Evidence map›Paper›PMID 33128789›Full record

ArticleBrain pathology (Zurich, Switzerland)2021

Isoform-specific upregulation of FynT kinase expression is associated with tauopathy and glial activation in Alzheimer's disease and Lewy body dementias.

Clara Y B Low, Jasinda H Lee, Frances T W Lim, Chingli Lee, Clive Ballard, Paul T Francis, Mitchell K P Lai, Michelle G K Tan

Open access · hybridAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Neuropsychiatric Symptoms Mimicking Dementia in a Patient Treated With Imatinib.Annals of clinical and translational neurology · 2026
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  8. PINK1 deficiency permits the development of Lewy body dementia with coexisting Aβ pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

8 authors at 4 institutions in 2 countries.

Clara Y B LowDepartment of Clinical Translational Research, Singapore General Hospital, Outram, Singapore.
Jasinda H LeeDepartment of Pharmacology, Yong Loo Lin School of Medicine, Kent Ridge, Singapore.
Frances T W LimDepartment of Clinical Translational Research, Singapore General Hospital, Outram, Singapore.
Chingli LeeDepartment of Clinical Translational Research, Singapore General Hospital, Outram, Singapore.
Clive BallardInstitute for Health Research, University of Exeter Medical School, Exeter, UK.
Paul T FrancisInstitute for Health Research, University of Exeter Medical School, Exeter, UK.
Mitchell K P LaiDepartment of Pharmacology, Yong Loo Lin School of Medicine, Kent Ridge, Singapore.ORCID 0000-0001-7685-1424
Michelle G K TanDepartment of Clinical Translational Research, Singapore General Hospital, Outram, Singapore.ORCID 0000-0002-3202-2023
National University of Singapore · SGSingapore General Hospital · SGKing's College London · GBUniversity of Exeter · GB

Funding

Medical Research Council G0400074
6 · The paper itself

Abstract

Cumulative data suggest the involvement of Fyn tyrosine kinase in Alzheimer's disease (AD). Previously, our group has shown increased immunoreactivities of the FynT isoform in AD neocortex (with no change in the alternatively spliced FynB isoform) which associated with neurofibrillary degeneration and reactive astrogliosis. Since both the aforementioned neuropathological features are also variably found in Lewy Body dementias (LBD), we investigated potential perturbations of Fyn expression in the post-mortem neocortex of patients with AD, as well as those diagnosed as having one of the two main subgroups of LBD: Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB). We found selective upregulation of FynT expression in AD, PDD, and DLB which also correlated with cognitive impairment. Furthermore, increased FynT expression correlated with hallmark neuropathological lesions, soluble β-amyloid, and phosphorylated tau, as well as markers of microglia and astrocyte activation. In line with the human post-mortem studies, cortical FynT expression in aged mice transgenic for human P301S tau was upregulated and further correlated with accumulation of aggregated phosphorylated tau as well as with microglial and astrocytic markers. Our findings provide further evidence for the involvement of FynT in neurodegenerative dementias, likely via effects on tauopathy and neuroinflammation.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAnimalsCerebral CortexFemaleHumansIsoenzymesLewy Body DiseaseMaleMiceMice, TransgenicProto-Oncogene Proteins c-fynUp-RegulationFYN protein, humanIsoenzymesProto-Oncogene Proteins c-fynalternative splicingAlzheimer's diseaseFyn kinaseglial activationLewy body dementiatauopathy

Identifiers

PMID33128789
PMCPMC8017997
OpenAlexW3095398750

What OpenQuestion holds

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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.