Evidence map›Paper›PMID 26307455›Full record

ReviewAgeing research reviews2015

Estrogen receptor β in Alzheimer's disease: From mechanisms to therapeutics.

Liqin Zhao, Sarah K Woody, Anindit Chhibber

Open access · greenAbstract readReview
In one paragraph

Review in Ageing research reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
5.2field-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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

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  17. Sex as a Determinant of Age-Related Changes in the Brain.International journal of molecular sciences · 2024
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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

3 authors at 1 institution in 1 country.

Liqin ZhaoDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, KS 66045, USA; Neuroscience Graduate Program, University of Kansas, Lawrence, KS 66045, USA. Electronic address: lzhao@ku.edu.
Sarah K WoodyDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, KS 66045, USA.
Anindit ChhibberDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, KS 66045, USA.
University of Kansas · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
Estrogen Receptor-beta phytoSERMs for Management of Menopause and Memory DeclineR01AG033288 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SCHNEIDER, LON S · 2010 to 2012
$1.6M
NIA NIH HHS P30 AG035982NIA NIH HHS P30AG035982NIA NIH HHS R01 AG033288NIA NIH HHS R01AG033288
6 · The paper itself

Abstract

Alzheimer's disease (AD) disproportionally affects women and men. The female susceptibility for AD has been largely associated with the loss of ovarian sex hormones during menopause. This review examines the current understanding of the role of estrogen receptor β (ERβ) in the regulation of neurological health and its implication in the development and intervention of AD. Since its discovery in 1996, research conducted over the last 15-20 years has documented a great deal of evidence indicating that ERβ plays a pivotal role in a broad spectrum of brain activities from development to aging. ERβ genetic polymorphisms have been associated with cognitive impairment and increased risk for AD predominantly in women. The role of ERβ in the intervention of AD has been demonstrated by the alteration of AD pathology in response to treatment with ERβ-selective modulators in transgenic models that display pronounced plaque and tangle histopathological presentations as well as learning and memory deficits. Future studies that explore the potential interactions between ERβ signaling and the genetic isoforms of human apolipoprotein E (APOE) in brain aging and development of AD-risk phenotype are critically needed. The current trend of lost-in-translation in AD drug development that has primarily been based on early-onset familial AD (FAD) models underscores the urgent need for novel models that recapitulate the etiology of late-onset sporadic AD (SAD), the most common form of AD representing more than 95% of the current human AD population. Combining the use of FAD-related models that generally have excellent face validity with SAD-related models that hold more reliable construct validity would together increase the predictive validity of preclinical findings for successful translation into humans.

Indexed as

AgingBrainEstrogen Receptor betaAlzheimer DiseaseBiobehavioral SciencesFemaleHumansMaleSex FactorsEstrogen Receptor betaAlzheimer’s diseaseApolipoprotein EERβ polymorphismEstrogen receptor βLate-onset AD modelsSex differences

Identifiers

PMID26307455
PMCPMC4661108
OpenAlexW1147961199

What OpenQuestion holds

Textmetadata
LicenceTDM
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.