Inflammation and Alzheimer's disease.

By Haruhiko Akiyama, Steven W. Barger, Scott R. Barnum, B. Bradt, J. Bauer, G. Cole, N. R. Cooper, P. Eikelenboom, M. Emmerling, B. L. Fiebich and 26 more. Neurobiology of Aging, 2000

4,581 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/306830c702c0547cc349a04c56cc3f148c39f595

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Citations in the corpus

• Inflammatory proteins in plasma and the risk of dementia: the rotterdam study. (2004, background): “Furthermore, inflammation has been demonstrated in AD-affected brains as is indicated by the presence of activated microglia and inflammatory proteins.(1) In addition to inflammation within the brain, the peripheral immune system of patients with dementia may be activated as well.”
• Inflammation as a central mechanism in Alzheimer's disease (2018, background): “IL-1 is a proinflammatory cytokine that is upregulated early in AD development and is considered crucial for b-amyloid plaque deposition [41].”
• Mechanisms Underlying Inflammation in Neurodegeneration (2010, unknown): “Moreover, microglia surrounding plaques stain positive for activation markers and proinflammatory mediators, including MHC class II, Cox-2, MCP-1, TNF-a, IL-1b, and IL-6 (Akiyama et al., 2000).”
• Neuropathologic changes in Alzheimer's disease. (2003, background): “Understanding the inflammatory and immunoregulatory processes of Alzheimer’s disease may enable researchers to develop antiinflammatory approaches that may not cure Alzheimer’s disease but may slow the progression or delay onset.(8,17,18,28) Therapies can then be rationally designed and possibly be ”
• Inflammatory processes in Alzheimer's disease. (2007, unknown): “For example, IL-1 has been implicated in the transformation of diffuse β-amyloid aggregates into βamyloid plaques (Akiyama et al., 2000).”
• Effects of rofecoxib or naproxen vs placebo on Alzheimer disease progression: a randomized controlled trial. (2003, background): “This approach is supported by a wealth of laboratory evidence that inflammatory mechanisms contribute to neuronal damage in AD.(1) Furthermore, many epidemiological studies suggest that antiinflammatory drugs have a protective effect, reducing the incidence of AD.”
• Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, background): “It is now clear that AD is associated with elevated serum and cerebrospinal fluid (CSF) levels of TNF-a, IL-6, and IL-1b (Akiyama et al., 2000; Shaftel et al., 2008).”
• Aggravation of Alzheimer’s disease due to the COX-2-mediated reciprocal regulation of IL-1β and Aβ between glial and neuron cells (2014, background): “Prior work suggests that COX-2, a critical inflammation inducer in peripheral tissues, is also involved in AD progression via inducing the activation of astrocytes or microglia cells (Akiyama et al., 2000).”
• Neuroinflammation in Alzheimer's disease: Current evidence and future directions (2016, background): “Indeed, Ab can stimulate the NF-kB–dependent pathway and, binding microglial cell surface, the activation of extracellular signal-regulated kinase and mitogen-activated protein kinase (MAPK) pathways, triggering pro-inflammatory gene expression [14,29].”