Neuroinflammation is greatly involved in the onset and pathology of neurological diseases such as neurodegenerative diseases, psychiatric disorders, cerebral ischemia, and dementia. Neuroinflammation is attributed to factors such as neuronal death after cerebral ischemia, viral infection, and immune response by autoantibodies. On the other hand, neuroinflammation is also affected by systematic inflammatory disease. For example, patients with ulcerative colitis and pneumonia have a high probability of developing depression. When depressive symptoms develop, it becomes difficult to proceed with treatment as planned, then delayed treatment leads to a vicious cycle of worsening the pathology of inflamed organs and becoming more severe depressive symptoms. In addition, it has been reported that children born after maternal-fetal transmission are more likely to develop autism, schizophrenia, and addiction, and that when patients with Parkinson's disease or amyotrophic lateral sclerosis suffer from systemic inflammation, their pathological conditions worsen. Furthermore, peripherally induced neuroinflammation is suggested to be greatly involved in the pathology of dementia. According to the 2009 World Alzheimer's Report, the annual cost of dementia worldwide is approximately $ 315 billion. Moreover, in Japan, where dementia is increasing in an aging society, it is reported that the social loss caused by dementia will reach about 21 trillion yen by 2030. Thus, the establishment of anti-neuroinflammatory treatment which can delay the onset and the worsening of dementia and depression is needed. Therefore, it is important to elucidate the mechanism of neuroinflammation induced by inflammation of other organs.
However, there are many unanswered questions. Why does neuroinflammation occur only in specific brain regions (e.g., hippocampus, prefrontal cortex)? Why do the inflamed brain regions differ depending on age or the diseases? Furthermore, it has been reported that the prevention and treatment of neuroinflammation is effective for the treatment of peripheral inflammatory diseases as well as neurological diseases, and that brain fitness which heals the patient’s mind, also exerts a beneficial effect on the inflamed organs. However, the detailed mechanism of these findings is still unknown.
In this topic, we focus on the link between neuroinflammation and dysfunction of peripheral organs and collect the latest findings regarding this. We hope this topic can contribute to finding novel regulatory mechanisms of neuroinflammation and developing therapies for neuroinflammation-related diseases.
Topic Editor Associate professor Takahide Itokaz belongs to the following endowed chair of which he receives sponsorship “Neuro-Medical Science, Graduate School of Medicine, Osaka University”. The Department of Neuro-Medical Science was co-founded by Osaka University and Mitsubishi Tanabe Pharma Corporation. The other Topic Editors declare no competing conflicts of interest.
Neuroinflammation is greatly involved in the onset and pathology of neurological diseases such as neurodegenerative diseases, psychiatric disorders, cerebral ischemia, and dementia. Neuroinflammation is attributed to factors such as neuronal death after cerebral ischemia, viral infection, and immune response by autoantibodies. On the other hand, neuroinflammation is also affected by systematic inflammatory disease. For example, patients with ulcerative colitis and pneumonia have a high probability of developing depression. When depressive symptoms develop, it becomes difficult to proceed with treatment as planned, then delayed treatment leads to a vicious cycle of worsening the pathology of inflamed organs and becoming more severe depressive symptoms. In addition, it has been reported that children born after maternal-fetal transmission are more likely to develop autism, schizophrenia, and addiction, and that when patients with Parkinson's disease or amyotrophic lateral sclerosis suffer from systemic inflammation, their pathological conditions worsen. Furthermore, peripherally induced neuroinflammation is suggested to be greatly involved in the pathology of dementia. According to the 2009 World Alzheimer's Report, the annual cost of dementia worldwide is approximately $ 315 billion. Moreover, in Japan, where dementia is increasing in an aging society, it is reported that the social loss caused by dementia will reach about 21 trillion yen by 2030. Thus, the establishment of anti-neuroinflammatory treatment which can delay the onset and the worsening of dementia and depression is needed. Therefore, it is important to elucidate the mechanism of neuroinflammation induced by inflammation of other organs.
However, there are many unanswered questions. Why does neuroinflammation occur only in specific brain regions (e.g., hippocampus, prefrontal cortex)? Why do the inflamed brain regions differ depending on age or the diseases? Furthermore, it has been reported that the prevention and treatment of neuroinflammation is effective for the treatment of peripheral inflammatory diseases as well as neurological diseases, and that brain fitness which heals the patient’s mind, also exerts a beneficial effect on the inflamed organs. However, the detailed mechanism of these findings is still unknown.
In this topic, we focus on the link between neuroinflammation and dysfunction of peripheral organs and collect the latest findings regarding this. We hope this topic can contribute to finding novel regulatory mechanisms of neuroinflammation and developing therapies for neuroinflammation-related diseases.
Topic Editor Associate professor Takahide Itokaz belongs to the following endowed chair of which he receives sponsorship “Neuro-Medical Science, Graduate School of Medicine, Osaka University”. The Department of Neuro-Medical Science was co-founded by Osaka University and Mitsubishi Tanabe Pharma Corporation. The other Topic Editors declare no competing conflicts of interest.
