Activity

Filter

Cancel
Date Panel Item Activity
5 actions
Early onset or syndromic epilepsy v8.176 OLA1 Ida Ertmanska Phenotypes for gene: OLA1 were changed from Ehlers-Danlos syndrome, hypermobility type, MONDO:0007523; neurodevelopmental disorder,MONDO:0700092; microcephaly, MONDO:0001149 to Ehlers-Danlos syndrome, hypermobility type, MONDO:0007523; neurodevelopmental disorder, MONDO:0700092; microcephaly, MONDO:0001149
Early onset or syndromic epilepsy v8.175 OLA1 Ida Ertmanska Classified gene: OLA1 as Amber List (moderate evidence)
Early onset or syndromic epilepsy v8.175 OLA1 Ida Ertmanska Added comment: Comment on list classification: There are 6 unrelated individuals reported with biallelic OLA1 variants and early onset seizures. Hence, this gene should be promoted to Green on Early onset or syndromic epilepsy.
Early onset or syndromic epilepsy v8.175 OLA1 Ida Ertmanska Gene: ola1 has been classified as Amber List (Moderate Evidence).
Early onset or syndromic epilepsy v8.174 OLA1 Ida Ertmanska gene: OLA1 was added
gene: OLA1 was added to Early onset or syndromic epilepsy. Sources: Literature
Q2_26_promote_green tags were added to gene: OLA1.
Mode of inheritance for gene: OLA1 was set to BIALLELIC, autosomal or pseudoautosomal
Publications for gene: OLA1 were set to 41887223
Phenotypes for gene: OLA1 were set to Ehlers-Danlos syndrome, hypermobility type, MONDO:0007523; neurodevelopmental disorder,MONDO:0700092; microcephaly, MONDO:0001149
Review for gene: OLA1 was set to GREEN
Added comment: PMID: 41887223 Alabdi et al., 2026
14 individuals from 9 families reported with homozygous loss of function variants in OLA1 with a phenotype characterised by a neurodevelopmental condition with connective tissue disorder.
All 14 individuals presented with intellectual disability / psychomotor delay. Seizures were reported in 6 unrelated individuals. Joint hypermobility was noted in 13/13 patients, 5 of them had skin laxity. 6 individuals had scoliosis or kyphoscoliosis. Several patients were diagnosed with Ehlers-Danos syndrome.
Microcephaly was noted in 4 individuals from unrelated families (severity details: -4.49 SD, -3SD, -4.6SD, and "HC 45cm at 9 years")

Functional evidence: C. elegans model with knock-in protein-truncating variants showed behavioural abnormalities (reduced bending, no response to touch), and reduced axon numbers in GABAergic neurons.
Variant in family 1 (p.Arg143Ter) was shown to cause complete loss of OLA1 protein on Western blot; RT-PCR was supportive of NMD taking place. Splice variant seen in Family 8 (c.728+5G>A) was demonstrated to cause exon 7 skipping.
Sources: Literature