| Resumo: |
Alzheimer's disease is a common neurodegenerative disorder. However, its exact etiology is still unknown. There were several mechanisms proposed such as the tau hypothesis and amyloid hypothesis. However, there is evidence challenging the above two hypotheses. Here, I propose the immune-amyloid hypothesis as a mechanism for Alzheimer's disease. Th17 related autoimmunity contributes to the disease pathogenesis. Accumulation of misfolded beta amyloid can trigger heat shock protein which in turn induces TH17 immunity. By microarray analysis of peripheral blood mononuclear cells, there is up-regulation of many TH17 related molecules after Alzheimer's disease. After knowing the exact disease pathogenesis, we can develop new therapeutic strategies to prevent or treat the detrimental disorder.
|
