Evidence map›Paper›PMID 39085262›Full record

ArticleNPJ Parkinson's disease2024

Plasma biomarkers of neurodegeneration in patients and high risk subjects with Lewy body disease.

Keita Hiraga, Makoto Hattori, Yuki Satake, Daigo Tamakoshi, Taiki Fukushima, Takashi Uematsu, Takashi Tsuboi, Maki Sato, Katsunori Yokoi, Keisuke Suzuki and 11 more

Abstract read
In one paragraph

Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. An exploratoryEuropean journal of nuclear medicine and molecular imaging · 2026
    Article
  3. Article
  4. Article
  5. Heterogeneity of dementia with lewy bodies: Insights from clinical presentations, neuropathology, and biomarkers.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  10. Article
  11. Article
  12. Article
4 · The record

Corrections and comments

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

21 authors.

Keita HiragaDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID http://orcid.org/0000-0002-0134-2956
Makoto HattoriDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuki SatakeDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Daigo TamakoshiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Taiki FukushimaDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takashi UematsuDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takashi TsuboiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID http://orcid.org/0000-0001-5042-3181
Maki SatoDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Katsunori YokoiDepartment of Neurology, National Hospital for Geriatric Medicine, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Keisuke SuzukiInnovation Center for Translational Research, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Yutaka ArahataDepartment of Neurology, National Hospital for Geriatric Medicine, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Yukihiko WashimiDepartment of Comprehensive Care and Research on Memory Disorders, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Akihiro HoriKumiai Kosei Hospital, Takayama, Gifu, Japan.
Masayuki YamamotoKumiai Kosei Hospital, Takayama, Gifu, Japan.
Hideaki ShimizuMedical Examination Center, Daido Clinic, Nagoya, Japan.
Masakazu WakaiChutoen General Medical Center, Kakegawa, Shizuoka, Japan.
Harutsugu TatebeDepartment of Functional Brain Imaging, Institute for Quantum Medical Science, National Institutes for Quantum Science and Technology, Chiba, Japan.
Takahiko TokudaDepartment of Functional Brain Imaging, Institute for Quantum Medical Science, National Institutes for Quantum Science and Technology, Chiba, Japan.
Akinori NakamuraDepartment of Biomarker Research, Center for Development of Advanced Medicine for Dementia, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Shumpei NiidaCore Facility Administration, Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.
Masahisa KatsunoDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan. katsuno.masahisa.i1@f.mail.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0001-9453-9311

Funding

Japan Agency for Medical Research and Development (AMED) JP20dm0107155Japan Agency for Medical Research and Development (AMED) JP20lk0201124Japan Agency for Medical Research and Development (AMED) JP22ae0101077Japan Agency for Medical Research and Development (AMED) JP22dk0207052Japan Agency for Medical Research and Development (AMED) JP22dk0207055MEXT | Japan Society for the Promotion of Science (JSPS) JP21K19443MEXT | Japan Society for the Promotion of Science (JSPS) JP23H00420National Center for Geriatrics and Gerontology (NCGG) 19-20National Center for Geriatrics and Gerontology (NCGG) 22-26
6 · The paper itself

Abstract

Comorbid Alzheimer's disease (AD) neuropathology is common in Lewy body disease (LBD); however, AD comorbidity in the prodromal phase of LBD remains unclear. This study investigated AD comorbidity in the prodromal and symptomatic phases of LBD by analyzing plasma biomarkers in patients with Parkinson's disease (PD) and dementia with Lewy bodies (DLB) and individuals at risk of LBD (NaT-PROBE cohort). Patients with PD (PD group, n = 84) and DLB (DLB group, n = 16) and individuals with LBD with ≥ 2 (high-risk group, n = 82) and without (low-risk group, n = 37) prodromal symptoms were enrolled. Plasma amyloid-beta (Aβ) composite was measured using immunoprecipitation-mass spectrometry assays. Plasma phosphorylated tau 181 (p-tau181), neurofilament light chain (NfL), and alpha-synuclein (aSyn) were measured using a single-molecule array. Plasma p-tau181 levels were higher in the PD and DLB groups than in the low-risk group. Aβ composite level was higher in the DLB group than in the high-risk group. AD-related biomarker levels were not elevated in the high-risk group. NfL levels were higher in the high-risk, PD, and DLB groups than in the low-risk group. In the PD group, Aβ composite was associated with cognitive function, p-tau181 with motor function and non-motor symptoms, and NfL with cognitive and motor functions and non-motor symptoms. In the high-risk group, NfL was associated with metaiodobenzylguanidine scintigraphy abnormalities. The PD and DLB groups exhibited comorbid AD neuropathology, though not in the prodromal phase. Elevated plasma NfL levels, even without elevated AD-related plasma biomarker levels, may indicate aSyn-induced neurodegeneration in the LBD prodromal phase.

Identifiers

PMID39085262
PMCPMC11292020

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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.