Evidence map›Paper›PMID 26303889›Full record

ReviewNeurobiology of disease2015

The relationship between iron dyshomeostasis and amyloidogenesis in Alzheimer's disease: Two sides of the same coin.

Douglas G Peters, James R Connor, Mark D Meadowcroft

Registry-linked trialOpen access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02878538 (An N of One Clinical Trial to Pilot the Feasibility of Using the Iron-Chelator Deferiprone on Mild Cognitive Impairment), which is not on this map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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.

NCT02878538 early_phase1withdrawnnot on this mapstarted 2018, after this paper: background citation

An N of One Clinical Trial to Pilot the Feasibility of Using the Iron-Chelator Deferiprone on Mild Cognitive Impairment

TypeinterventionalSponsorThe University of Texas Health Science Center at San AntonioRan2018 to 2023Enrolled0ConditionsMild Cognitive ImpairmentArmsDeferiprone, Placebo phase
3 · Its place in the literature

Who cites it

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Pooled it
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  16. Observational
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15 more citing papers are in PubMed but not listed here.

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.

Douglas G PetersDepartment of Neurosurgery, The Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA; Department of Neural and Behavioral Sciences, The Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA.
James R ConnorDepartment of Neurosurgery, The Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA.
Mark D MeadowcroftDepartment of Neurosurgery, The Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA; Department of Radiology, The Center for NMR Research, The Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey, PA, USA. Electronic address: markmeadowcroft@psu.edu.
Pennsylvania State University · US

Funding

Micro-histological MRI of White Matter Cytoarchitecture in Alzheimers DiseaseR03AG047461 · NIA · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI MEADOWCROFT, MARK DAVID · 2014 to 2015
$158k
NIA NIH HHS R03 AG047461NIA NIH HHS R03AG047461
6 · The paper itself

Abstract

The dysregulation of iron metabolism in Alzheimer's disease is not accounted for in the current framework of the amyloid cascade hypothesis. Accumulating evidence suggests that impaired iron homeostasis is an early event in Alzheimer's disease progression. Iron dyshomeostasis leads to a loss of function in several enzymes requiring iron as a cofactor, the formation of toxic oxidative species, and the elevated production of beta-amyloid proteins. Several common genetic polymorphisms that cause increased iron levels and dyshomeostasis have been associated with Alzheimer's disease but the pathoetiology is not well understood. A full picture is necessary to explain how heterogeneous circumstances lead to iron loading and amyloid deposition. There is evidence to support a causative interplay between the concerted loss of iron homeostasis and amyloid plaque formation. We hypothesize that iron misregulation and beta-amyloid plaque pathology are synergistic in the process of neurodegeneration and ultimately cause a downward cascade of events that spiral into the manifestation of Alzheimer's disease. In this review, we amalgamate recent findings of brain iron metabolism in healthy versus Alzheimer's disease brains and consider unique mechanisms of iron transport in different brain cells as well as how disturbances in iron regulation lead to disease etiology and propagate Alzheimer's pathology.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHomeostasisHumansIronPlaque, AmyloidAmyloid beta-PeptidesIronADAlzheimer's diseaseAmyloidogenesisBeta-amyloidDyshomeostasisIronMetallosisPathology

Identifiers

PMID26303889
PMCPMC4672943
OpenAlexW1593684700

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

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.