PKCδ serves as a potential biomarker and therapeutic target for microglia-mediated neuroinflammation in Alzheimer's disease.
Ying DuTiantian GuoYunfeng HaoChuan LiLinghui TangXia LiXiaoxiao ZhangLin LiDan YaoXia XuHuaxing SiJinghan ZhangNana ZhaoTong YuYingjun ZhaoWei ZhangHuaxi XuPublished in: Alzheimer's & dementia : the journal of the Alzheimer's Association (2024)
Protein kinase C delta (PKCδ) levels increase in cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), and positively correlate with elevated inflammatory cytokines in human subjects. PKCδ is expressed mainly in microglia in vivo, whereas amyloid beta (Aβ) stimulation increases PKCδ expression and secretion, causing upregulation of the nuclear factor kappa B (NF-κB) pathway and production of inflammatory cytokines. Downregulation or inhibition of PKCδ attenuates Aβ-enhanced NF-κB signaling and cytokine production in microglia and improves cognitive function in AD mice. PKCδ serves as a potential biomarker and therapeutic target for microglia-mediated neuroinflammation in AD.
Keyphrases
- nuclear factor
- protein kinase
- inflammatory response
- lps induced
- toll like receptor
- signaling pathway
- cerebrospinal fluid
- neuropathic pain
- lipopolysaccharide induced
- poor prognosis
- cell proliferation
- cognitive decline
- endothelial cells
- oxidative stress
- pi k akt
- spinal cord injury
- spinal cord
- metabolic syndrome
- cognitive impairment
- type diabetes
- cerebral ischemia
- brain injury
- subarachnoid hemorrhage
- high fat diet induced
- induced pluripotent stem cells