Evidence map›Paper›PMID 27143416›Full record

ArticleNeurobiology of aging2016

Oxidative stress and hippocampal synaptic protein levels in elderly cognitively intact individuals with Alzheimer's disease pathology.

Stephen W Scheff, Mubeen A Ansari, Elliott J Mufson

Abstract read
In one paragraph

Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.8field-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

53 citing papers in PubMed, 95 citations in OpenAlex.

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  9. SV2A PET shows hippocampal synaptic loss in cognitively unimpaired APOE ε4/ε4 homozygotes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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  18. Synaptic Compensatory Plasticity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Review
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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 2 institutions in 1 country.

Stephen W ScheffDepartment of Anatomy and Neurobiology, Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA. Electronic address: sscheff@email.uky.edu.
Mubeen A AnsariDepartment of Anatomy and Neurobiology, Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Elliott J MufsonDepartment of Neurobiology, Barrow Neurological Institute, Phoenix, AZ, USA.
University of Kentucky · USBarrow Neurological Institute · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI IKONOMOVIC, MILOS D · 1997 to 2024
$39.7M
University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI SCHMITT, FREDERICK · 2006 to 2020
$23.3M
Cellular and Molecular Medial Temporal Lobe Pathology in Elderly PreMCI subjectsR01AG043375 · NIA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI GINSBERG, STEPHEN D, MUFSON, ELLIOTT JAY · 2013 to 2017
$3.6M
CELLULAR CHANGES ALTERING SYNAPTIC CONNECTIVITY IN PRECLINICAL ADR01AG042475 · NIA · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2013 to 2017
$1.5M
NIA NIH HHS P01 AG014449NIA NIH HHS P30 AG010161NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG042475NIA NIH HHS R01 AG043375
6 · The paper itself

Abstract

Neuritic amyloid plaques and neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) and are major components used for the clinical diagnosis of this disorder. However, many individuals with no cognitive impairment (NCI) also present at autopsy with high levels of these AD pathologic hallmarks. In this study, we evaluated 15 autopsy cases from NCI individuals with high levels of AD-like pathology (high pathology no cognitive impairment) and compared them to age- and postmortem-matched cohorts of individuals with amnestic mild cognitive impairment and NCI cases with low AD-like pathology (low pathology no cognitive impairment [LPNCI]). Individuals classified as high pathology no cognitive impairment or amnestic mild cognitive impairment had a significant loss of both presynaptic and postsynaptic proteins in the hippocampus compared with those in the LPNCI cohort. In addition, these 2 groups had a significant increase in 3 different markers of oxidative stress compared with that in the LPNCI group. The changes in levels of synaptic proteins are strongly associated with levels of oxidative stress. These data suggest that cognitively older subjects without dementia but with increased levels of AD-like pathology may represent a very early preclinical stage of AD.

Indexed as

CognitionOxidative StressAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EFemaleGenotypeHippocampusHumansLipid PeroxidationMaleNerve Tissue ProteinsPeptide FragmentsSynapsesAmyloid beta-Peptidesamyloid beta-protein (1-42)Apolipoproteins ENerve Tissue ProteinsPeptide FragmentsAgingAmyloidDementiaHippocampusNeurodegenerationSynapsesTemporal lobe

Identifiers

PMID27143416
PMCPMC4857887
OpenAlexW2294586018

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.