Evidence map›Paper›PMID 30467822›Full record

ArticleJournal of molecular neuroscience : MN2019

Apolipoprotein D Upregulation in Alzheimer's Disease but Not Frontotemporal Dementia.

Surabhi Bhatia, Woojin Scott Kim, Claire E Shepherd, Glenda M Halliday

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Dysregulation of Monounsaturated Fatty Acids is Related to α-Synuclein in Multiple System Atrophy.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Apolipoprotein D as a Potential Biomarker in Neuropsychiatric Disorders.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. MScience signaling · 2022
    Article
  20. 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

4 authors at 2 institutions in 1 country.

Surabhi BhatiaCentral Clinical School and Brain and Mind Centre, Faculty of Medicine and Health Sciences, The University of Sydney, 94 Mallet Street, Camperdown, NSW, Australia. surabhi.bhatia@sydney.edu.au.ORCID http://orcid.org/0000-0001-7991-5569
Woojin Scott KimCentral Clinical School and Brain and Mind Centre, Faculty of Medicine and Health Sciences, The University of Sydney, 94 Mallet Street, Camperdown, NSW, Australia.
Claire E ShepherdNeuroscience Research Australia, Sydney, NSW, Australia.
Glenda M HallidayCentral Clinical School and Brain and Mind Centre, Faculty of Medicine and Health Sciences, The University of Sydney, 94 Mallet Street, Camperdown, NSW, Australia.
The University of Sydney · AUUNSW Sydney · AU

Funding

Brain Tissue Resource Centre for Alcohol ResearchR28AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI Greg Trevor Sutherland · 2012 to 2026
$7.0M
National Health and Medical Research Council APP1108882NIAAA NIH HHS R28 AA012725
6 · The paper itself

Abstract

Frontotemporal dementia (FTD) and Alzheimer's disease (AD) are the two common forms of dementia. FTD syndromes are characterized by lobar atrophy (frontotemporal lobar degeneration or FTLD) and the presence of either cellular TDP43 (FTLD-TDP), tau (FTLD-tau), or FUS aggregates, while extracellular β-amyloid plaques and hyperphosphorylated tau tangles develop in AD. Oxidative stress can induce these pathological modifications in disease models, and is thought to play a role in these syndromes. Apolipoprotein D (apoD) is a glial-expressed lipocalin known to protect against oxidative stress, with increased levels in AD, supporting a protective role. The expression of apoD has not been studied in FTLD. This study assesses apoD expression in FTLD-TDP and FTLD-tau in comparison to AD and controls. It also analyzes the effect of apoD on TARDBP (TDP43 gene) and β-amyloid precursor protein (APP). The expression of apoD was analyzed by Western blotting in FTLD-TDP, FTLD-tau, AD, and control post-mortem brain tissue. An apoD-overexpressing cell model was used to study the impact of increased apoD on APP and TARDBP expression. We confirm that apoD expression was increased in AD but surprisingly it was not affected in either of the two main pathological forms of FTLD. Under oxidative stress conditions, apoD had no effect on TDP43 expression but it did decrease APP expression. This suggests that apoD does not act as a neuroprotective factor in FTLD in the same way as in AD. This could contribute to the more rapid degeneration observed in FTLD.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseApolipoproteins DBrainCell Line, TumorFemaleFrontotemporal DementiaHumansMaleUp-RegulationApolipoproteins DApolipoprotein DFrontotemporal dementiaNeurodegenerationOxidative stressTDP43

Identifiers

PMID30467822
PMCPMC6344390
OpenAlexW2901092742

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.