Microglial Gene Expression Alterations in the Brains of Patients with Psychiatric Disorders

Abstract

Abstract.As recent studies have shown that microglia play a key role in inflammation and immunological challenges as well as have broader roles in synaptic modulation in the brain, studies on psychiatric disorders have increasingly focused on microglia. Microglial abnormalities have consistently been observed in psychiatric postmortem brain studies, including altered microglial activation and changes in the protein and mRNA expression levels of microglial marker molecules, such as major histocompatibility complex, class II, DR (HLA-DR), complement receptor type 3 (CD11b), ionized calcium binding adaptor molecule 1 (IBA-1), macrosialin (CD68) and glucose transporter type 5 (GLUT5). Microglial abnormalities have also been observed in positron emission tomography (PET) studies. Recent advances in omics-based microglial gene expression profiling of psychiatric brains may elucidate microglial involvement in the pathogeneses of psychiatric disorders. In the present paper, we review the current status of research on expression profiling of microglia-relevant molecules in psychiatric postmortem and imaging studies and we discuss future research directions.

Deficient Autophagy in Microglia Aggravates Repeated Social Defeat Stress-Induced Social Avoidance

“…The microglial activation function in pruning and removing dead cells and releasing humoral factors for immune responses may be involved in the pathogenesis of MDD [ 15 , 54 , 55 ]. Recently, various studies have suggested the essential role of autophagy in microglia in the pathophysiology in the CNS.…”

The influence of tissue pH and RNA integrity number on gene expression of human postmortem brain

“…Now, investigating the pathology of the human postmortem brain at the molecular level is critical for elucidating the pathophysiology of schizophrenia. For example, abnormal expression level of transcripts related to various biological components including γ-aminobutyric acid (GABA) signaling (3,4), glutamatergic signaling (5), inflammatory system (6), astrocyte (7), oligodendrocyte (8), microglia (9) have been repeatedly reported and it is certain that these system are profoundly included in pathophysiology of schizophrenia. Moreover, effects of schizophrenia-associated single nucleotide polymorphisms (SNPs) on gene expression in the brain have been investigated and the increase of SNPs has been associated with aberrant gene expression and the abnormal brain structure of patients with schizophrenia (10)(11)(12).…”