Evidence map›Paper›PMID 35453600›Full record

ReviewBiomedicines2022

Development of Alzheimer's Disease Biomarkers: From CSF- to Blood-Based Biomarkers.

Sakulrat Mankhong, Sujin Kim, Seongju Lee, Hyo-Bum Kwak, Dong-Ho Park, Kyung-Lim Joa, Ju-Hee Kang

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 3% of its field
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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  14. How well do plasma Alzheimer's disease biomarkers reflect the CSF amyloid status?Journal of neurology, neurosurgery, and psychiatry · 2025
    Article
  15. Blood biomarker profiles in young-onset neurocognitive disorders: A cohort study.The Australian and New Zealand journal of psychiatry · 2025
    Article
  16. Review
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  20. Plasma membrane repair defect in Alzheimer's disease neurons is driven by the reduced dysferlin expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    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

7 authors at 1 institution in 1 country.

Sakulrat MankhongDepartment of Pharmacology, Research Center for Controlling Intercellular Communication, College of Medicine, Inha University, Incheon 22212, Korea.ORCID 0000-0002-8972-2274
Sujin KimDepartment of Pharmacology, Research Center for Controlling Intercellular Communication, College of Medicine, Inha University, Incheon 22212, Korea.ORCID 0000-0001-7674-8873
Seongju LeeProgram in Biomedical Science and Engineering, Inha University, Incheon 22212, Korea.
Hyo-Bum KwakProgram in Biomedical Science and Engineering, Inha University, Incheon 22212, Korea.ORCID 0000-0003-0451-4554
Dong-Ho ParkProgram in Biomedical Science and Engineering, Inha University, Incheon 22212, Korea.ORCID 0000-0003-1863-0652
Kyung-Lim JoaDepartment of Physical & Rehabilitation Medicine, College of Medicine, Inha University, Incheon 22212, Korea.ORCID 0000-0002-3747-9831
Ju-Hee KangDepartment of Pharmacology, Research Center for Controlling Intercellular Communication, College of Medicine, Inha University, Incheon 22212, Korea.ORCID 0000-0001-5235-8993
Inha University · KR

Funding

National Research Foundation of Korea NRF-2021R1A5A2031612, NRF-2019S1A5C2A03082727
6 · The paper itself

Abstract

In the 115 years since the discovery of Alzheimer's disease (AD), our knowledge, diagnosis, and therapeutics have significantly improved. Biomarkers are the primary tools for clinical research, diagnostics, and therapeutic monitoring in clinical trials. They provide much insightful information, and while they are not clinically used routinely, they help us to understand the mechanisms of this disease. This review charts the journey of AD biomarker discovery and development from cerebrospinal fluid (CSF) amyloid-beta 1-42 (Aβ42), total tau (T-tau), and phosphorylated tau (p-tau) biomarkers and imaging technologies to the next generation of biomarkers. We also discuss advanced high-sensitivity assay platforms for CSF Aβ42, T-tau, p-tau, and blood analysis. The recently proposed Aβ deposition/tau biomarker/neurodegeneration or neuronal injury (ATN) scheme might facilitate the definition of the biological status underpinning AD and offer a common language among researchers across biochemical biomarkers and imaging. Moreover, we highlight blood-based biomarkers for AD that offer a scalable alternative to CSF biomarkers through cost-saving and reduced invasiveness, and may provide an understanding of disease initiation and development. We discuss different groups of blood-based biomarker candidates, their advantages and limitations, and paths forward, from identification and analysis to clinical validation. The development of valid blood-based biomarkers may facilitate the implementation of future AD therapeutics and diagnostics.

Indexed as

Alzheimer’s biomarkeramyloid-betablood-based biomarkercerebrospinal fluidclinical trialtau

Identifiers

PMID35453600
PMCPMC9025524
OpenAlexW4224325755

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.