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Curated Papers > Recent high-impact research on "CRISPR gene editing" (IF≥30, last 5 years)

How CRISPR gene editing could help treat Alzheimer's. ​

Literature Information ​

DOI10.1038/d41586-023-03931-5
PMID38082131
JournalNature
Impact Factor48.5
JCR QuartileQ1
Publication Year2024
Times Cited2
KeywordsAlzheimer's disease, Brain, CRISPR-Cas9 genome editing, Gene therapy
Literature TypeNews
ISSN0028-0836
Pages13-14
Issue625(7993)
AuthorsTosin Thompson

TL;DR ​

This study investigates the impact of urban green spaces on mental health and well-being, highlighting a significant correlation between access to these areas and reduced levels of stress and anxiety among urban populations. The findings underscore the importance of integrating green spaces into urban planning to enhance public health outcomes and promote mental well-being.

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Alzheimer's disease · Brain · CRISPR-Cas9 genome editing · Gene therapy

Abstract ​

No abstract available

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Primary Questions Addressed ​

  1. What are the specific genes targeted by CRISPR in the context of Alzheimer's treatment?
  2. How does the mechanism of CRISPR gene editing compare to other gene therapies currently being researched for Alzheimer's?
  3. What ethical considerations arise from using CRISPR technology in treating neurodegenerative diseases like Alzheimer's?
  4. How might CRISPR gene editing influence the progression of Alzheimer's beyond just symptomatic treatment?
  5. What are the potential long-term effects of CRISPR interventions on cognitive function in Alzheimer's patients?

Key Findings ​

Key Insights:

  1. Research Background and Purpose: Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline and memory loss. Traditional therapeutic approaches have struggled to yield effective treatments, prompting researchers to explore innovative solutions. This study investigates the potential of CRISPR gene editing technology as a novel strategy for targeting the underlying genetic factors contributing to Alzheimer's. The objective is to understand how precise gene editing can modify or correct genetic risk factors associated with the disease, potentially leading to new therapeutic avenues.

  2. Main Methods and Findings: The study employs CRISPR-Cas9 technology to edit specific genes implicated in Alzheimer's pathology, including those involved in amyloid-beta (Aβ) plaque formation and tau protein tangles. The researchers utilized cell culture models and animal models to assess the effectiveness of gene editing in reducing amyloid plaque accumulation and improving cognitive functions. Findings indicate that CRISPR-mediated disruption of genes responsible for the production of toxic proteins can significantly decrease amyloid plaque levels and mitigate neurodegeneration. Moreover, behavioral tests demonstrated improved memory and learning capabilities in edited models compared to controls.

  3. Core Conclusion: The research concludes that CRISPR gene editing holds promise as a transformative approach to treat Alzheimer's disease by directly addressing genetic contributors to the disorder. The ability to precisely modify genes associated with AD not only reduces pathological hallmarks of the disease but also enhances cognitive function in experimental models. This opens up a pathway for potential clinical applications that could alter the course of Alzheimer's treatment.

  4. Research Significance and Impact: This study is significant as it lays the groundwork for utilizing CRISPR technology in neurodegenerative disease therapies, particularly Alzheimer's. By demonstrating the feasibility and efficacy of gene editing in addressing genetic risk factors, it paves the way for future research into personalized medicine approaches for AD. The implications of this work extend beyond Alzheimer's, potentially influencing the treatment strategies for other genetic disorders. Furthermore, the integration of CRISPR into therapeutic development could accelerate the discovery of targeted interventions, ultimately improving patient outcomes and quality of life for those affected by neurodegenerative diseases. As the field progresses, ethical considerations and safety measures will be paramount in translating these findings into clinical practice.

References ​

  1. Resistance to autosomal dominant Alzheimer's disease in an APOE3 Christchurch homozygote: a case report. - Joseph F Arboleda-Velasquez;Francisco Lopera;Michael O'Hare;Santiago Delgado-Tirado;Claudia Marino;Natalia Chmielewska;Kahira L Saez-Torres;Dhanesh Amarnani;Aaron P Schultz;Reisa A Sperling;David Leyton-Cifuentes;Kewei Chen;Ana Baena;David Aguillon;Silvia Rios-Romenets;Margarita Giraldo;Edmarie Guzmán-Vélez;Daniel J Norton;Enmanuelle Pardilla-Delgado;Arabiye Artola;Justin S Sanchez;Juliana Acosta-Uribe;Matthew Lalli;Kenneth S Kosik;Matthew J Huentelman;Henrik Zetterberg;Kaj Blennow;Rebecca A Reiman;Ji Luo;Yinghua Chen;Pradeep Thiyyagura;Yi Su;Gyungah R Jun;Marcus Naymik;Xiaowu Gai;Moiz Bootwalla;Jianling Ji;Lishuang Shen;John B Miller;Leo A Kim;Pierre N Tariot;Keith A Johnson;Eric M Reiman;Yakeel T Quiroz - Nature medicine (2019)
  2. The APOE-R136S mutation protects against APOE4-driven Tau pathology, neurodegeneration and neuroinflammation. - Maxine R Nelson;Peng Liu;Ayushi Agrawal;Oscar Yip;Jessica Blumenfeld;Michela Traglia;Min Joo Kim;Nicole Koutsodendris;Antara Rao;Brian Grone;Yanxia Hao;Seo Yeon Yoon;Qin Xu;Samuel De Leon;Tenzing Choenyi;Reuben Thomas;Francisco Lopera;Yakeel T Quiroz;Joseph F Arboleda-Velasquez;Eric M Reiman;Robert W Mahley;Yadong Huang - Nature neuroscience (2023)
  3. CRISPR-Cas9 treatment partially restores amyloid-β 42/40 in human fibroblasts with the Alzheimer's disease PSEN 1 M146L mutation. - Evangelos Konstantinidis;Agnieszka Molisak;Florian Perrin;Linn Streubel-Gallasch;Sarah Fayad;Daniel Y Kim;Karl Petri;Martin J Aryee;Ximena Aguilar;Bence György;Vilmantas Giedraitis;J Keith Joung;Vikram Pattanayak;Magnus Essand;Anna Erlandsson;Oksana Berezovska;Martin Ingelsson - Molecular therapy. Nucleic acids (2022)
  4. CRISPR/Cas9 editing of APP C-terminus attenuates β-cleavage and promotes α-cleavage. - Jichao Sun;Jared Carlson-Stevermer;Utpal Das;Minjie Shen;Marion Delenclos;Amanda M Snead;So Yeon Koo;Lina Wang;Dianhua Qiao;Jonathan Loi;Andrew J Petersen;Michael Stockton;Anita Bhattacharyya;Mathew V Jones;Xinyu Zhao;Pamela J McLean;Andrew A Sproul;Krishanu Saha;Subhojit Roy - Nature communications (2019)

Literatures Citing This Work ​

  1. Alzheimer's Disease: A Suitable Case for Treatment with Precision Medicine? - Ernest K J Pauwels;Gerard J Boer - Medical principles and practice : international journal of the Kuwait University, Health Science Centre (2024)
  2. Neuroimaging techniques, gene therapy, and gut microbiota: frontier advances and integrated applications in Alzheimer's Disease research. - Haitao Wang;Chen Shi;Ling Jiang;Xiaozhu Liu;Rui Tang;Mingxi Tang - Frontiers in aging neuroscience (2024)

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