Evidence map›Paper›PMID 29440425›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Bryostatin-1 alleviates experimental multiple sclerosis.

Michael D Kornberg, Matthew D Smith, Hasti Atashi Shirazi, Peter A Calabresi, Solomon H Snyder, Paul M Kim

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Therapeutic Potential of Ziyuglycosides fromDrug design, development and therapy · 2026
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  20. Prodrugs of PKC modulators show enhanced HIV latency reversal and an expanded therapeutic window.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

6 authors at 1 institution in 1 country.

Michael D KornbergDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287.ORCID 0000-0003-2588-7325
Matthew D SmithDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
Hasti Atashi ShiraziDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
Peter A CalabresiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
Solomon H SnyderDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287; ssnyder@jhmi.edu pmkim@jhmi.edu.
Paul M KimDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287; ssnyder@jhmi.edu pmkim@jhmi.edu.
Johns Hopkins University · US

Funding

NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR01MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2019
$10.8M
The Role of KV1.3 in Effector T cellsR01NS041435 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI CALABRESI, PETER A · 2000 to 2025
$5.8M
Mechanisms by which effector T cells modulate endogenous remyelinationR37NS041435 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CALABRESI, PETER A · 2013 to 2019
$3.0M
NIMH NIH HHS R01 MH018501NINDS NIH HHS R01 NS041435NINDS NIH HHS R37 NS041435
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory disorder targeting the central nervous system (CNS). The relapsing-remitting phase of MS is largely driven by peripheral activation of autoreactive T-helper (Th) 1 and Th17 lymphocytes. In contrast, compartmentalized inflammation within the CNS, including diffuse activation of innate myeloid cells, characterizes the progressive phase of MS, the most debilitating phase that currently lacks satisfactory treatments. Recently, bryostatin-1 (bryo-1), a naturally occurring, CNS-permeable compound with a favorable safety profile in humans, has been shown to act on antigen-presenting cells to promote differentiation of lymphocytes into Th2 cells, an action that might benefit Th1-driven inflammatory conditions such as MS. In the present study, we show that bryo-1 provides marked benefit in mice with experimental autoimmune encephalomyelitis (EAE), an experimental MS animal model. Preventive treatment with bryo-1 abolishes the onset of neurologic deficits in EAE. More strikingly, bryo-1 reverses neurologic deficits after EAE onset, even when treatment is initiated at a late stage of disease when peak adaptive immunity has subsided. Treatment with bryo-1 in vitro promotes an anti-inflammatory phenotype in antigen-presenting dendritic cells, macrophages, and to a lesser extent, lymphocytes. These findings suggest the potential for bryo-1 as a therapeutic agent in MS, particularly given its established clinical safety. Furthermore, the benefit of bryo-1, even in late treatment of EAE, combined with its targeting of innate myeloid cells suggests therapeutic potential in progressive forms of MS.

Indexed as

AnimalsAntibodiesBryostatinsCD4-Positive T-LymphocytesCentral Nervous SystemEncephalomyelitis, Autoimmune, ExperimentalFemaleMiceMice, Inbred C57BLMultiple SclerosisAntibodiesbryostatin 1BryostatinsbryostatinEAEmultiple sclerosisneuroimmunology

Identifiers

PMID29440425
PMCPMC5834718
OpenAlexW2794246339

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.