Evidence map›Paper›PMID 35573283›Full record

ReviewFrontiers in neuroscience2022

Alzheimer's Disease Biomarkers Revisited From the Amyloid Cascade Hypothesis Standpoint.

Deborah O T Alawode, Nick C Fox, Henrik Zetterberg, Amanda J Heslegrave

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

Review in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  15. Ghrelin system in Alzheimer's disease.Current opinion in neurobiology · 2023
    Review
  16. Early Diagnosis of Alzheimer's Disease with Blood Test; Tempting but Challenging.International journal of molecular and cellular medicine · 2023
    Review
  17. Review
  18. Article
  19. Article
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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

4 authors at 3 institutions in 2 countries.

Deborah O T AlawodeDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, United Kingdom.
Nick C FoxUK Dementia Research Institute at UCL, London, United Kingdom.
Henrik ZetterbergDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, United Kingdom.
Amanda J HeslegraveDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, United Kingdom.
UK Dementia Research Institute · GBSahlgrenska University Hospital · SEUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease worldwide. Amyloid beta (Aβ) is one of the proteins which aggregate in AD, and its key role in the disease pathogenesis is highlighted in the amyloid cascade hypothesis, which states that the deposition of Aβ in the brain parenchyma is a crucial initiating step in the future development of AD. The sensitivity of instruments used to measure proteins in blood and cerebrospinal fluid has significantly improved, such that Aβ can now successfully be measured in plasma. However, due to the peripheral production of Aβ, there is significant overlap between diagnostic groups. The presence of pathological Aβ within the AD brain has several effects on the cells and surrounding tissue. Therefore, there is a possibility that using markers of tissue responses to Aβ may reveal more information about Aβ pathology and pathogenesis than looking at plasma Aβ alone. In this manuscript, using the amyloid cascade hypothesis as a starting point, we will delve into how the effect of Aβ on the surrounding tissue can be monitored using biomarkers. In particular, we will consider whether glial fibrillary acidic protein, triggering receptor expressed on myeloid cells 2, phosphorylated tau, and neurofilament light chain could be used to phenotype and quantify the tissue response against Aβ pathology in AD.

Indexed as

amyloid-betablood biomarkersglial fibrillary acidic protein (GFAP)neurodegenerationneurofilament light (NfL)phosphorylated tau (p-tau)triggering receptor expressed on myeloid cells 2 (TREM2)

Identifiers

PMID35573283
PMCPMC9091905
OpenAlexW4224928623

What OpenQuestion 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 OpenQuestion graph.