Evidence map›Paper›PMID 9033258›Full record

ArticleThe American journal of pathology1997

Presenilin-1-immunoreactive neurons are preserved in late-onset Alzheimer's disease.

P Giannakopoulos, C Bouras, E Kövari, J Shioi, N Tezapsidis, P R Hof, N K Robakis

Abstract read
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
6.4field-weighted citation impact, top 3% 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, 53 citations in OpenAlex.

  1. Presenilin1/γ-secretase protects neurons from glucose deprivation-induced death by regulating miR-212 and PEA15.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Overexpression in neurons of human presenilin-1 or a presenilin-1 familial Alzheimer disease mutant does not enhance apoptosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  7. Article
  8. Article
  9. Interaction of presenilins with the filamin family of actin-binding proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  10. Presenilin-1 is associated with Alzheimer's disease amyloid.The American journal of pathology · 1997
    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

7 authors at 1 institution in 1 country.

P GiannakopoulosDepartment of Psychiatry, University of Geneva School of Medicine, Switzerland.
C Bouras
E Kövari
J Shioi
N Tezapsidis
P R Hof
N K Robakis
University of Geneva · CH

Funding

STRUCTURE &EXPRESSION OF THE B-PROTEIN-PRECURSOR GENER01AG008200 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI ROBAKIS, NIKOLAOS K · 1988 to 2017
$5.6M
NIA NIH HHS AG05138NIA NIH HHS AG08200
6 · The paper itself

Abstract

Recent studies have suggested that missense mutations in the presenilin-1 gene are causally related to the majority of familial early-onset Alzheimer's disease (AD). To examine the possible involvement of presenilin-1 in late-onset sporadic AD, a quantitative analysis of its distribution in the cerebral cortex of nondemented and AD patients was performed using immunocytochemistry. Stereological analyses revealed that AD brains showed a marked neuronal loss in the CA1 field of the hippocampus and hilus of the dentate gyrus, subiculum, and entorhinal cortex. In these areas, however, the fraction of neurofibrillary tangle (NFT)-free neurons showing presenilin-1 immunoreactivity was increased compared with nondemented controls. In contrast, cortical areas, which displayed no neuronal loss, did not show any significant increase in the fraction of presenilin-1-positive neurons. Moreover, presenilin-1 immunoreactivity was reduced in NFT-containing neurons. Thus, in AD, the fraction of NFT-free neurons that contained presenilin-1 varied from 0.48 to 0.77, whereas the fraction of NFT-containing neurons that were presenilin-1 positive varied from 0.1 to 0.24. Together, these observations indicate that presenilin-1 may have a neuroprotective role and that in AD low cellular expression of this protein may be associated with increased neuronal loss and NFT formation.

Indexed as

AgedAged, 80 and overAge of OnsetAlzheimer DiseaseFemaleHumansImmunohistochemistryMaleMembrane ProteinsNeurofibrillary TanglesNeuronsPresenilin-1Reference ValuesTissue DistributionMembrane ProteinsPresenilin-1PSEN1 protein, human

Identifiers

PMID9033258
PMCPMC1858297
OpenAlexW1416457013

What OpenQuestion holds

Textmetadata
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.