4.6 Review

Antibody-Based Therapeutic Interventions for Amyotrophic Lateral Sclerosis: A Systematic Literature Review

期刊

FRONTIERS IN NEUROSCIENCE
卷 15, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2021.790114

关键词

amyotrophic lateral sclerosis; antibody-based therapy; systematic review; knowledge synthesis; passive immunization

资金

  1. ALS Canada Foundation
  2. ALS Canada Foundation
  3. ALS Canada Foundation
  4. ALS Canada Foundation
  5. Vincent Bourque Foundation
  6. Vincent Bourque Foundation
  7. Vincent Bourque Foundation
  8. Vincent Bourque Foundation
  9. CIHR-INMHA [ICT-171454]
  10. CIHR-INMHA

向作者/读者索取更多资源

ALS is a mid-life onset neurodegenerative disease with no known cure, but antibody-based therapeutic interventions are gaining attention. Research has shown some efficacy of antibody-based treatments in ALS patients and animal models, targeting extracellular molecules and intracellular pathogenic proteins. The potentials and limitations of these therapeutic interventions have been described and discussed in the literature review.
Amyotrophic Lateral Sclerosis (ALS) is a mid-life onset neurodegenerative disease that manifests its symptomatology with motor impairments and cognitive deficits overlapping with Frontotemporal Lobar Degeneration (FTLD). The etiology of ALS remains elusive, with various mechanisms and cellular targets implicated, and no treatment can reverse or stop the progression of the pathology. Therapeutic interventions based on passive immunization are gaining attention for neurodegenerative diseases, and FDA recently approved the first antibody-based approach for Alzheimer's disease. The present systematic review of the literature aims to highlight the efforts made over the past years at developing antibody-based strategies to cure ALS. Thirty-one original research papers have been selected where the therapeutic efficacy of antibodies were investigated and described in patients and animal models of ALS. Antibody-based interventions analyzed, target both extracellular molecules implicated in the pathology and intracellular pathogenic proteins known to drive the disease, such as SOD1, TDP-43 or C9ORF72 repeats expansions. The potentials and limitations of these therapeutic interventions have been described and discussed in the present review.

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