Evidence map›Paper›PMID 37719154›Full record

ArticleFrontiers in neuroscience2023

Nicotine-mediated effects in neuronal and mouse models of synucleinopathy.

Mohamed Bilal Fares, Omar Alijevic, Stephanie Johne, Cassia Overk, Makoto Hashimoto, Athanasios Kondylis, Anthony Adame, Remi Dulize, Dariusz Peric, Catherine Nury and 11 more

Erratum issuedAbstract read
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In one paragraph

Article in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

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

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors.

Mohamed Bilal FaresPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Omar AlijevicPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Stephanie JohnePMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Cassia OverkDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Makoto HashimotoDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Athanasios KondylisPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Anthony AdameDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Remi DulizePMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Dariusz PericPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Catherine NuryPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
James BatteyPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Emmanuel GuedjPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Nicolas SierroPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Damian Mc HughPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Edward RockensteinDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Changyoun KimDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Robert A RissmanDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Julia HoengPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Manuel C PeitschPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Eliezer MasliahDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
Carole MathisPMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.

Funding

USCADRC Diversity Supplement PachicanoP30AG066530 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HELENA Chang CHUI · 2020 to 2026
$27.8M
NIA NIH HHS P30 AG066530
6 · The paper itself

Abstract

Introduction: Alpha-synuclein (α-Syn) aggregation, transmission, and contribution to neurotoxicity represent central mechanisms underlying Parkinson's disease. The plant alkaloid "nicotine" was reported to attenuate α-Syn aggregation in different models, but its precise mode of action remains unclear. Methods: In this study, we investigated the effect of 2-week chronic nicotine treatment on α-Syn aggregation, neuroinflammation, neurodegeneration, and motor deficits in D-line α-Syn transgenic mice. We also established a novel humanized neuronal model of α-Syn aggregation and toxicity based on treatment of dopaminergic neurons derived from human induced pluripotent stem cells (iPSC) with α-Syn preformed fibrils (PFF) and applied this model to investigate the effects of nicotine and other compounds and their modes of action. Results and discussion: Overall, our results showed that nicotine attenuated α-Syn-provoked neuropathology in both models. Moreover, when investigating the role of nicotinic acetylcholine receptor (nAChR) signaling in nicotine's neuroprotective effects in iPSC-derived dopaminergic neurons, we observed that while α4-specific antagonists reduced the nicotine-induced calcium response, α4 agonists (e.g., AZD1446 and anatabine) mediated similar neuroprotective responses against α-Syn PFF-provoked neurodegeneration. Our results show that nicotine attenuates α-Syn-provoked neuropathology

Indexed as

induced pluripotent stem cell (iPSC)neuroprotectionnicotinenicotinic acetylcholine receptors (nAChR)synucleinopathytransgenic mice

Identifiers

PMID37719154
PMCPMC10501483

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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.