{"id":4342,"date":"2026-04-27T14:20:23","date_gmt":"2026-04-27T12:20:23","guid":{"rendered":"https:\/\/www.ub.edu\/ibub\/?p=4342"},"modified":"2026-04-30T14:27:58","modified_gmt":"2026-04-30T12:27:58","slug":"a-study-expands-the-genetic-basis-of-an-encephalopathy-associated-with-epilepsy-and-autism","status":"publish","type":"post","link":"https:\/\/www.ub.edu\/ibub\/a-study-expands-the-genetic-basis-of-an-encephalopathy-associated-with-epilepsy-and-autism\/","title":{"rendered":"A study expands the genetic basis of an encephalopathy associated with epilepsy and autism"},"content":{"rendered":"\n

SYNGAP1 encephalopathy is a rare genetic disorder for which there is no treatment, causing epilepsy, intellectual disability, psychomotor delay and, frequently, autism. It is caused by mutations in the SYNGAP1<\/em> gene, which produces a protein essential for brain and cognitive development. Now, a multicentre study describes the wide variability in clinical symptoms among patients and reveals that the severity of the disease does not depend exclusively on the SYNGAP1<\/em> gene, but on other genetic factors that may modulate its clinical expression.<\/strong><\/p>\n\n\n\n

The study, published in the journal Neurobiology of Disease<\/em><\/a>, opens up new avenues for better understanding how variants in the SYNGAP1<\/em> gene influence the severity of the disease, which has highly complex and variable clinical manifestations. Furthermore, the study has identified four novel variants of the SYNGAP1<\/em> gene, which expand our understanding of the genetic basis of the condition. The findings could help anticipate potential clinical trajectories and better guide therapeutic decisions in the management of this genetic condition, affecting one in every 16,000 people.<\/p>\n\n\n\n

The lead authors of the study are the experts Marina Mitjans, Bru Cormand and Ferran Casals, from the Faculty of Biology and the Institute of Biomedicine at the University of Barcelona (IBUB), the Sant Joan de D\u00e9u Research Institute (IRSJD) and the CIBER Area for Mental Health (CIBERSAM) and the Area for Rare Diseases (CIBERER); \u00c0lex Bay\u00e9s, from the Sant Pau Research Institute (IR Sant Pau) and the Universitat Aut\u00f2noma de Barcelona (UAB), and \u00c0ngels Garc\u00eda-Cazorla, from IRSJD.<\/p>\n\n\n\n

The study also highlights the contribution of researchers Selena Aranda (UB\u2019s Faculty of Biology and IBUB), Juliana Ribeiro (UB\u2019s Faculty of Medicine and Health Sciences and IRSJD) and Alba Trist\u00e1n (UB\u2019s Faculty of Biology and IR Sant Pau).<\/p>\n\n\n\n

There is a correlation between gentoype and phenotype in this encephalopathy, but it is complex.<\/p>\n\n\n\n

Clinical symptoms and mutations: What is the link?<\/strong><\/p>\n\n\n\n

To date, various mutations in the SYNGAP1<\/em> gene associated with encephalopathy have been identified, but the catalogue of variants continues to grow as more patients are studied.<\/p>\n\n\n\n

The new study examines the genotype-phenotype correlation in the condition, that is, how alterations in the SYNGAP1<\/em> gene manifest as clinical symptoms. For this purpose, the team analysed a cohort of 44 patients \u2014 all of whom were well characterized clinically \u2014 from 16 hospitals across Spain, all carrying a dominant mutation in the SYNGAP1<\/em> gene.<\/p>\n\n\n\n

\u201cThe first key finding of the study is that there is considerable clinical variability among patients, even when they share mutations in the same gene,\u201d says Professor Bru Cormand, head of the UB\u2019s Neurogenetics Research Group and an ICREA Academia 2021 researcher.<\/p>\n\n\n\n

\u201cSecondly \u2014 he continues \u2014 a link has been discovered between genetic characteristics and symptoms, although it is neither direct nor straightforward.\u201d<\/p>\n\n\n\n

Another significant finding suggests that the severity of the disease does not depend solely on mutations in the SYNGAP1<\/em> gene, \u201cbut also on other genetic factors that may influence its clinical presentation,\u201d notes Marina Mitjans, a researcher with the Ram\u00f3n y Cajal programme at the UB\u2019s Department of Genetics, Microbiology and Statistics.<\/p>\n\n\n\n

The study has also identified four new variants of the SYNGAP1<\/em> gene, \u201cwhich are likely to be pathogenic and had not been described previously; specifically, the variants p.Ala591Pro, p.Val447Leufs*5, p.Thr674Profs*36 and p.Arg143Glnfs*9\u201d, notes Professor Ferran Casals, from the same department at the UB. He also adds that \u201cin cases where we could analyse the parents\u2019 DNA, we could confirm that these variants have arisen de novo<\/em>; in other words, they are new mutations that have not been inherited from the parents.\u201d<\/p>\n\n\n\n

Can mutations in the gene predict disease severity?<\/strong><\/p>\n\n\n\n

One of the key questions raised by the study was whether the type of genetic variant can predict the severity of the disease.<\/p>\n\n\n\n

Although this association is only partial, some significant patterns have been identified. \u201cFor example, we know that the location of the variant within the gene is an important factor. More specifically, variants located in the PH domain of the gene are associated with a milder phenotype, with less impairment of language, fewer cases of epilepsy and lower overall severity,\u201d says Bru Cormand.<\/p>\n\n\n\n

\u201cFor this reason, we suggest that a correlation between genotype and phenotype does exist in this encephalopathy, but it is complex. It is not just a question of which variant is present, but also where it is located and the patient\u2019s overall genetic context,\u201d adds Cormand.<\/p>\n\n\n\n

Another significant finding is that patients with the same SYNGAP1<\/em> mutation can show markedly different clinical manifestations. \u201cThis finding suggests that the severity of the disease does not depend solely on the specific SYNGAP1<\/em> mutation, but probably also on other genetic modifier factors,\u201d say Mitjans and Casals.<\/p>\n\n\n\n

It is also worth noting that two-thirds of patients affected by this encephalopathy have also been diagnosed with autism. \u201cFor this reason, we are talking about one of the monogenic forms of autism spectrum disorder, which is usually of polygenic origin,\u201d the team points out.<\/p>\n\n\n\n

To obtain these results, the team analysed whole-genome sequencing data covering all the exons in many of the patients \u2014 that is, around 200,000 segments comprising some 40 million nucleotides.<\/p>\n\n\n\n

\u201cThese sequences have enabled the detection, in addition to the alteration in the SYNGAP1<\/em> gene, of other mutations in genes whose products interact with the SYNGAP1 protein, such as SHANK1, SHANK3<\/em> and NLGN2<\/em>, among others. In general, patients with rare mutations in these genes appear to have a more severe form of the disease\u201c, the researchers conclude.<\/p>\n\n\n\n

Reference article:<\/strong><\/p>\n\n\n\n

Aranda, Selena et al<\/em>.<\/em> \u201cGenotype-phenotype correlations and putative modifier genes in SYNGAP1<\/em> Encephalopathy\u201d<\/a>. Neurobiology of Disease<\/em>, March 2026. DOI: 10.1016\/j.nbd.2026.107357.<\/p>\n\n\n\n

<\/p>\n\n\n\n

UB News [+]<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"

SYNGAP1 encephalopathy is a rare genetic disorder for which there is no treatment, causing epilepsy, intellectual disability, psychomotor delay and, frequently, autism. It is caused by mutations in the SYNGAP1 gene, which produces a protein essential for brain and cognitive development. Now, a multicentre study describes the wide variability in clinical symptoms among patients and … Read more<\/a><\/p>\n","protected":false},"author":4,"featured_media":4343,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[3],"tags":[227,224,229],"class_list":["post-4342","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-news","tag-clinical","tag-encephalopathy","tag-therapeutic"],"acf":[],"yoast_head":"\nA study expands the genetic basis of an encephalopathy associated with epilepsy and autism - IBUB - Institut de Biomedicina de la Universitat de Barcelona<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.ub.edu\/ibub\/a-study-expands-the-genetic-basis-of-an-encephalopathy-associated-with-epilepsy-and-autism\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"A study expands the genetic basis of an encephalopathy associated with epilepsy and autism - IBUB - Institut de Biomedicina de la Universitat de Barcelona\" \/>\n<meta property=\"og:description\" content=\"SYNGAP1 encephalopathy is a rare genetic disorder for which there is no treatment, causing epilepsy, intellectual disability, psychomotor delay and, frequently, autism. 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