Evidence map›Paper›PMID 30022305›Full record

ArticleJournal of inherited metabolic disease2018

Presynaptic disorders: a clinical and pathophysiological approach focused on the synaptic vesicle.

Elisenda Cortès-Saladelafont, Noa Lipstein, Àngels García-Cazorla

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Article in Journal of inherited metabolic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 16 citations in OpenAlex.

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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

3 authors at 2 institutions in 2 countries.

Elisenda Cortès-SaladelafontDepartment of Neurology, Neurometabolic Unit and Synaptic Metabolism Laboratory, Institut Pediàtric de Recerca and CIBERER, ISCIII, Hospital Sant Joan de Déu, Passeig Sant Joan de Déu, 2, 08950, Esplugues, Barcelona, Spain.
Noa LipsteinDepartment of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Àngels García-CazorlaDepartment of Neurology, Neurometabolic Unit and Synaptic Metabolism Laboratory, Institut Pediàtric de Recerca and CIBERER, ISCIII, Hospital Sant Joan de Déu, Passeig Sant Joan de Déu, 2, 08950, Esplugues, Barcelona, Spain. agarcia@hsjdbcn.org.
Hospital Sant Joan de Déu Barcelona · ESMax Planck Institute of Experimental Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this report is to present a tentative clinical and pathophysiological approach to diseases affecting the neuronal presynaptic terminal, with a major focus on synaptic vesicles (SVs). Diseases are classified depending on which step of the neurobiology of the SV is predominantly affected: (1) biogenesis of vesicle precursors in the neuronal soma; (2) transport along the axon; (3) vesicle cycle at the presynaptic terminal (exocytosis-endocytosis cycle, with the main purpose of neurotransmitter release). Given that SVs have been defined as individual organelles, we highlight the link between the biological processes disturbed by genetic mutations and the clinical presentation of these disorders. The great majority of diseases may present as epileptic encephalopathies, intellectual disability (syndromic or nonsyndromic) with/without autism spectrum disorder (and other neuropsychiatric symptoms), and movement disorders. These symptoms may overlap and present in patients as a combination of clinical signs that results in the spectrum of the synaptopathies. A small number of diseases may also exhibit neuromuscular signs. In general, SV disorders tend to be severe, early encephalopathies that interfere with neurodevelopment. As a consequence, developmental delay and intellectual disability are constant in almost all the defects described. Considering that some of these diseases might mimic other neurometabolic conditions (and in particular treatable disorders), an initial extensive metabolic workup should always be considered. Further knowledge into pathophysiological mechanisms and biomarkers, as well as descriptions of new presynaptic disorders, will probably take place in the near future.

Indexed as

Synaptic TransmissionAutism Spectrum DisorderBrain Diseases, Metabolic, InbornEndocytosisEpilepsyExocytosisHumansIntellectual DisabilityMovement DisordersNeurodegenerative DiseasesNeuromuscular DiseasesPresynaptic TerminalsSynaptic Vesicles

Identifiers

PMID30022305
OpenAlexW2884818053

What OpenQuestion holds

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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.