Evidence map›Paper›PMID 27185734›Full record

ReviewBehavioural brain research2016

Molecular and cellular pathophysiology of preclinical Alzheimer's disease.

Elliott J Mufson, Milos D Ikonomovic, Scott E Counts, Sylvia E Perez, Michael Malek-Ahmadi, Stephen W Scheff, Stephen D Ginsberg

Open access · greenAbstract readReview
In one paragraph

Review in Behavioural brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
10.1field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.

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  20. Alcohol Use Disorder and Dementia: A Review.Alcohol research : current reviews · 2024
    Review

8 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

7 authors at 6 institutions in 1 country.

Elliott J MufsonDepartments of Neurobiology and Neurology, Barrow Neurological Institute, Phoenix, AZ, United States. Electronic address: Elliott.Mufson@dignityhealth.org.
Milos D IkonomovicDepartments of Neurology and Psychiatry, University of Pittsburgh, and Geriatric Research Education and Clinical Center, VA Pittsburgh Healthcare System, Pittsburgh, PA, United States.
Scott E CountsDepartment of Translational Science and Molecular Medicine, Department of Family Medicine, Hauenstien Neuroscience Institute, Mercy Health Saint Mary's Hospital, Grand Rapids, MI, United States.
Sylvia E PerezDepartments of Neurobiology and Neurology, Barrow Neurological Institute, Phoenix, AZ, United States.
Michael Malek-AhmadiBanner Alzheimer's Institute, Phoenix, AZ, United States.
Stephen W ScheffSanders Brown Center on Aging, University of Kentucky, Lexington, KY, United States.
Stephen D GinsbergCenter for Dementia Research, Nathan Kline Institute, Department of Psychiatry, Department of Neuroscience & Physiology, New York University Langone Medical Center, Orangeburg, NY, United States.
Barrow Neurological Institute · USBanner Alzheimer’s InstituteGeriatric Research Education and Clinical Center · USMercy Health Saint Mary's · USNathan Kline Institute for Psychiatric Research · USUniversity of Kentucky · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI LEURGANS, SUE E. · 1991 to 2020
$49.1M
Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0M
TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI COUNTS, SCOTT E · 1997 to 2024
$39.7M
University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI GOLD, BRIAN TIMOTHY, VAN ELDIK, LINDA J · 2006 to 2020
$23.3M
Michigan Alzheimer's Disease Core CenterP30AG053760 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALBIN, ROGER L · 2016 to 2020
$10.1M
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
Neuroprotective microRNA pathwaysR21AG042146 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI COUNTS, SCOTT E · 2012 to 2013
$409k
Proteomics of mild cognitive impairment in the elderlyR21AG026032 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI COUNTS, SCOTT E · 2005 to 2006
$342k
NIA NIH HHS P01 AG014449NIA NIH HHS P01 AG017617NIA NIH HHS P30 AG010161NIA NIH HHS P30 AG028383NIA NIH HHS P30 AG053760NIA NIH HHS R01 AG043375NIA NIH HHS R21 AG026032NIA NIH HHS R21 AG042146
6 · The paper itself

Abstract

Although the two pathological hallmarks of Alzheimer's disease (AD), senile plaques composed of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau, have been studied extensively in postmortem AD and relevant animal and cellular models, the pathogenesis of AD remains unknown, particularly in the early stages of the disease where therapies presumably would be most effective. We and others have demonstrated that Aβ plaques and NFTs are present in varying degrees before the onset and throughout the progression of dementia. In this regard, aged people with no cognitive impairment (NCI), mild cognitive impairment (MCI, a presumed prodromal AD transitional state, and AD all present at autopsy with varying levels of pathological hallmarks. Cognitive decline, a requisite for the clinical diagnosis of dementia associated with AD, generally correlates better with NFTs than Aβ plaques. However, correlations are even higher between cognitive decline and synaptic loss. In this review, we illustrate relevant clinical pathological research in preclinical AD and throughout the progression of dementia in several areas including Aβ and tau pathobiology, single population expression profiling of vulnerable hippocampal and basal forebrain neurons, neuroplasticity, neuroimaging, cerebrospinal fluid (CSF) biomarker studies and their correlation with antemortem cognitive endpoints. In each of these areas, we provide evidence for the importance of studying the pathological hallmarks of AD not in isolation, but rather in conjunction with other molecular, cellular, and imaging markers to provide a more systematic and comprehensive assessment of the multiple changes that occur during the transition from NCI to MCI to frank AD.

Indexed as

Alzheimer DiseaseAnimalsHumansNeuronsProdromal Symptoms

Identifiers

PMID27185734
PMCPMC4931948
OpenAlexW2356948138

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.