Evidence map›Paper›PMID 32347461›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2020

Immunotherapies for Aging-Related Neurodegenerative Diseases-Emerging Perspectives and New Targets.

Somin Kwon, Michiyo Iba, Changyoun Kim, Eliezer Masliah

Abstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026
    Review
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  11. A brain-penetrant bispecific antibody lowers oligomeric alpha-synuclein and activates microglia in a mouse model of alpha-synuclein pathology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  12. Review
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  15. Article
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  18. Single-Domain Antibody-Based Protein Degrader for Synucleinopathies.bioRxiv : the preprint server for biology · 2024
    Article
  19. Recombinant Antibody Fragments for Immunotherapy of Parkinson's Disease.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024
    Review
  20. Article
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.

Somin KwonLaboratory of Neurogenetics, Molecular Neuropathology Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.
Michiyo IbaLaboratory of Neurogenetics, Molecular Neuropathology Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.
Changyoun KimLaboratory of Neurogenetics, Molecular Neuropathology Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.
Eliezer MasliahLaboratory of Neurogenetics, Molecular Neuropathology Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA. eliezer.masliah@nih.gov.

Funding

Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
6 · The paper itself

Abstract

Neurological disorders such as Alzheimer's disease (AD), Lewy body dementia (LBD), frontotemporal dementia (FTD), and vascular dementia (VCID) have no disease-modifying treatments to date and now constitute a dementia crisis that affects 5 million in the USA and over 50 million worldwide. The most common pathological hallmark of these age-related neurodegenerative diseases is the accumulation of specific proteins, including amyloid beta (Aβ), tau, α-synuclein (α-syn), TAR DNA-binding protein 43 (TDP43), and repeat-associated non-ATG (RAN) peptides, in the intra- and extracellular spaces of selected brain regions. Whereas it remains controversial whether these accumulations are pathogenic or merely a byproduct of disease, the majority of therapeutic research has focused on clearing protein aggregates. Immunotherapies have garnered particular attention for their ability to target specific protein strains and conformations as well as promote clearance. Immunotherapies can also be neuroprotective: by neutralizing extracellular protein aggregates, they reduce spread, synaptic damage, and neuroinflammation. This review will briefly examine the current state of research in immunotherapies against the 3 most commonly targeted proteins for age-related neurodegenerative disease: Aβ, tau, and α-syn. The discussion will then turn to combinatorial strategies that enhance the effects of immunotherapy against aggregating protein, followed by new potential targets of immunotherapy such as aging-related processes.

Indexed as

Agingalpha-SynucleinAmyloid beta-PeptidesAnimalsBrainClinical Trials as TopicDrug Delivery SystemsGene-Environment InteractionHumansImmunologic FactorsImmunotherapyNeurodegenerative Diseasestau Proteinsalpha-SynucleinAmyloid beta-PeptidesImmunologic Factorstau ProteinsAlzheimer’s diseaseAβImmunotherapytauvaccinationα-synuclein

Identifiers

PMID32347461
PMCPMC7222955

What OpenQuestion holds

Textmetadata
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.