Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism.

By M. Block, Jau-Shyong Hong. Progress in neurobiology, 2005

1,572 citations recorded by the source corpus.

Subfields: Immunology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/182f55c0fddad3231873d51bb46849355f168b0e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. P. Whitton
2. Melinda E Lull
3. M. Goldberg
4. M. Tansey
5. M. Block

In Neurology

1. M. Tansey
2. M. Goldberg
3. P. Whitton
4. Melinda E Lull
5. M. Block
6. S. Duty
7. P. Jenner
8. Elias K. Michaelis

In Physiology

1. P. Whitton
2. Melinda E Lull
3. M. Goldberg
4. M. Block
5. M. Tansey

Citations in the corpus

• Neuroinflammation in Parkinson’s disease: its role in neuronal death and implications for therapeutic intervention (2009, background): “…including chronic inflammatory syndromes (rheumatoid arthritis, arthrosclerosis, type 2 diabetes, Crohn’s disease, and multiple sclerosis) and environmental toxins (pesticides, particulate matter, etc.) (Aloisi, 1999; Streit, 2000; Block and Hong, 2005; Hirsch et al., 2005; Minghetti et al., 2005).”
• Inflammation as a causative factor in the aetiology of Parkinson's disease (2007, background): “Elevated levels of proinflammatory cytokines such as tumour necrosis factor-a (TNF-a), interleukin (IL)-1b and IL-6 in the colony-stimulating factor (CSF) and striatum in PD brains have also been demonstrated (Mogi et al., 1994; Blum-Degen et al., 1995; Muller et al., 1998).”
• Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, neutral): “, 2001) and eventually even to apoptosis and neurodegeneration (Block and Hong, 2005).”
• Microglial Activation & Chronic Neurodegeneration (2010, background): “Although the detailed components of the microglial response can be stimulus specific, there are common factors of microglial activation.(46) LPS is a cell wall component of gram-negative bacteria and is a potent stimulus of the microglial innate immune response.”
• Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, neutral): “…neurotoxic effects by releasing multiple cytotoxic substances, including pro-inflammatory cytokines (e.g. interleukin (IL)-1b, tumor necrosis factor-a (TNFa), and interferon-c (IFNc)) and oxidative metabolites (e.g. nitric oxide, reactive oxygen and nitrogen species) (Block and Hong, 2005).”
• Neuroinflammation in Parkinson’s disease and its potential as therapeutic target (2015, background): “Although a variety of possible pathogenetic mechanisms have been proposed over the years, including excessive release of oxygen free radicals during enzymatic dopamine breakdown, impairment of mitochondrial function, loss of trophic support, abnormal kinase activity, disruption of calcium homeostasi”