Evidence map›Paper›PMID 30029687›Full record

ArticleActa neuropathologica communications2018

The presubiculum is preserved from neurodegenerative changes in Alzheimer's disease.

Christina E Murray, Priya Gami-Patel, Eleni Gkanatsiou, Gunnar Brinkmalm, Erik Portelius, Oliver Wirths, Wendy Heywood, Kaj Blennow, Jorge Ghiso, Janice L Holton and 4 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
0.4field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Estrogen Receptors: A New Frontier in Alzheimer's Disease Therapy.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. The fate of interneurons, GABABrain pathology (Zurich, Switzerland) · 2023
    Review
  9. Article
  10. Article
  11. 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

14 authors at 7 institutions in 4 countries.

Christina E MurrayThe Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, WC1N 3BG, UK.
Priya Gami-PatelThe Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, WC1N 3BG, UK.
Eleni GkanatsiouInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Gunnar BrinkmalmInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Erik PorteliusInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Oliver WirthsDepartment of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, Goettingen, Germany.
Wendy HeywoodCentre for Translational Omics, Great Ormond Street Institute of Child health, UCL, London, UK.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Jorge GhisoNew York University, New York, NY, USA.
Janice L HoltonThe Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, WC1N 3BG, UK.
Kevin MillsCentre for Translational Omics, Great Ormond Street Institute of Child health, UCL, London, UK.
Henrik ZetterbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Tamas ReveszThe Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, WC1N 3BG, UK.
Tammaryn LashleyThe Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, WC1N 3BG, UK. T.Lashley@ucl.ac.uk.ORCID 0000-0001-7389-0348
Wellcome Centre for Human Neuroimaging · GBSahlgrenska University Hospital · SEGreat Ormond Street Hospital · GBUniversity of Gothenburg · SEAllen Institute for Brain Science · USNew York University · USUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the majority of affected brain regions the pathological hallmarks of Alzheimer's disease (AD) are β-amyloid (Aβ) deposits in the form of diffuse and neuritic plaques, tau pathology in the form of neurofibrillary tangles, neuropil threads and plaque-associated abnormal neurites in combination with an inflammatory response. However, the anatomical area of the presubiculum, is characterised by the presence of a single large evenly distributed 'lake-like' Aβ deposit with minimal tau deposition or accumulation of inflammatory markers. Post-mortem brain samples from sporadic AD (SAD) and familial AD (FAD) and two hereditary cerebral amyloid diseases, familial British dementia (FBD) and familial Danish dementia (FDD) were used to compare the morphology of the extracellular proteins deposited in the presubiculum compared to the entorhinal cortex. The level of tau pathology and the extent of microglial activation were quantitated in the two brain regions in SAD and FAD. Frozen tissue was used to investigate the Aβ species and proteomic differences between the two regions. Consistent with our previous investigations of FBD and FDD cases we were able to establish that the 'lake-like' pre-amyloid deposits of the presubiculum were not a unique feature of AD but they also found two non-Aβ amyloidosis. Comparing the presubiculum to the entorhinal cortex the number of neurofibrillary tangles and tau load were significantly reduced; there was a reduction in microglial activation; there were differences in the Aβ profiles and the investigation of the whole proteome showed significant changes in different protein pathways. In summary, understanding why the presubiculum has a different morphological appearance, biochemical and proteomic makeup compared to surrounding brain regions severely affected by neurodegeneration could lead us to understanding protective mechanisms in neurodegenerative diseases.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAnnexin A1Computational BiologyCytokinesEntorhinal CortexFemaleHumansLaser Capture MicrodissectionMacrophage-1 AntigenMaleMass SpectrometryMiddle AgedNeurodegenerative DiseasesNeurofibrillary TanglesAnnexin A1CytokinesMacrophage-1 AntigenAlzheimer’s diseaseAmyloidNeuroinflammationPresubiculumTau

Identifiers

PMID30029687
PMCPMC6053705
OpenAlexW2884669466

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.