Evidence map›Paper›PMID 32457210›Full record

ArticleNeurology2020

Effect of ApoE isoforms on mitochondria in Alzheimer disease.

Junxiang Yin, Eric M Reiman, Thomas G Beach, Geidy E Serrano, Marwan N Sabbagh, Megan Nielsen, Richard J Caselli, Jiong Shi

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 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
5.8field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. bioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Exploratory associations between APOE-εFrontiers in neurology · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Proteomic and metabolic profiling revealsbioRxiv : the preprint server for biology · 2025
    Article
  16. THRA1/PGC-1α/SIRT3 pathway regulates oxidative stress and is implicated in hypertension of maternal hypothyroid rat offspring.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Article

18 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 2 countries.

Junxiang YinFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.
Eric M ReimanFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.ORCID 0000-0002-0705-3696
Thomas G BeachFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.
Geidy E SerranoFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.
Marwan N SabbaghFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.
Megan NielsenFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.
Richard J CaselliFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing.
Jiong ShiFrom the Barrow Neurological Institute (J.Y., M.N.S., M.N., J.S.), St. Joseph Hospital and Medical Center, Phoenix, AZ; Banner Alzheimer's Institute (E.M.R.), Phoenix, AZ; Civin Laboratory for Neuropathology (T.G.B., G.E.S.), Banner Sun Health Research Institute, Sun City, AZ; Cleveland Clinic Lou Ruvo Center for Brain Health (M.N.S.), Las Vegas, NV; School of Life Sciences (M.N.), Arizona State University, Tempe; Department of Neurology (R.J.C.), Mayo Clinic Arizona, Scottsdale; Advanced Innovation Center for Human Brain Protection (J.S.), Capital Medical University, Beijing, China; and China National Clinical Research Center for Neurological Diseases (J.S.), Beijing Tiantan Hospital, Capital Medical University, Beijing. jshi2000@yahoo.com.ORCID 0000-0001-7694-1366
Alzheimer's Association · US

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI REIMAN, ERIC MICHAEL · 2001 to 2020
$32.5M
National Brain and Tissue Resource for Parkinson's Disease and Related DisordersU24NS072026 · NINDS · BANNER SUN HEALTH RESEARCH INSTITUTE · PI BEACH, THOMAS G · 2011 to 2015
$7.8M
NIA NIH HHS P30 AG019610NINDS NIH HHS U24 NS072026
6 · The paper itself

Abstract

objectiveTo test the hypothesis that ApoE isoforms affect mitochondrial structure and function that are related to cognitive impairment in Alzheimer disease (AD), we systematically investigated the effects of ApoE isoforms on mitochondrial biogenesis and dynamics, oxidative stress, synapses, and cognitive performance in AD.

methodsWe obtained postmortem human brain tissues and measured proteins that are responsible for mitochondrial biogenesis (peroxisome proliferator-activated receptor-gamma coactivator-1α [PGC-1α] and sirtuin 3 [SIRT3]), for mitochondrial dynamics (mitofusin 1 [MFN1], mitofusin 2 [MFN2], and dynamin-like protein 1 [DLP1]), for oxidative stress (superoxide dismutase 2 [SOD2] and forkhead-box protein O3a [Foxo3a]), and for synapses (postsynaptic density protein 95 [PSD95] and synapsin1 [Syn1]). A total of 46 cases were enrolled, including ApoE-ɛ4 carriers (n = 21) and noncarriers (n = 25).

resultsLevels of these proteins were compared between ApoE-ɛ4 carriers and noncarriers. ApoE-ɛ4 was associated with impaired mitochondrial structure and function, oxidative stress, and synaptic integrity in the human brain. Correlation analysis revealed that mitochondrial proteins and the synaptic protein were strongly associated with cognitive performance.

conclusionApoE isoforms influence mitochondrial structure and function, which likely leads to alteration in oxidative stress, synapses, and cognitive function. These mitochondria-related proteins may be a harbinger of cognitive decline in ApoE-ɛ4 carriers and provide novel therapeutic targets for prevention and treatment of AD.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseApolipoprotein E4Apolipoproteins EBrain ChemistryFemaleHumansMaleMental Status and Dementia TestsMitochondriaMitochondrial DynamicsMitochondrial ProteinsNerve Tissue ProteinsNeuronal PlasticityOrganelle BiogenesisApoE protein, humanApolipoprotein E4Apolipoproteins EMitochondrial ProteinsNerve Tissue ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanProtein IsoformsSIRT3 protein, humanSirtuin 3

Identifiers

PMID32457210
PMCPMC7455369
OpenAlexW3031542208

What OpenQuestion holds

Textmetadata
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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.