ArticleActa neuropathologica communications2020
Influence of APOE genotype in primary age-related tauopathy.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- A critical appraisal of the link between apolipoprotein E and Tau.Current opinion in neurology · 2026Review
- Primary age-related tauopathy.Acta neuropathologica · 2025Review
- Cognitive and neuropsychological trajectories in patients with mixed neurodegenerative pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Hippocampal tau distribution in primary age-related tauopathy: The Vantaa 85+ Study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Protection against APOE4-associated phenotypes with the longevity-promoting intervention 17α-estradiol in middle-aged male mice.Communications medicine · 2025Article
- Lewy body co-pathology in Alzheimer's disease and primary age-related tauopathy contributes to differential neuropathological, cognitive, and brain atrophy patterns.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Novel Role of Pin1-Cis P-Tau-ApoE Axis in the Pathogenesis of Preeclampsia and Its Connection with Dementia.Biomedicines · 2024Review
- Prevalence and clinicopathological features of primary age-related tauopathy (PART): A large forensic autopsy study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Histopathologic brain age estimation via multiple instance learning.Acta neuropathologica · 2023Article
- The relationship between hippocampal amyloid beta burden and spatial distribution of neurofibrillary degeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Hypothesis review: Alzheimer's overture guidelines.Brain pathology (Zurich, Switzerland) · 2023Review
- Cognitive and Neuropsychological Profiles in Alzheimer's Disease and Primary Age-Related Tauopathy and the Influence of Comorbid Neuropathologies.Journal of Alzheimer's disease : JAD · 2023Article
- APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer's disease pathology and brain diseases.Molecular neurodegeneration · 2022Review
- Primary age-related tauopathy in a Finnish population-based study of the oldest old (Vantaa 85+).Neuropathology and applied neurobiology · 2022Article
- The Frequency of Cerebral Amyloid Angiopathy in Primary Age-Related Tauopathy.Journal of neuropathology and experimental neurology · 2022Article
- Apolipoprotein E Genotype e2: Neuroprotection and Its Limits.Frontiers in aging neuroscience · 2022Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The term "Primary age-related tauopathy" (PART) was coined in 2014 to describe the common neuropathological observation of neurofibrillary tangles without associated beta-amyloid (Aβ) pathology. It is possible for PART pathology to be present in both cognitively normal and cognitively impaired individuals. Genetically, Apolipoprotein E (APOE) ε4 has been shown to occur less commonly in PART than in Alzheimer's disease (AD). Here, we investigate the relationships between PART, AD and those pathologically normal for age, with an emphasis on APOE and cognition, using 152 selected participants from The University of Manchester Longitudinal Study of Cognition in Normal Healthy Old Age and the Manchester arm of the Brains for Dementia Research cohort. APOE genotype differed between PART and AD with APOE ε2 more common in the former and APOE ε4 more common in the latter. Individuals with definite PART were less likely to be cognitively impaired than those with AD and those with pathology considered pathologically normal for age. We postulate that the lack of Aβ in definite PART cases may be due either to an increased frequency of APOE ε2 or decreased frequency of APOE ε4 as their resulting protein isoforms have differing binding properties in relation to Aβ. Similarly, an increased frequency of APOE ε2 or decreased frequency of APOE ε4 may lead to decreased levels of cognitive impairment, which raises questions regarding the impact of Aβ pathology on overall cognition in elderly subjects. We suggest that it may be possible to use the increased frequency of APOE ε2 in definite PART to assist neuropathological diagnosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.