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Blood brain barrier permeability increases with age in individuals with 22q11.2 deletion syndrome. | LitMetric

AI Article Synopsis

  • 22q11.2 deletion syndrome (22q11.2DS) is linked to high rates of psychotic disorders and immune issues, with blood-brain barrier (BBB) permeability being a key factor for schizophrenia.
  • The study assessed BBB permeability biomarkers (s100β and neuron-specific enolase) in adults and children with 22q11.2DS to explore the relationship between psychosis and BBB permeability.
  • Results showed elevated biomarker levels in adults with 22q11.2DS, especially in the non-psychotic group, indicating that increased BBB permeability may develop in early adulthood and could shed light on new pathways to psychosis in this population.

Article Abstract

Unlabelled: 22q11.2 deletion syndrome (22q11.2DS) is characterised by high rates of psychotic disorders and immune abnormalities. Blood-brain barrier (BBB) permeability is known to be a risk factor for schizophrenia and immune aberrations.

Objective: To evaluate the relationship between psychosis and BBB permeability in this population.

Methods: We examined two biomarkers for BBB permeability, s100β and neuron-specific enolase (NSE), in 22q11.2DS individuals with/without psychosis. The first cohort of this Israeli-Belgium study was comprised of 20 22q11.2DS adults (30.58 ± 9.42 years) afflicted with a psychotic disorder, another group of 69 non-psychotic 22q11.2DS adults (23.42 ± 8.36 years), and 58 healthy controls (26.39 ± 7.77 years). A second cohort was comprised of 18 non-psychotic 22q11.2DS Israeli children (5.83 ± 1.55 years) and 14 healthy controls (5.34 ± 1.43 years). NSE and s100β serum levels were detected in all participants.

Results: Both factors were elevated in adults with 22q11.2DS compared to healthy controls, specifically in the non-psychotic sub-group. In contrast, there were no significant differences in their levels between the two groups of the paediatric cohort.

Conclusions: Increased BBB permeability seems to be a trait of 22q11.2DS that evolves sometime in early adulthood. Our findings are in line with previous reports on non-syndromic schizophrenia, and suggest potential novel neural pathways to psychosis in 22q11.2DS.

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Source
http://dx.doi.org/10.1080/15622975.2021.2013090DOI Listing

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