Inflammatory processes in Alzheimer's disease.

By Michael T. Heneka, M. O’Banion. Journal of Neuroimmunology, 2007

1,015 citations recorded by the source corpus.

Subfields: Neurology, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/6b166be766a8541a45d7f5588ce7b38b216a20b3

How researchers see this paper

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

In Neurology

1. C. Cunningham
2. V. Perry
3. R. Ransohoff
4. B. Barres
5. M. Sofroniew
6. C. Iadecola

In Physiology

1. C. Cunningham
2. V. Perry
3. R. Ransohoff
4. J. Morillas-Ruiz
5. J. M. Rubio-Pérez
6. C. Serhan

In Surgery

1. C. Serhan
2. K. Moore
3. P. Calder
4. T. Kern
5. Johnny Tang

Citations in the corpus

• A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease. (2005, background): “Amyloid peptide–mediated oxidative stress, the activation of microglia associated with Aβ peptide deposition, and excessive production of microglial-derived cytokines such as IL-1β and TNF-α support progressive inflammatory episodes in AD (4, 32, 38, 47).”
• A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “This activation is thought to result from the glial reaction to the events related to the ongoing deposition of Aβ [16–18].”
• NLRP3 is activated in Alzheimer´s disease and contributes to pathology in APP/PS1 mice (2012, neutral): “AD-associated inflammation interferes with APP metabolism and with mechanisms of A β aggregation and clearance at multiple levels 9,10 .”
• Microglial physiology: unique stimuli, specialized responses. (2009, background): “The role of inflammation in AD has been extensively researched and exhaustively reviewed (103, 104), but the contributions to the disease of the microglia and the associated innate inflammatory response are by no means clear.”
• Central and Systemic Endotoxin Challenges Exacerbate the Local Inflammatory Response and Increase Neuronal Death during Chronic Neurodegeneration (2005, background): “There is much speculation on the role of CNS inflammation in the progression of neurodegenerative diseases such as Alzheimer’s disease (AD) (Akiyama et al., 2000; Mrak and Griffin, 2001; McGeer and McGeer, 2003).”
• The blood-brain barrier in brain homeostasis and neurological diseases. (2009, neutral): “[198,199].”
• Selective COX-1 inhibition: A therapeutic target to be reconsidered. (2010, background): “An innate immune response is mediated by microglia that contributes to the progression of the diseases [63-65].”
• CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer (2009, background): “We therefore tested whether fibrillar β-amyloid peptide (1-42) (Aβ1-42) could activate TLR4-TLR6 signaling via CD36.”