Evidence map›Paper›PMID 32005122›Full record

ReviewMolecular neurodegeneration2020

Therapeutic approaches targeting Apolipoprotein E function in Alzheimer's disease.

Tosha Williams, David R Borchelt, Paramita Chakrabarty

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 3 pooled it
12.2field-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

88 citing papers in PubMed, 3 syntheses or guidelines pooled it, 167 citations in OpenAlex.

  1. Beneficial Effect of Societal Factors on APOE-ε2 and ε4 Carriers' Brain Health: A Systematic Review.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Pooled it
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  4. Japanese participant data from three gantenerumab trials in early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Trial
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  10. Open veterinary journal · 2025
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28 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

3 authors at 1 institution in 1 country.

Tosha WilliamsCenter for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
David R BorcheltCenter for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
Paramita ChakrabartyCenter for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA. pchakrabarty@ufl.edu.ORCID 0000-0002-6226-3776
University of Florida · US

Funding

APOE as a modifier of prion-like spread in dementiaRF1AG057933 · NIA · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, CHAKRABARTY, PARAMITA · 2018 to 2018
$2.6M
Towards understanding the role of immune regulation of Apolipoprotein E function in Alzheimer's disease proteostasisR01AG055798 · NIA · UNIVERSITY OF FLORIDA · PI CHAKRABARTY, PARAMITA · 2017 to 2022
$1.9M
Clinical and Translational Predoctoral training in Alzheimers Disease and Related DementiasT32AG061892 · NIA · UNIVERSITY OF FLORIDA · PI PARAMITA CHAKRABARTY, JADA M LEWIS · 2018 to 2026
$1.8M
APOE as a modifier of prion-like spread in dementiaR56AG057933 · NIA · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, CHAKRABARTY, PARAMITA · 2017 to 2017
$690k
NIA NIH HHS R01 AG055798NIA NIH HHS R56 AG057933NIA NIH HHS RF1 AG057933NIA NIH HHS RF1AG057933NIA NIH HHS T32 AG061892
6 · The paper itself

Abstract

One of the primary genetic risk factors for Alzheimer's disease (AD) is the presence of the Ɛ4 allele of apolipoprotein E (APOE). APOE is a polymorphic lipoprotein that is a major cholesterol carrier in the brain. It is also involved in various cellular functions such as neuronal signaling, neuroinflammation and glucose metabolism. Humans predominantly possess three different allelic variants of APOE, termed E2, E3, and E4, with the E3 allele being the most common. The presence of the E4 allele is associated with increased risk of AD whereas E2 reduces the risk. To understand the molecular mechanisms that underlie APOE-related genetic risk, considerable effort has been devoted towards developing cellular and animal models. Data from these models indicate that APOE4 exacerbates amyloid β plaque burden in a dose-dependent manner. and may also enhance tau pathogenesis in an isoform-dependent manner. Other studies have suggested APOE4 increases the risk of AD by mechanisms that are distinct from modulation of Aβ or tau pathology. Further, whether plasma APOE, by influencing systemic metabolic pathways, can also possibly alter CNS function indirectly is not complete;y understood. Collectively, the available studies suggest that APOE may impact multiple signaling pathways and thus investigators have sought therapeutics that would disrupt pathological functions of APOE while preserving or enhancing beneficial functions. This review will highlight some of the therapeutic strategies that are currently being pursued to target APOE4 towards preventing or treating AD and we will discuss additional strategies that holds promise for the future.

Indexed as

Alzheimer DiseaseAnimalsApolipoprotein E4Genetic Predisposition to DiseaseHumansApolipoprotein E4Alzheimer’s diseaseAmyloid βApolipoprotein ETauTherapy

Identifiers

PMID32005122
PMCPMC6995170
OpenAlexW3009292846

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.