Systemic inflammation and disease progression in Alzheimer disease

By C. Holmes, C. Cunningham, E. Zotova, J. Woolford, C. Dean, S. Kerr, D. Culliford, V. Perry. Neurology, 2009

1,051 citations recorded by the source corpus.

Subfields: Biological Psychiatry, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/cbac9326b978c2365dec0a3f265816a795105bb1

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

1. C. Cunningham

In Neurology

1. Paul Edison
2. V. Calsolaro
3. O. Maier
4. Roman Fischer
5. L. Zuo
6. Wen-Ying Wang
7. Zewen Liu
8. Jin-Tai Yu

In Physiology

1. Paul Edison
2. V. Calsolaro
3. O. Maier
4. Roman Fischer
5. L. Zuo
6. Wen-Ying Wang
7. Zewen Liu
8. Jin-Tai Yu

Citations in the corpus

• Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF (2015, background): “Interestingly, increased serum TNF levels due to systemic inflammation have been associated with an increased cognitive decline in AD and PD suggesting a link between systemic inflammation and neurodegeneration [5, 153].”
• Microglia and neurodegeneration: The role of systemic inflammation (2013, background): “While those with elevated serum TNF-a or with carer-reported infection showed greater decline, those with both of these features showed considerably greater decline (Holmes et al., 2009).”
• Neuroinflammation in Alzheimer's disease: Current evidence and future directions (2016, background): “The M1 phenotype responds to lipopolysaccharide (LPS) in combination with interferon-g (IFN-g) and produces a massive inflammatory response releasing interleukin-1b (IL-1b), IL-12, tumor necrosis factor-a (TNF-a), and inducible nitric oxide synthase (iNOS).”
• Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications (2017, background): “Inflammation is responsible for increased expression of cytokines, ROS levels, and cellular toxicity, thereby exacerbating AD progression [50, 51].”
• Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease. (2015, background): “In addition, several studies (48,49) suggest that sustained inflammation from the periphery can cause proinflammatory cytokines in the CNS by crossing the bloodbrain barrier (BBB) and can contribute to cognitive decline in AD patients.”
• The blood-brain barrier in systemic inflammation. (2017, neutral): “Alzheimer’s disease Both acute and chronic systemic inflammation accelerate the progression of AD (Holmes et al., 2009).”