Evidence map›Paper›PMID 15972961›Full record

ArticleThe American journal of pathology2005

Perturbed neurogenesis in the adult hippocampus associated with presenilin-1 A246E mutation.

Nathalie L Chevallier, Salvador Soriano, David E Kang, Eliezer Masliah, Gloria Hu, Edward H Koo

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

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 144 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Nathalie L ChevallierDepartment of Neurosciences, University of California-San Diego, School of Medicine, La Jolla, California 92093-0691, USA.
Salvador Soriano
David E Kang
Eliezer Masliah
Gloria Hu
Edward H Koo
University of California, San Diego · US

Funding

STROKE THERAPY MECHANISMS WITH NEUROTROPHIC FACTORSP01NS028121 · NINDS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI ZIVIN, JUSTIN A. · 1990 to 2004
$6.4M
B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
NIA NIH HHS AG18440NIA NIH HHS R01 AG018440NIA NIH HHS R37 AG018440NINDS NIH HHS NS28121NINDS NIH HHS P01 NS028121
6 · The paper itself

Abstract

In addition to its well-established role in gamma-secretase cleavage, presenilin (PS) also plays a role in regulating the stability of cytosolic beta-catenin, a protein involved in Wnt signaling. Several familial Alzheimer's disease-associated PS1 mutations have been shown to increase the stability of the signaling pool of beta-catenin, correlating with enhanced cell proliferation. Accordingly, we hypothesized that in the setting of PS1 mutations, abnormal activation of Wnt/beta-catenin signaling leads to increased cell division. We tested this hypothesis by examining whether there is evidence of increased neurogenesis in the hippocampus of adult transgenic mice that overexpress the PS1 A246E mutation. In PS1/PS2-deficient fibroblasts, expression of PS1 A246E Familial AD mutation failed to restore the rapid turnover of beta-catenin compared with wild-type PS1. We then examined whether the same mutation enhanced neurogenesis in vivo in adult hippocampus of PS1-deficient mice when restored by wild-type human PS1 (PS1(-/-)WT) or A246E PS1 mutation (PS1(-/-)AE). The PS1 A246E mutation stimulated the proliferation of progenitor cells in the dentate gyrus of adult mice, as assessed by 5-bromo-2-deoxyuridine incorporation, but did not influence their survival or differentiation. These observations suggest that the PS1 A246E mutation influences cell growth putatively via abnormal beta-catenin signaling in vivo.

Indexed as

Alzheimer DiseaseAnimalsbeta CateninCell DeathCell DifferentiationCell ProliferationCell SurvivalCytoskeletal ProteinsFluorescent Antibody TechniqueHippocampusHumansImmunoblottingMembrane ProteinsMiceMice, TransgenicMutationbeta CateninCTNNB1 protein, humanCTNNB1 protein, mouseCytoskeletal ProteinsMembrane ProteinsPresenilin-1PSEN1 protein, humanTrans-Activators

Identifiers

PMID15972961
PMCPMC1603433
OpenAlexW2087260334

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.