Evidence map›Paper›PMID 42570139›Full record

ReviewNeurogenetics2026

PPP1R21-Related neurodevelopmental disorder: Phenotypic delineation, variant spectrum, and pathophysiological mechanisms.

Francesco Fabrizio Comisi, Gabriele Di Pasquale, Andrea Maria Comisi, Giuseppe Donato Mangano, Piero Pavone, Alessandro Ferretti, Vincenzo Salpietro, Pasquale Parisi, Alberto Spalice

Abstract readReview
In one paragraph

Review in Neurogenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Francesco Fabrizio ComisiPediatric Clinic and Rare Diseases, Microcitemico Hospital "A. Cao", University of Cagliari, 09124, Cagliari, Italy.
Gabriele Di PasqualeDepartment of Biotechnological and Applied Clinical Sciences, Academic Unit of Pediatrics, University of L'Aquila, L'Aquila, Italy.
Andrea Maria ComisiDepartment of Clinical and Experimental Medicine, University of Catania, 95131, Catania, Italy. a.comisi@studium.unict.it.ORCID http://orcid.org/0009-0004-5479-4333
Giuseppe Donato ManganoDepartment of Medicine and Surgery, Kore University of Enna, Enna, Italy.
Piero PavoneDepartment of Clinical and Experimental Medicine, University of Catania, 95131, Catania, Italy.
Alessandro FerrettiDepartment of Neuroscience, Mental Health and Sensory Organs (NESMOS), Sant'Andrea University Hospital, Sapienza University of Rome, Rome, Italy.
Vincenzo SalpietroDepartment of Biotechnological and Applied Clinical Sciences, Academic Unit of Pediatrics, University of L'Aquila, L'Aquila, Italy.
Pasquale ParisiDepartment of Neuroscience, Mental Health and Sensory Organs (NESMOS), Sant'Andrea University Hospital, Sapienza University of Rome, Rome, Italy.
Alberto SpaliceDepartment of Maternal, Infantile and Urological Sciences, La Sapienza University of Rome, 00161, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PPP1R21-related neurodevelopmental disorder (PPP1R21-NDD) is an ultra-rare autosomal-recessive encephalopathy caused by dysfunction of the Five-subunit Endosomal Rab5 and RNA/ribosome intermediarY (FERRY) complex. To delineate the clinical, neuroimaging, and molecular spectrum of PPP1R21-NDD and outline diagnostic and research priorities. Targeted searches of PubMed, EMBASE, Scopus, Web of Science, and Google Scholar through January 2026 were performed. Eligible reports included molecularly confirmed biallelic PPP1R21 cases and related functional studies. Two researchers independently extracted individual-level data following narrative review quality criteria. Twenty-five individuals from 21 families harbored 17 distinct variants (15 loss-of-function, 2 missense), all homozygous, reflecting high consanguinity. Profound global developmental delay/intellectual disability was universal; hypotonia near-universal (22/25, 88%). Ambulation was delayed and ataxic when achieved; expressive language was minimal or absent. A recognizable coarse facial gestalt was observed with thick eyebrows, broad nasal bridge, thick lips, and low-set ears. Systemic features included feeding dysfunction and respiratory morbidity requiring gastrostomy or tracheostomy in severe cases. Mortality was 17% (4/24). Neuroimaging showed callosal thinning, white-matter volume loss, ventricular enlargement, and vermian hypoplasia. Patient fibroblasts showed delayed transferrin clearance and elevated proteasome activity, suggesting endosomal dysfunction and proteasome hyperactivation. PPP1R21-NDD is a severe recessive encephalopathy with a convergent phenotype and evidence of endo-lysosomal dysfunction. Diagnosis should be pursued with exome or genome sequencing in patients with characteristic clinical and neuroimaging features, particularly in consanguineous families. Research priorities include natural history studies, standardized magnetic resonance imaging (MRI) protocols, neural disease models, and therapeutic strategies targeting endosomal trafficking.

Indexed as

Neurodevelopmental DisordersAdolescentChildChild, PreschoolFemaleHumansInfantMaleMutationPhenotypeEndosomal dysfunctionFERRY complexHypomyelinationIntellectual disabilityNeurodevelopmental disorderPPP1R21

Identifiers

PMID42570139
PMCPMC13452748

What Socratic 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 Socratic graph.