Evidence map›Paper›PMID 16785601›Full record

ReviewEndocrine2006

The role of gonadotropins in Alzheimer's disease: potential neurodegenerative mechanisms.

Anna M Barron, Giuseppe Verdile, Ralph N Martins

Abstract readReview
PubMed Publisher
In one paragraph

Review in Endocrine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 38 citations in OpenAlex.

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  11. Animal models for aberrations of gonadotropin action.Reviews in endocrine & metabolic disorders · 2011
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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.

Anna M BarronCentre for Aging and Alzheimer's Disease, Edith Cowan University, Joondalup, WA, Australia.
Giuseppe Verdile
Ralph N Martins
Edith Cowan University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to the classical role of gonadotropins as a modulator of sex hormone production, it is now becoming apparent that the gonadotropins may have actions within the central nervous system. Evidence is also mounting that age-related increases in levels of the gonadotropin, luteinizing hormone (LH), may exert neurodegenerative effects such as those seen in Alzheimer's disease (AD). LH has been implicated in key cellular and biochemical processes that contribute to the pathogenesis of AD. These processes include the altered metabolism of key proteins in AD pathology, beta amyloid (Abeta), and its parent molecule, the amyloid precursor protein (APP). Evidence in the literature suggests that gonadotropins may be involved in processes that contribute to the etiology/pathogenesis of AD such as inflammation, cholesterol homeostasis, and insulin status. Here we examine the potential mechanisms by which gonadotropins could influence neurodegenerative processes. The role of gonadotropins in the brain and potential direct neuropathological effects of elevated gonadotropin levels is an exciting new topic in neuroendocrinology that in turn will lead to the development of novel therapeutic approaches for AD.

Indexed as

Age FactorsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCholesterolGonadal Steroid HormonesGonadotropinsHumansInflammationLuteinizing HormoneMaleModels, BiologicalNeurodegenerative DiseasesSex FactorsAmyloid beta-PeptidesCholesterolGonadal Steroid HormonesGonadotropinsLuteinizing Hormone

Identifiers

PMID16785601
OpenAlexW2006630401

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.