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
- lipopolysaccharide induced
- cerebrospinal fluid
- neuropathic pain
- poor prognosis
- traumatic brain injury
- cell proliferation
- cognitive decline
- oxidative stress
- cognitive impairment
- adipose tissue
- pi k akt
- metabolic syndrome
- spinal cord
- induced pluripotent stem cells
- high fat diet induced
- blood brain barrier