Neuroinflammation in Alzheimer's disease.
|Title||Neuroinflammation in Alzheimer's disease.|
|Publication Type||Journal Article|
|Year of Publication||2015|
|Authors||Heneka MT, Carson MJ, Khoury JEl, Landreth GE, Brosseron F, Feinstein DL, Jacobs AH, Wyss-Coray T, Vitorica J, Ransohoff RM, Herrup K, Frautschy SA, Finsen B, Brown GC, Verkhratsky A, Yamanaka K, Koistinaho J, Latz E, Halle A, Petzold GC, Town T, Morgan D, Shinohara ML, V Perry H, Holmes C, Bazan NG, Brooks DJ, Hunot S, Joseph B, Deigendesch N, Garaschuk O, Boddeke E, Dinarello CA, Breitner JCS, Cole GM, Golenbock DT, Kummer MP|
|Date Published||2015 Apr|
|Keywords||Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Astrocytes, Biomarkers, Brain Injuries, Clinical Trials as Topic, Disease Models, Animal, Disease Progression, Humans, Immunity, Innate, Immunization, Inflammation, Inflammation Mediators, Locus Coeruleus, Microglia, Nootropic Agents, Obesity, Phagocytosis, Protein Folding, Risk Factors, Severity of Illness Index|
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.
|Alternate Journal||Lancet Neurol|
|Grant List||I01 BX001257 / BX / BLRD VA / United States |
R01 AG021975 / AG / NIA NIH HHS / United States
R01 AT006816 / AT / NCCIH NIH HHS / United States
RC1 AG035878 / AG / NIA NIH HHS / United States