Evidence map›Paper›PMID 29018524›Full record

ArticleBiomarker research2017

Re-evaluation of soluble APP-α and APP-β in cerebrospinal fluid as potential biomarkers for early diagnosis of dementia disorders.

Wataru Araki, Kotaro Hattori, Kazutomi Kanemaru, Yuma Yokoi, Yoshie Omachi, Harumasa Takano, Masuhiro Sakata, Sumiko Yoshida, Tadashi Tsukamoto, Miho Murata and 13 more

Abstract read
In one paragraph

Article in Biomarker research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Amyloid-βAlzheimer's research & therapy · 2020
    Article
  7. Article
  8. Article
  9. 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

23 authors.

Wataru ArakiDepartment of Demyelinating Disease and Aging, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502 Japan.ORCID 0000-0001-8467-6937
Kotaro HattoriMedical Genome Center, NCNP, Tokyo, Japan.
Kazutomi KanemaruTokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo, Japan.
Yuma YokoiNational Center Hospital, NCNP, Tokyo, Japan.
Yoshie OmachiNational Center Hospital, NCNP, Tokyo, Japan.
Harumasa TakanoNational Center Hospital, NCNP, Tokyo, Japan.
Masuhiro SakataNational Center Hospital, NCNP, Tokyo, Japan.
Sumiko YoshidaNational Center Hospital, NCNP, Tokyo, Japan.
Tadashi TsukamotoNational Center Hospital, NCNP, Tokyo, Japan.
Miho MurataNational Center Hospital, NCNP, Tokyo, Japan.
Yuko SaitoNational Center Hospital, NCNP, Tokyo, Japan.
Hiroshi KunugiDepartment of Mental Disorder Research, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Yu-Ichi GotoMedical Genome Center, NCNP, Tokyo, Japan.
Utako NagaokaTokyo Metropolitan Neurological Hospital, Tokyo, Japan.
Masahiro NagaoTokyo Metropolitan Neurological Hospital, Tokyo, Japan.
Takashi KomoriTokyo Metropolitan Neurological Hospital, Tokyo, Japan.
Kunimasa ArimaKomoro Kogen Hospital, Komoro, Japan.
Kenji IshiiTokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo, Japan.
Shigeo MurayamaTokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo, Japan.
Hiroshi MatsudaIntegrative Brain Imaging Center, NCNP, Tokyo, Japan.
Hisateru TachimoriDepartment of Mental Health Policy and Evaluation, National Institute of Mental Health, NCNP, Tokyo, Japan.
Yumiko M ArakiDepartment of Demyelinating Disease and Aging, National Institute of Neuroscience, National Center of Neurology and Psychiatry (NCNP), 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502 Japan.
Hidehiro MizusawaNational Center Hospital, NCNP, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBecause soluble (or secreted) amyloid precursor protein-β (sAPPβ) and -α (sAPPα) possibly reflect pathological features of Alzheimer's disease (AD), they are potential biomarker candidates for dementia disorders, including AD and mild cognitive impairment (MCI) due to AD (MCI-AD). However, controversial results have been reported regarding their alterations in the cerebrospinal fluid (CSF) of AD and MCI-AD patients. In this study, we re-assessed the utility of sAPPα and sAPPβ in CSF as diagnostic biomarkers of dementia disorders.

methodsWe used a modified and sensitive detection method to analyze sAPPs levels in CSF in four groups of patients: AD (

resultsA strong correlation was observed between sAPPα and sAPPβ, consistent with previous reports. Both sAPPα and sAPPβ were highly correlated with p-tau and total tau, suggesting that sAPPs possibly reflect neuropathological changes in the brain. Levels of sAPPα were significantly higher in MCI-AD cases compared with non-AD and disease control cases, and those of sAPPβ were also significantly higher in MCI-AD and AD cases relative to other cases. A logistic regression analysis indicated that sAPPα and sAPPβ have good discriminative power for the diagnosis of MCI-AD.

conclusionsOur findings collectively suggest that both sAPPs are pathologically relevant and potentially useful biomarkers for early and accurate diagnosis of dementia disorders. We also suggest that careful measurement is important in assessing the diagnostic utility of CSF sAPPs.

Indexed as

Alzheimer’s diseaseBiomarkerCerebrospinal fluidMild cognitive impairmentSoluble amyloid precursor proteinTau

Identifiers

PMID29018524
PMCPMC5610422

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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.