Behrang Mahjani

Behrang Mahjani

Forskningsspecialist

Vi studerar utvecklingsursprung och förlopp för neuropsykiatriska tillstånd, inklusive psykiatrisk-somatisk samsjuklighet (LUTS), och hur genetiska profiler påverkar långsiktiga behandlingsutfall. &#1

E-postadress: behrang.mahjani@ki.se
Besöksadress: D4:53, Eugeniavägen 3, 17164 Stockholm
Postadress: K1 Molekylär medicin och kirurgi, K1 MMK Urologi, 171 76 Stockholm
Del av:

Om mig

  • Vår forskargrupp undersöker utvecklingsmässiga ursprung och förlopp för neuropsykiatriska tillstånd, med särskilt fokus på autismspektrumtillstånd och ADHD. Dessa neuropsykiatriska funktionsnedsättningar uppträder tidigt i barndomen till följd av komplexa interaktioner mellan genetiska och miljömässiga faktorer. Vi utforskar psykiatrisk-somatisk samsjuklighet, särskilt den oväntade överlappningen mellan ADHD och nedre urinvägssymtom (LUTS), vilket avslöjar gemensamma neuroendokrina mekanismer som involverar HPA-axeln och det autonoma nervsystemet. Dessutom undersöker vi farmakogenetiska interaktioner vid ADHD, där vi granskar hur genetiska profiler påverkar både behandlingsutfall av centralstimulantia och risken för att utveckla psykotiska tillstånd och bipolär sjukdom hos behandlade ungdomar.


    Vi studerar även svåra psykiatriska tillstånd efter förlossning, särskilt postpartumpsykos, vilket representerar ett kritiskt fönster för att förstå psykiatrisk sårbarhet. Genom analyser av sällsynta varianter och storskaliga genomiska kohorter karakteriserar vi den genetiska arkitekturen för dessa tillstånd och identifierar graviditetsrelaterade utlösande faktorer.

Artiklar

Alla övriga publikationer

Forskningsbidrag

  • The Role of Stimulant Medication for Psychotic and Bipolar Disorders in Youth with ADHD
    Vetenskapsrådet
    1 January 2026 - 31 December 2029
  • Mechanism of Association Between Childhood Psychiatric Disorder and Lower Urinary Tract Symptoms
    Vetenskapsrådet
    1 January 2026 - 31 December 2028
  • Swedish Research Council
    1 January 2026 - 31 December 2028
    This project explores the bidirectional relationship between psychiatric disorders (ADHD, OCD, anxiety) and urinary problems in children. We aim to: (1) identify genetic factors in neuroendocrine pathways contributing to this co-occurrence
    (2) determine how these genetic factors influence gene expression in relevant tissues
    and (3) track how these conditions develop over time and are affected by environmental factors.Spanning five years, this project brings together experts in urology, psychiatry, and genetics from Karolinska Institutet and Mount Sinai. We will analyze data from Swedish registers, international cohorts (All of Us, ABCD Study), and Swedish Twin Registry. The first two years will focus on genetic analysis, the third year on gene expression, and the final two years on developmental trajectories and data integration. The project employs pathway-specific genetic risk scores, sex-stratified analyses, and longitudinal modeling.This research reframes urinary symptoms as potential markers of broader neuroendocrine dysfunction affecting both body and brain. By understanding how stress-response systems connect these conditions, we can identify children at highest risk and determine optimal timing for intervention. This approach targeting shared biological mechanisms will improve outcomes for these vulnerable children.
  • Swedish Research Council
    1 January 2026 - 31 December 2029
    This five-year project investigates how stimulant treatment influences the risk of psychotic and bipolar disorders in youth with ADHD. While stimulants provide significant therapeutic benefits, they may precipitate severe psychiatric complications in vulnerable individuals. To identify risk and protective factors, we will examine: (1) stimulant type, dose, and duration effects
    (2) shared genetic and environmental factors
    (3) individual vulnerabilities and stressors
    and (4) ADHD symptom-specific contributions.We will analyze two complementary datasets: Swedish national registers (1,269,516 individuals, 86,705 with ADHD) and detailed clinical data from Uppsala´s Child and Adolescent Psychiatric unit (6,000 individuals). Using advanced statistical methods, including time-to-event analyses, family-based quasi-experimental designs, and statistical genetic models, we will distinguish medication effects from familial influences.Given the 119% increase in ADHD diagnoses in Sweden over the past decade, this research addresses an urgent public health concern. Findings will improve risk assessment, inform safer prescribing practices, and guide personalized ADHD treatment to prevent severe psychiatric outcomes, including suicide, in high-risk youth.
  • National Institute of Mental Health
    1 July 2025 - 30 April 2030
    Project Summary Considerable progress has been made in identifying highly penetrant genes for autism spectrum disorder (ASD), particularly those involving deleterious de novo mutations that are evolutionarily constrained and crucial for developmental processes. These mutations typically result in syndromic forms of ASD with severe symptoms, but they are rare and do not account for the majority of ASD cases. In contrast, identifying genes with a moderate effect size (MES), which may explain the more heritable, mild, and broader ASD spectrum, has been limited. This project aims to identify and characterize MES risk genes by integrating both rare and common genetic variation. Our central hypothesis is that MES genes significantly contribute to ASD liability and manifestation, particularly among individuals with a high genetic load of common variation. The central hypothesis will be tested by pursuing four specific aims: (1) Identify and characterize MES risk genes using rare variation stratified by common variation
    (2) Identify MES risk genes on chromosome X using rare variation stratified by common variation
    (3) Identify MES risk genes contributing to ASD co-occurring conditions
    and (4) Cluster MES risk genes to identify biological pathways relevant to ASD heterogeneity. This research is significant because it sheds light on the role of MES risk genes in ASD liability and presentation, enhancing diagnostic accuracy and supporting clinical applications such as genetic counseling and individualized treatment options. The most innovative parts of our proposal include (1) a novel gene discovery approach targeting MES risk genes typically overlooked due to their subtler effects, (2) the integration of both common and rare genetic variations to comprehensively understand their interplay in ASD, (3) investigating sex- and genetic ancestry-specific ASD risk factors, particularly on chromosome X, and (4) identifying genetic factors that correspond to the heterogeneity within ASD. Importantly, although methodologically innovative, we use large, established collections of individuals diagnosed with ASD, their family members, and population controls, re-purposing these datasets to produce novel and clinically useful findings.
  • National Institute of Mental Health
    15 January 2023 - 31 December 2024
  • Swedish Research Council
    1 January 2022 - 31 December 2024

Anställningar

  • Forskningsspecialist, Molekylär medicin och kirurgi, Karolinska Institutet, 2022-
  • Forskningsspecialist, Medicinsk epidemiologi och biostatistik, Karolinska Institutet, 2023-2026

Nyheter från KI

Kalenderhändelser från KI