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Record W2073170499 · doi:10.1093/brain/awv057

<i>PMPCA</i>mutations cause abnormal mitochondrial protein processing in patients with non-progressive cerebellar ataxia

2015· article· en· W2073170499 on OpenAlexafffund
Rebekah Jobling, Mirna Assoum, Oleksandr Gakh, Susan Blasér, Julian Raiman, Cyril Mignot, Emmanuel Roze, Alexandra Dürr, Alexis Brice, Nicolas Lévy, Chitra Prasad, Tara Paton, Andrew D. Paterson, Nicole M. Roslin, Christian R. Marshall, Jean‐Pierre Desvignes, Nathalie Roeckel-Trévisiol, Stephen W. Scherer, Guy A. Rouleau, André Mégarbané, Grazia Isaya, Valérie Delague, Grace Yoon

Bibliographic record

VenueBrain · 2015
Typearticle
Languageen
FieldNeuroscience
TopicGenetic Neurodegenerative Diseases
Canadian institutionsMcGill UniversityUniversity of TorontoSickKids FoundationMontreal Neurological Institute and HospitalHospital for Sick ChildrenLondon Health Sciences Centre
FundersNational Institute on AgingNational Institutes of HealthAkademie Věd České RepublikyUniversity of TorontoYale University
KeywordsAtaxiaCerebellar ataxiaCerebellumMutationNeuroscienceMedicineGeneticsBiologyGene

Abstract

fetched live from OpenAlex

Non-progressive cerebellar ataxias are a rare group of disorders that comprise approximately 10% of static infantile encephalopathies. We report the identification of mutations in PMPCA in 17 patients from four families affected with cerebellar ataxia, including the large Lebanese family previously described with autosomal recessive cerebellar ataxia and short stature of Norman type and localized to chromosome 9q34 (OMIM #213200). All patients present with non-progressive cerebellar ataxia, and the majority have intellectual disability of variable severity. PMPCA encodes α-MPP, the alpha subunit of mitochondrial processing peptidase, the primary enzyme responsible for the maturation of the vast majority of nuclear-encoded mitochondrial proteins, which is necessary for life at the cellular level. Analysis of lymphoblastoid cells and fibroblasts from patients homozygous for the PMPCA p.Ala377Thr mutation and carriers demonstrate that the mutation impacts both the level of the alpha subunit encoded by PMPCA and the function of mitochondrial processing peptidase. In particular, this mutation impacts the maturation process of frataxin, the protein which is depleted in Friedreich ataxia. This study represents the first time that defects in PMPCA and mitochondrial processing peptidase have been described in association with a disease phenotype in humans. Mitochondrial dysfunction is a common cause of cerebellar disorders. Jobling et al. identify homozygous or compound heterozygous mutations in PMPCA, which encodes the alpha subunit of mitochondrial processing peptidase, in 17 patients from four families with non-progressive cerebellar ataxia. The mutations disrupt maturation of nuclear-encoded mitochondrial proteins, particularly frataxin.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.001
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.214
Threshold uncertainty score0.803

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.022
GPT teacher head0.259
Teacher spread0.237 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations77
Published2015
Admission routes2
Has abstractyes

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