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Article in English | MEDLINE | ID: mdl-28782486

ABSTRACT

Alzheimer's disease is the most common form of dementia. It is characterized by betaamyloid peptide fibrils which are extracellular deposition of a specific protein, accompanied by extensive neuroinflammation. Various studies show the presence of a number of inflammation markers in the AD brain: elevated inflammatory cytokines and chemokines, and an accumulation of activated microglia in the damaged regions. NF-κB is a family of redox sensitive transcriptional factors, and it is known that NF-κB has binding sites in the promoter region of the genes involved in amyloidogenesis and inflammation. Long-term use of non-steroidal anti-inflammatory drugs prevents progression of AD and delays its onset, suggesting that there is a close correlation between NF-κB and AD pathogenesis. This study aims to (1) assess the association between NF-κB activity and AD through discussion of a variety of experimental and clinical studies on AD and (2) review treatment strategies designed to treat or prevent AD with NF-κB inhibitors.


Subject(s)
Alzheimer Disease/metabolism , Alzheimer Disease/pathology , Brain/metabolism , Brain/pathology , Encephalitis/metabolism , NF-kappa B/metabolism , Alzheimer Disease/complications , Alzheimer Disease/drug therapy , Animals , Encephalitis/complications , Humans , Models, Neurological , NF-kappa B/antagonists & inhibitors
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