Investigation of Prefrontal Cortex Pathology in Df(h22q11)/+ and Df(h15q13)/+ Genetic Mouse Models of Schizophrenia

2021.01.14 | Graduate School of Health

On Thursday 4 February at 14:00, Abdel-Rahman Al-Absi defends his PhD dissertation entitled "Investigation of Prefrontal Cortex Pathology in Df(h22q11)/+ and Df(h15q13)/+ Genetic Mouse Models of Schizophrenia".

Schizophrenia is a severe and debilitating disorder with tremendous social and economic burden. The majority of the currently applied treatments against schizophrenia are only partially efficacious. During the past years, copy number variations (CNVs) have been identified in the human genome that associate with multiple brain disorders, including schizophrenia. Among these CNVs, both the 22q11.2 and 15q13.3 deletions are reported to significantly increase the risk of schizophrenia. The brains prefrontal cortex (PFC) is a key structure known to regulate multiple functions that are impaired in the 22q11.2 and 15q13.3 deletion syndromes. Several mouse models have been generated that mimic the human 22q11.2 and 15q13.3 hemizygous deletions. This includes the Df(h22q11)/+ and Df(h15q13)/+ mouse models. Both models display multiple functional and behavioral abnormalities with relevance to schizophrenia. Findings from both models uncovered alterations affecting different cellular components of PFC. Collectively, PFC in the Df(h22q11)/+ and Df(h15q13)/+ models reveal changes at the molecular, functional, and structural levels implicating both neuronal and non-neuronal circuits. Results emerged from the two models identify molecular substrates that could potentially explain part of the schizophrenia-related phenotype observed in the 22q11.2 and 15q13.3 deletion syndromes.

The summary is written by the PhD student.    

The defence is public and takes place online via Zoom. Please read the attached press release for more information.

Contact:

PhD student Abdel-Rahman Al-Absi

Mail: abd.alabsi@clin.au.dk

Phone: (+45) 71515087

Read full press release