Evidence map›Paper›PMID 26721507›Full record

ReviewNeurochemical research2016

Neuroprotection as a Potential Therapeutic Perspective in Neurodegenerative Diseases: Focus on Antiepileptic Drugs.

D Caccamo, L R Pisani, P Mazzocchetti, R Ientile, P Calabresi, F Pisani, C Costa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 17 citations in OpenAlex.

  1. Selective Reduction of CaMolecular neurobiology · 2024
    Article
  2. Review
  3. Review
  4. 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

7 authors at 4 institutions in 1 country.

D CaccamoDepartment of Biomedical Sciences, Dental Sciences and Morpho-Functional Imaging, University of Messina, AOU Policlinico "G. Martino", Messina, Italy.
L R PisaniIRCCS Centro Neurolesi "Bonino-Pulejo", Messina, Italy.
P MazzocchettiDepartment of Medicine, Neurological Clinic, University of Perugia, S. Maria della Misericordia Hospital, S. Andrea delle Fratte, 06156, Perugia, Italy.
R IentileDepartment of Biomedical Sciences, Dental Sciences and Morpho-Functional Imaging, University of Messina, AOU Policlinico "G. Martino", Messina, Italy.
P CalabresiDepartment of Medicine, Neurological Clinic, University of Perugia, S. Maria della Misericordia Hospital, S. Andrea delle Fratte, 06156, Perugia, Italy.
F PisaniDepartment of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
C CostaDepartment of Medicine, Neurological Clinic, University of Perugia, S. Maria della Misericordia Hospital, S. Andrea delle Fratte, 06156, Perugia, Italy. cinzia.costa@unipg.it.
University of Messina · ITUniversity of Perugia · ITCentro Neurolesi Bonino Pulejo · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroprotection is conceived as one of the potential tool to prevent or slow neuronal death and hence a therapeutic hope to treat neurodegenerative diseases, like Parkinson's and Alzheimer's diseases. Increase of oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation have been identified as main causes of neuronal death and adopted as targets to test experimentally the putative neuroprotective effects of various classes of drugs. Among these agents, antiepileptic drugs (AEDs), both the old and the newer generations, have shown to exert protective effects in different experimental models. Their mechanism of action is mediated mainly by modulating the activity of sodium, calcium and potassium channels as well as the glutamatergic and GABAergic (gamma-aminobutyric acid) synapses. Neurological pathologies in which a neuroprotective action of AEDs has been demonstrated in specific experimental models include: cerebral ischemia, Parkinson's disease, and Alzheimer's disease. Although the whole of experimental data indicating that neuroprotection can be achieved is remarkable and encouraging, no firm data have been produced in humans so far and, at the present time, neuroprotection still remains a challenge for the future.

Indexed as

AnimalsAnticonvulsantsDisease ProgressionHumansNeurodegenerative DiseasesAnticonvulsantsAEDsExperimental animal modelsNeuroprotection

Identifiers

PMID26721507
OpenAlexW2199153959

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.