Evidence map›Paper›PMID 32759188›Full record

ArticleNeurology2020

Limbic-predominant age-related TDP-43 encephalopathy in Black and White decedents.

Sukriti Nag, Lisa L Barnes, Lei Yu, Robert S Wilson, David A Bennett, Julie A Schneider

Open access · greenAbstract read
In one paragraph

Article in Neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  8. Evaluating the updated LATE-NC staging criteria using data from NACC.Alzheimer's & dementia : the journal of the Alzheimer's Association · 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

6 authors at 1 institution in 1 country.

Sukriti NagFrom the Rush Alzheimer Disease Center (S.N., L.L.B., L.Y., R.S.W., D.A.B., J.A.S.) and Departments of Pathology (Neuropathology) (S.N., J.A.S.), Neurological Sciences (L.L.B., L.Y., R.S.W., D.A.B., J.A.S.), and Psychiatry and Behavioral Sciences (L.L.B., R.S.W.), Rush University Medical Center, Chicago, IL. Sukriti_Nag@rush.edu.ORCID 0000-0002-5193-1177
Lisa L BarnesFrom the Rush Alzheimer Disease Center (S.N., L.L.B., L.Y., R.S.W., D.A.B., J.A.S.) and Departments of Pathology (Neuropathology) (S.N., J.A.S.), Neurological Sciences (L.L.B., L.Y., R.S.W., D.A.B., J.A.S.), and Psychiatry and Behavioral Sciences (L.L.B., R.S.W.), Rush University Medical Center, Chicago, IL.
Lei YuFrom the Rush Alzheimer Disease Center (S.N., L.L.B., L.Y., R.S.W., D.A.B., J.A.S.) and Departments of Pathology (Neuropathology) (S.N., J.A.S.), Neurological Sciences (L.L.B., L.Y., R.S.W., D.A.B., J.A.S.), and Psychiatry and Behavioral Sciences (L.L.B., R.S.W.), Rush University Medical Center, Chicago, IL.
Robert S WilsonFrom the Rush Alzheimer Disease Center (S.N., L.L.B., L.Y., R.S.W., D.A.B., J.A.S.) and Departments of Pathology (Neuropathology) (S.N., J.A.S.), Neurological Sciences (L.L.B., L.Y., R.S.W., D.A.B., J.A.S.), and Psychiatry and Behavioral Sciences (L.L.B., R.S.W.), Rush University Medical Center, Chicago, IL.
David A BennettFrom the Rush Alzheimer Disease Center (S.N., L.L.B., L.Y., R.S.W., D.A.B., J.A.S.) and Departments of Pathology (Neuropathology) (S.N., J.A.S.), Neurological Sciences (L.L.B., L.Y., R.S.W., D.A.B., J.A.S.), and Psychiatry and Behavioral Sciences (L.L.B., R.S.W.), Rush University Medical Center, Chicago, IL.
Julie A SchneiderFrom the Rush Alzheimer Disease Center (S.N., L.L.B., L.Y., R.S.W., D.A.B., J.A.S.) and Departments of Pathology (Neuropathology) (S.N., J.A.S.), Neurological Sciences (L.L.B., L.Y., R.S.W., D.A.B., J.A.S.), and Psychiatry and Behavioral Sciences (L.L.B., R.S.W.), Rush University Medical Center, Chicago, IL.
Rush University Medical Center · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI LEURGANS, SUE E. · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Risk Factors for Cognitive Decline in African-AmericansR01AG022018 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BARNES, LISA L · 2004 to 2025
$18.2M
Characterizing TDP-43 related hippocampal degeneration and memory loss in agingR01AG067482 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI SCHNEIDER, JULIE A. · 2020 to 2024
$6.8M
Racial Differences in Late-Life Cognitive Decline and Risk of Alzheimer's DiseaseRF1AG022018 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BARNES, LISA L · 2016 to 2019
$6.6M
Epidemiologic Study of TDP-43 Pathology in Aging and DementiaR01AG042210 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI SCHNEIDER, JULIE A. · 2012 to 2018
$2.4M
NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG022018NIA NIH HHS R01 AG042210NIA NIH HHS R01 AG067482NIA NIH HHS RF1 AG022018
6 · The paper itself

Abstract

objectiveThe association of limbic-predominant age-related transactive response DNA-binding protein 43 encephalopathy neuropathologic change (LATE-NC) with cognition and dementia was assessed in community-dwelling Black elders, and racial differences in these associations were tested.

methodsBlack (n = 76) and White (n = 152) decedents from 4 longitudinal clinical pathologic studies of aging were matched 2 to 1 by age at death, sex, years of education, dementia status, and follow-up time. LATE-NC detected by immunohistochemistry was dichotomized into none/mild and moderate/severe groups. Distribution and clinical and pathologic characteristics of LATE-NC and its association with cognitive profiles and odds of dementia were determined in Black decedents, and racial differences in these associations were assessed.

resultsThe overall frequency of LATE-NC in Black and White decedents was similar (40.8% vs 45.4%). Black decedents with moderate/severe LATE-NC were older, had significantly lower global cognition scores, particularly in memory domains, and had higher frequency of Alzheimer disease, hippocampal sclerosis, and cerebral amyloid angiopathy than the LATE-NC none/mild group. LATE-NC in Black decents was independently associated with impaired global cognition, episodic and semantic memory, and visuospatial abilities. There were no racial differences in clinical features or pathologic distribution of LATE-NC except for a significant increase in the mean cytoplasmic inclusions in the entorhinal and mid temporal cortices in White compared to Black decedents. In addition, no racial differences in the cognitive profiles or the odds of dementia were observed in Black vs White decedents.

conclusionsConsistent with findings in White decedents, LATE-NC in Black decedents is associated with impaired cognition, including memory domains.

Indexed as

Aged, 80 and overAge FactorsAlzheimer DiseaseBlack or African AmericanCognitive DysfunctionComorbidityFemaleHumansIllinoisLate Onset DisordersLongitudinal StudiesMaleNeuropsychological TestsRace FactorsTDP-43 ProteinopathiesWhite People

Identifiers

PMID32759188
PMCPMC7713750
OpenAlexW3047297093

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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.