Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors.
Linbin DaiProgram of Bone-Brain Axis Research, Department of Orthopedics, Institute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID http://orcid.org/0000-0001-5825-1505
Bjørn-Eivind KirsebomDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Chenxi WangNeurodegenerative Disorder Research Center, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Mengguo ZhangNeurodegenerative Disorder Research Center, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Qiong WangNeurodegenerative Disorder Research Center, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Ming NiDepartment of Radiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Fernando Gonzalez-OrtizDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID http://orcid.org/0000-0001-7897-9456
Kaj BlennowNeurodegenerative Disorder Research Center, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. kaj.blennow@clinchem.gu.se.ORCID http://orcid.org/0000-0002-1890-4193
Jiong ShiNeurodegenerative Disorder Research Center, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. jshi2022@ustc.edu.cn.
Feng GaoNeurodegenerative Disorder Research Center, Hefei National Laboratory for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. fenggao7@ustc.edu.cn.ORCID http://orcid.org/0000-0002-7539-6455
Yong ShenProgram of Bone-Brain Axis Research, Department of Orthopedics, Institute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. yongshen@ustc.edu.cn.ORCID http://orcid.org/0000-0002-5048-8134
Funding
National Natural Science Foundation of China (National Science Foundation of China) 82501685, U23A20422National Natural Science Foundation of China (National Science Foundation of China) W2411069,82030034
6 · The paper itself
Abstract
Identifying biomarkers that precisely track the neurodegenerative component of Alzheimer's disease (AD) is essential for effective clinical management. Here we show that cerebrospinal fluid (CSF) levels of the synaptic proteins NPTX1 and NPTXR are robust indicators of disease severity and future clinical progression. In two independent, multi-ethnic cohorts spanning the AD continuum (n = 635), lower CSF NPTX levels correlate strongly with cognitive impairment and cortical thinning in AD-vulnerable regions. Longitudinally, baseline NPTX levels predict accelerated brain atrophy and the clinical transition from mild cognitive impairment to dementia, frequently outperforming or complementing established markers such as pTau181 and neurofilament light chain. These findings establish NPTX1 and NPTXR as sensitive, stage-specific markers of synaptic integrity and neurodegeneration. By accurately forecasting disease progression, these biomarkers offer significant potential to enhance patient stratification and provide a crucial tool for monitoring the efficacy of disease-modifying therapies in clinical trials.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Cerebrospinal fluid NPTX1 and NPTXR predict neurodegeneration and clinical progression in Alzheimer's disease. · full record | OpenQuestion