Besides emotional symptoms, cognitive symptoms have been characterized as main symptoms across a range of psychiatric disorders, and they have been increasingly recognized as an important risk factor for the pathogenesis, prognosis and drug response of these diseases.
The elucidation of the pathophysiological mechanisms underlying cognitive dysfunction is therefore very important for an objective diagnosis as well as an integrative treatment of psychiatric disorders. Latest developments of multidisciplinary knowledge have demonstrated that cognitive function is regulated by a bi-directional interaction of our nervous and immune systems.
The main pathophysiological basis of cognitive dysfunction is believed to be represented by an impairment of the neural and synaptic plasticity, which is in turn regulated by neuron-glia integrity.
Microglia, which is, in fact, one of the main brain cells actively involved in immune defense in the central nervous system, interacts with neurons via the release of multiple immune and neurotrophic factors, and its disturbance is closely connected to the emotional and cognitive dysfunction typical of some psychiatric disorders.
Consistently, several immune abnormalities have been observed in patients as well as animal models of psychiatric disorders, including depression, schizophrenia, post-traumatic stress disorder (PTSD), etc. However, the exact role of various immune alterations in cognitive symptomatology of diseases remains to be clarified.
It is generally accepted that both genetic and environmental factors affect the onset and development of psychiatric disorders. Exposure to adverse life experiences, especially during early child development, strongly increases individuals’ risk of developing various psychiatric disorders later in life.
After birth, the development of the brain immune system follows a stepwise program, actively engaging in the formation, maintenance and remodeling of neuronal circuits and cognitive function mediated. It is now becoming clear that long-term immune function can be altered by experiences during early life critical windows. We welcome contributions investigating how early life stress causes long-term effects on brain structure and function through disturbing the development of brain immunity, and its relationship with cognitive alterations.
The scope of this Research Topic is to deepen our understanding of the brain-immune interaction mechanisms underlying cognitive dysfunction in psychiatric disorders, and therefore developing better integrative therapeutic approaches.
Contributions investigating all approaches, from behavioral to molecular and cellular analyses, in human patients as well as animal models of psychiatric disorders will be welcome. Topics will include but won’t be limited to:
1) The role of immune molecules and relevant signaling pathways in the context of cognitive dysfunction, such as pro- and anti-inflammatory cytokines, pro- and anti-inflammatory M1 and M2 signaling pathway, etc.
2) The role of neuron-glia interactions in cognitive dysfunction and synaptic plasticity mechanisms. All the main types of glia, astroglia, microglia, and oligodendrocyte, are included.
3) The role of stress exposure, especially during sensitive time windows at early life stages of life, in the context of cognitive dysfunction and underlying neuro-immunological mechanisms.
Besides emotional symptoms, cognitive symptoms have been characterized as main symptoms across a range of psychiatric disorders, and they have been increasingly recognized as an important risk factor for the pathogenesis, prognosis and drug response of these diseases.
The elucidation of the pathophysiological mechanisms underlying cognitive dysfunction is therefore very important for an objective diagnosis as well as an integrative treatment of psychiatric disorders. Latest developments of multidisciplinary knowledge have demonstrated that cognitive function is regulated by a bi-directional interaction of our nervous and immune systems.
The main pathophysiological basis of cognitive dysfunction is believed to be represented by an impairment of the neural and synaptic plasticity, which is in turn regulated by neuron-glia integrity.
Microglia, which is, in fact, one of the main brain cells actively involved in immune defense in the central nervous system, interacts with neurons via the release of multiple immune and neurotrophic factors, and its disturbance is closely connected to the emotional and cognitive dysfunction typical of some psychiatric disorders.
Consistently, several immune abnormalities have been observed in patients as well as animal models of psychiatric disorders, including depression, schizophrenia, post-traumatic stress disorder (PTSD), etc. However, the exact role of various immune alterations in cognitive symptomatology of diseases remains to be clarified.
It is generally accepted that both genetic and environmental factors affect the onset and development of psychiatric disorders. Exposure to adverse life experiences, especially during early child development, strongly increases individuals’ risk of developing various psychiatric disorders later in life.
After birth, the development of the brain immune system follows a stepwise program, actively engaging in the formation, maintenance and remodeling of neuronal circuits and cognitive function mediated. It is now becoming clear that long-term immune function can be altered by experiences during early life critical windows. We welcome contributions investigating how early life stress causes long-term effects on brain structure and function through disturbing the development of brain immunity, and its relationship with cognitive alterations.
The scope of this Research Topic is to deepen our understanding of the brain-immune interaction mechanisms underlying cognitive dysfunction in psychiatric disorders, and therefore developing better integrative therapeutic approaches.
Contributions investigating all approaches, from behavioral to molecular and cellular analyses, in human patients as well as animal models of psychiatric disorders will be welcome. Topics will include but won’t be limited to:
1) The role of immune molecules and relevant signaling pathways in the context of cognitive dysfunction, such as pro- and anti-inflammatory cytokines, pro- and anti-inflammatory M1 and M2 signaling pathway, etc.
2) The role of neuron-glia interactions in cognitive dysfunction and synaptic plasticity mechanisms. All the main types of glia, astroglia, microglia, and oligodendrocyte, are included.
3) The role of stress exposure, especially during sensitive time windows at early life stages of life, in the context of cognitive dysfunction and underlying neuro-immunological mechanisms.