Evidence map›Paper›PMID 34555265›Full record

ArticleBrain and behavior2021

Effects of ApoE genotype on clinical phenotypes in early-onset and late-onset Alzheimer's disease in China: Data from the PUMCH dementia cohort.

Liling Dong, Jie Li, Caiyan Liu, Chenhui Mao, Jie Wang, Dan Lei, Xinying Huang, Shanshan Chu, Bo Hou, Feng Feng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. International journal of molecular sciences · 2025
    Article
  2. Altered Heme and Redox Homeostasis Underpin Late-onset Alzheimer's Disease.International journal of biological sciences · 2025
    Article
  3. Association ofFrontiers in aging neuroscience · 2023
    Article
  4. Article
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

13 authors at 1 institution in 1 country.

Liling DongNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Jie LiNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Caiyan LiuNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.ORCID 0000-0001-6035-7456
Chenhui MaoNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Jie WangNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Dan LeiNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Xinying HuangNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Shanshan ChuNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Bo HouDepartment of Radiology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.
Feng FengDepartment of Radiology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.ORCID 0000-0002-3507-1154
Longze ShaInstitute of Basic Medical Sciences, Peking Union Medical College, Dongcheng, Beijing, China.
Qi XuInstitute of Basic Medical Sciences, Peking Union Medical College, Dongcheng, Beijing, China.
Jing GaoNeurology Department, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Dongcheng, Beijing, China.ORCID 0000-0001-7458-4334
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTo investigate the heterogeneous effect of Apolipoprotein E (ApoE) genotype on clinical phenotypes in early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD), respectively.

methods785 probable AD patients were enrolled from the dementia cohort of Peking Union Medical College Hospital (PUMCH), China. There were 386 EOAD and 399 LOAD cases. All individuals finished history inquiry, neurological examination, blood biochemical test, neuropsychological screening test, electroencephalography, brain CT/MRI, and ApoE genotyping. Some participants had neuropsychological domain assessment (n = 317), MRI morphometry (n = 130), CSF testing of Aβ42, p-tau, t-tau (n = 144), or DNA sequencing (n = 690). The variables were compared mainly between ɛ4 carriers and non-carriers in EOAD and LOAD, respectively.

resultsIn LOAD, ɛ4 carriers showed female predominance; worse performance in trail making test, delayed recall of auditory verbal learning test (AVLT) and rey complex figure; smaller hippocampal, parahippocampal, and entorhinal volume, as compared to ɛ4 non-carriers. In EOAD, ɛ4 carriers had lower scores in AVLT, episodic memory and modified Luria's tapping task; but less cortical atrophy in entorhinal, middle cingulate, inferior frontal, and parieto-occipital regions, in comparison to ɛ4 non-carriers. 6.2% (43/690) subjects harbored potential causative mutations in APP, PSEN1, and PSEN2. In both EOAD and LOAD, no differences were observed between ɛ4 carriers and non-carriers in CSF levels of Aβ42, p-tau, t-tau, or mutation frequency.

conclusionsApoE exerts a heterogeneous effect on clinical phenotypes in EOAD and LOAD, which might be related to the different genetic and pathological basis underlying them.

Indexed as

Alzheimer DiseaseApolipoprotein E4Apolipoproteins EFemaleGenotypeHospitalsHumansPhenotypeApoE protein, humanApolipoprotein E4Apolipoproteins EApoEcognitive functioncortical atrophyearly-onset Alzheimer's diseaselate-onset Alzheimer's diseasetau burden

Identifiers

PMID34555265
PMCPMC8613405
OpenAlexW3201049513

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.