Evidence map›Paper›PMID 30090689›Full record

ArticleJournal of Alzheimer's disease & Parkinsonism2018

The Potential of CRISPR/Cas9 Gene Editing as a Treatment Strategy for Alzheimer's Disease.

Troy T Rohn, Nayoung Kim, Noail F Isho, Jacob M Mack

Open access · hybridAbstract read
In one paragraph

Article in Journal of Alzheimer's disease & Parkinsonism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Alzheimer's and Parkinson's disease therapies in the clinic.Bioengineering & translational medicine · 2023
    Review
  11. Review
  12. Review
  13. CRISPR-Cas9: A Preclinical and Clinical Perspective for the Treatment of Human Diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Can mouse models mimic sporadic Alzheimer's disease?Neural regeneration research · 2020
    Review
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

4 authors at 1 institution in 1 country.

Troy T RohnDepartment of Biological Sciences, Science Building, Room 228, Boise State University, Boise, Idaho, USA.
Nayoung KimDepartment of Biological Sciences, Science Building, Room 228, Boise State University, Boise, Idaho, USA.
Noail F IshoDepartment of Biological Sciences, Science Building, Room 228, Boise State University, Boise, Idaho, USA.
Jacob M MackDepartment of Biological Sciences, Science Building, Room 228, Boise State University, Boise, Idaho, USA.
Boise State University · US

Funding

Women's health: interplay of maternal diet and key demographics on neurological health in the rural frontier and remote WestP20GM103408 · NIGMS · UNIVERSITY OF IDAHO · PI Scott A Minnich · 2012 to 2026
$59.8M
VPS35 D620N inhibits autophagy through disrupted hyaluronic acid-CD44 signalingP20GM109095 · NIGMS · BOISE STATE UNIVERSITY · PI OXFORD, JULIA THOM · 2014 to 2023
$22.7M
Nuclear Localization of an Amino-Terminal Fragment of Apolipoprotein E4 in the Alzheimer's Disease BrainR15AG042781 · NIA · BOISE STATE UNIVERSITY · PI ROHN, TROY T · 2013 to 2022
$1.1M
NIA NIH HHS R15 AG042781NIGMS NIH HHS P20 GM103408NIGMS NIH HHS P20 GM109095
6 · The paper itself

Abstract

Despite a wealth of knowledge gained in the past three decades concerning the molecular underpinnings of Alzheimer's disease (AD), progress towards obtaining effective, disease modifying therapies has proven to be challenging. In this manner, numerous clinical trials targeting the production, aggregation, and toxicity of beta-amyloid, have failed to meet efficacy standards. This puts into question the beta-amyloid hypothesis and suggests that additional treatment strategies should be explored. The recent emergence of CRISPR/Cas9 gene editing as a relatively straightforward, inexpensive, and precise system has led to an increased interest of applying this technique in AD. CRISPR/Cas9 gene editing can be used as a direct treatment approach or to help establish better animal models that more faithfully mimic human neurodegenerative diseases. In this manner, this technique has already shown promise in other neurological disorders, such as Huntington's disease. The purpose of this review is to examine the potential utility of CRISPR/Cas9 as a treatment option for AD by targeting specific genes including those that cause early-onset AD, as well as those that are significant risk factors for late-onset AD such as the apolipoprotein E4 (APOE4) gene.

Indexed as

Alzheimer’s diseaseCRISPR/Cas9Gene editingHuntington’s diseaseiPSC neuronsTreatment

Identifiers

PMID30090689
PMCPMC6078432
OpenAlexW2883317091

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.