Reserve University; 3 N.N.
② [（全文补选）] Semenov Federal Research Center for Chemical Physics Russian Academy of Sciences, Moscow, Russia * Corresponding author; email: axs848@case.edu http://orcid.org/0000-0001-7469-8331NairSandeep1http://orcid.org/0000-0003-1812-6691JoshiPrajakta2FilyushkinaVeronika3SayfulinaKsenia4GuhaAratrik2SedovAlexey5ShaikhAasef G26axs848@case.edu2026 15102026 15102026 2026.10.13.26365259 13102026 13102026 15102026 © 2026, Posted by openRxiv2026The copyright holder for this pre-print is the author.
③ [（全文补选）] Methods: Twelve participants undergoing bilateral subthalamic deep brain stimulation contributed 30 contacts (14 dorsal, 16 ventral).
④ [（全文补选）] Results: Levodopa suppressed beta power more strongly dorsally than ventrally (-2.473 versus -0.120 dB; p=0.0438).
⑤ [（全文补选）] Dorsal theta power increased, with a trend toward an increase after baseline normalization (p=0.07).

数据速览（正文抽取）：2026 · 36525910 · 64898 · 10 · 13 · 263652592026

保留意见/局限（原文摘录）：① Background: Dopamine replacement reshapes subthalamic activity in Parkinson's disease, but whether this response reflects anatomically organized network reconfiguration remains unclear.

对本栏价值（自动评估）：★★☆

一句话贡献（摘要首句摘录）：Parkinson's disease progression is difficult to measure clinically because of variability in symptom presentation, disease trajectory, and response to symptomatic therapy.

核心要点（正文原句摘录）：
① [（全文补选）] Here, we develop proteomic quality-control measures and refine clinical metrics of disease progression for longitudinal, high-throughput proteomic profiling of 850 plasma and 1,200 CSF biosamples from 832 Parkinson's Precision Medicine Initiative participants.
② [（全文补选）] We identify 68 plasma and 3 CSF biomarkers of disease burden and 4 plasma biomarkers of disease activity.
③ [（全文补选）] We associate 96 plasma and 34 CSF proteins to drug dosage across 12 antiparkinsonian medications.
④ [（全文补选）] PPMI participant IDs for data visualized in Figure 2a, Extended Data Figure 1, and Extended Data Figure 11 are available upon request from signatories to the PPMI data use agreement.

数据速览（正文抽取）：850 · 200 · 832 · 68 · 96 · 34

保留意见/局限（原文摘录）：① （全文未设专门局限节，亦未检出限定表述句——按纪律不做推断，标「未报告」。）

对本栏价值（自动评估）：★☆☆

同窗口 bioRxiv 宽口径命中 146 篇，均为衰老相关预印本，但本环境出口 IP 被 bioRxiv Cloudflare WAF 封禁（真实 DOI 连续探测恒定 403，内容页/JATS/PDF 全链路），全文无法取得。按「取不到全文就不做深度解读」的纪律，本批不纳入 bioRxiv 条目；待通道恢复（代理或官方 S3）后单独补发。本条为说明，不是内容缺失的借口。