Evidence map›Paper›PMID 31748522›Full record

ArticleScientific reports2019

Neuropathological characterization of Lemur tyrosine kinase 2 (LMTK2) in Alzheimer's disease and neocortical Lewy body disease.

János Bencze, Máté Szarka, Viktor Bencs, Renáta Nóra Szabó, Máté Smajda, Dag Aarsland, Tibor Hortobágyi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. LMTK2 and CRB1 are two novel risk genes for Alzheimer's disease in Han Chinese.The journal of prevention of Alzheimer's disease · 2025
    Article
  3. Review
  4. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons.Frontiers in molecular neuroscience · 2020
    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 2 institutions in 3 countries.

János BenczeDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Máté SzarkaHorvath Csaba Memorial Institute of Bioanalytical Research, Research Centre for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
Viktor BencsDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Renáta Nóra SzabóMTA-DE Cerebrovascular and Neurodegenerative Research Group, Department of Neurology, University of Debrecen, Debrecen, Hungary.
Máté SmajdaVitrolink Ltd., Debrecen, Hungary.
Dag AarslandDepartment of Old Age Psychiatry, Institute of Psychiatry Psychology and Neuroscience, King's College London, London, UK.
Tibor HortobágyiMTA-DE Cerebrovascular and Neurodegenerative Research Group, Department of Neurology, University of Debrecen, Debrecen, Hungary. tibor.hortobagyi@kcl.ac.uk.ORCID http://orcid.org/0000-0001-5732-7942
University of Debrecen · HUKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) and neocortical Lewy body disease (LBD) are the most common neurodegenerative dementias, with no available curative treatment. Elucidating pathomechanism and identifying novel therapeutic targets are of paramount importance. Lemur tyrosine kinase 2 (LMTK2) is involved in several physiological and pathological cellular processes. Herewith a neuropathological characterization is presented in AD and neocortical LBD samples using chromogenic and fluorescent LMTK2 immunohistochemistry on post-mortem brain tissues and compared them to age-matched controls (CNTs). LMTK2 immunopositivity was limited to the neuronal cytoplasm. Neurons, including tau-positive tangle-bearing ones, showed decreased chromogenic and immunofluorescent labelling in AD in every cortical layer compared to CNT and neocortical LBD. Digital image analysis was performed to measure the average immunopositivity of groups. Mean grey values were calculated for each group after measuring the grey scale LMTK2 signal intensity of each individual neuron. There was significant difference between the mean grey values of CNT vs. AD and neocortical LBD vs. AD. The moderate decrease in neocortical LBD suggests the effect of coexisting AD pathology. We provide neuropathological evidence on decreased neuronal LMTK2 immunolabelling in AD, with implications for pathogenesis.

Indexed as

Alzheimer DiseaseBiomarkersCase-Control StudiesFemaleHumansLewy Body DiseaseMaleMembrane ProteinsMiddle AgedNeocortexPrognosisProtein Serine-Threonine KinasesBiomarkersLMTK2 protein, humanMembrane ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID31748522
PMCPMC6868282
OpenAlexW2989881793

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.