Evidence map›Paper›PMID 24305808›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Synaptic plasticity and PDGF signaling defects underlie clinical progression in multiple sclerosis.

Francesco Mori, Silvia Rossi, Sonia Piccinin, Caterina Motta, Dalila Mango, Hajime Kusayanagi, Alessandra Bergami, Valeria Studer, Carolina G Nicoletti, Fabio Buttari and 6 more

3 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this 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
5.1field-weighted citation impact, top 4% 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.

NCT03228524 early_phase1unknown statusnot on this mapstarted 2017, after this paper: background citation

Promotion of Synaptic Plasticity With D-Aspartate to Favour Recovery Form Cerebral Damage

TypeinterventionalSponsorNeuromed IRCCSRan2017 to 2022Enrolled100ConditionsBrain InjuriesArmsD-Aspartate, Therapeutic exercise, Placebo Oral Tablet
NCT05811013 narecruitingnot on this mapstarted 2023, after this paper: background citation

Effects of Transcranial Static Magnetic Field Stimulation (tSMS) in Progressive Multiple Sclerosis

TypeinterventionalSponsorNeuromed IRCCSRan2023 to 2026Enrolled40ConditionsProgressive Multiple SclerosisArmsTranscranial static magnetic field stimulation (tSMS), Sham Transcranial static magnetic field stimulation (tSMS)
NCT06900959 nanot yet recruitingnot on this mapstarted 2025, after this paper: background citation

Transcranial Static Field Stimulation (tSMS) and Transcranial Direct Current Stimulation (tDCS) for the Treatment of Neurological Symptoms

TypeinterventionalSponsorNeuromed IRCCSRan2025 to 2026Enrolled40ConditionsNeurological Diseases or ConditionsArmstranscranial static field stimulation (tSMS) and transcranial (tDCS)
3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Cladribine tablets in the new multiple sclerosis era.Therapeutic advances in neurological disorders · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. The X factor in neurodegeneration.The Journal of experimental medicine · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

16 authors at 4 institutions in 1 country.

Francesco MoriIstituto Di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia, 00143 Rome, Italy, Clinica Neurologica, Dipartimento di Medicina dei Sistemi, Università Tor Vergata, 00133 Rome, Italy, Dipartimento di Fisiologia e Farmacologia, Università di Roma La Sapienza, 00185, Rome, Italy, Laboratorio di Farmacologia della Plasticità Sinaptica, European Brain Research Institute, 00143 Rome, Italy, and Neuroimmunology Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, 20132 Milan, Italy.
Silvia Rossi
Sonia Piccinin
Caterina Motta
Dalila Mango
Hajime Kusayanagi
Alessandra Bergami
Valeria Studer
Carolina G Nicoletti
Fabio Buttari
Francesca Barbieri
Nicola B Mercuri
Gianvito Martino
Roberto Furlan
Robert Nisticò
Diego Centonze
University of Rome Tor Vergata · ITFondazione Santa Lucia · ITVita-Salute San Raffaele University · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroplasticity is essential to prevent clinical worsening despite continuing neuronal loss in several brain diseases, including multiple sclerosis (MS). The precise nature of the adaptation mechanisms taking place in MS brains, ensuring protection from disability appearance and accumulation, is however unknown. Here, we explored the hypothesis that long-term synaptic potentiation (LTP), potentially able to minimize the effects of neuronal loss by providing extra excitation of denervated neurons, is the most relevant form of adaptive plasticity in stable MS patients, and it is disrupted in progressing MS patients. We found that LTP, explored by means of transcranial magnetic theta burst stimulation over the primary motor cortex, was still possible, and even favored, in stable relapsing-remitting (RR-MS) patients, whereas it was absent in individuals with primary progressive MS (PP-MS). We also provided evidence that platelet-derived growth factor (PDGF) plays a substantial role in favoring both LTP and brain reserve in MS patients, as this molecule: (1) was reduced in the CSF of PP-MS patients, (2) enhanced LTP emergence in hippocampal mouse brain slices, (3) was associated with more pronounced LTP in RR-MS patients, and (4) was associated with the clinical compensation of new brain lesion formation in RR-MS. Our results show that brain plasticity reserve, in the form of LTP, is crucial to contrast clinical deterioration in MS. Enhancing PDGF signaling might represent a valuable treatment option to maintain brain reserve and to attenuate the clinical consequences of neuronal damage in the progressive phases of MS and in other neurodegenerative disorders.

Indexed as

AdultAnimalsBrainCerebral CortexDisease ProgressionElectric StimulationElectrophysiological PhenomenaEvoked PotentialsFemaleHumansLong-Term PotentiationMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLMultiple SclerosisPlatelet-Derived Growth Factor

Identifiers

PMID24305808
PMCPMC6618776
OpenAlexW2123219661

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.