Role of CaM Kinase II in the Neuropsychiatry Disorders and Drug Addiction

Dear Colleagues,

Age-related cognitive impairments are the major cause of dementia worldwide. Research on cognitive impairments has identified several critical molecules such as the Calcium-/calmodulin-dependent protein kinase II (CaMKII), Brain-derived neurotrophic factor (BDNF) and cAMP-response element binding protein (CREB) in the brain’s memory consolidation. Moreover, synaptic signature molecules have been identified in the synaptic plasticity of learning-related neuronal networks. However, it remains unclear how the dysregulation of synaptic signatures is related to neuropsychiatry diseases such as schizophrenia, depression and autism spectrum disorders. Interestingly, memory decline in AD has also been linked to the abnormality in expressing these memory-related molecular signatures. The de novo mutation studies on CaMKII have elucidated the novel molecular targets inducing neuropsychiatry diseases and abnormal synaptic plasticity. Hence, we will explore the role of these memory-related molecular signatures in long-term memory consolidation in rodents and its disturbance in neuropsychiatry diseases in humans. Additionally, we will address the downstream molecules causing neuropsychiatry disorders and drug dependence, except for the CaMKII/CREB/BDNF pathways.

Prof. Dr. Kohji Fukunaga
Dr. Ichiro Kawahata
Guest Editors

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• CaMKII
• neuropsychiatry disorders
• drug addiction
• synaptic plasticity
• aging