Systemic infections and inflammation affect chronic neurodegeneration
By V. Perry, C. Cunningham, C. Holmes. Nature reviews. Immunology, 2007
1,027 citations recorded by the source corpus.
Subfields: Biological Psychiatry, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/3cb9c5e078e04f5c19f105b2137275f4d79dff9f
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Biological Psychiatry
- C. Cunningham
- M. Sofroniew
- J. Burda
- R. Ransohoff
- V. Perry
- T. Wyss‐Coray
- Ygor P. Silva
- B. K. Pedersen
In Neurology
In Physiology
- B. K. Pedersen
- R. Ransohoff
- T. Wyss‐Coray
- Christoph Handschin
- J. Burda
- B. Spiegelman
- C. Cunningham
- M. Sofroniew
Citations in the corpus
- Microglia and neurodegeneration: The role of systemic inflammation (2013, methodology): “The terminology we adopted at that time (Perry et al., 2007) was derived from the original description of peripheral macrophage priming (Johnson et al.”
- Mechanisms Underlying Inflammation in Neurodegeneration (2010, neutral): “Activation of the systemic innate immune system by infection may be involved in the early stages of AD pathogenesis (Perry et al., 2007).”
- Microglial physiology: unique stimuli, specialized responses. (2009, background): “Investigators have proposed that the microglia in the prion diseased brain are primed by the ongoing pathology and that a secondary stimulus, the signaling of systemic inflammation across the BBB, switches these cells to an aggressive phenotype (98).”
- Inflammation: The Common Pathway of Stress-Related Diseases (2017, background): “Activation of the systemic innate immune system by infection may participate in the early stages of AD pathogenesis (Perry et al., 2007).”
- Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer’s disease (2009, background): “Elderly, demented patients often have systemic comorbidities, such as pneumonia and other infections, and it has been shown that infectious disease outside the CNS can profoundly influence microglial activation [23, 27, 36].”
- The diseasome of physical inactivity – and the role of myokines in muscle–fat cross talk (2009, background): “Moreover, in addition to the neuroinflammation found in many neurodegenerative disorders, systemic inflammation may further exacerbate the progression of neurodegeneration (Perry et al. 2007).”
- Repertoire of microglial and macrophage responses after spinal cord injury (2011, background): “Such microglial responses were seen in a mouse model of prion disease challenged with inoculation with LP”
- Differential roles of microglia and monocytes in the inflamed central nervous system (2014, background): “Despite this apparent uniformity, gene expression by morphologically identical microglia can differ drastically contingent on context (Perry et al., 2007).”
- Regulation of learning and memory by meningeal immunity: a key role for IL-4 (2010, background): “Innate immune cells, both peripheral and CNS resident, were proposed as the source of proinflammatory cytokines that are secreted in response to any deviation from physiological homeostasis as a result of stress, disease, or injury (Perry et al., 2007).”
- A meta-analysis of cytokines in Alzheimer's disease. (2010, background): “Thereore, over time, it has been suggested that the net effect of icroglial activation might be to further increase amyloid- depoition, perpetuating the neurodegenerative cascade (19,151).”