The role of inflammation in Alzheimer's disease.

By E. Tuppo, H. Arias. International Journal of Biochemistry and Cell Biology, 2005

751 citations recorded by the source corpus.

Considerable evidence gained over the past decade has supported the conclusion that neuroinflammation is associated with Alzheimer's disease (AD) pathology. Inflammatory components related to AD neuroinflammation include brain cells such as microglia and astrocytes, the classic and alternate pathways of the complement system, the pentraxin acute-phase proteins, neuronal-type nicotinic acetylcholine receptors (AChRs), peroxisomal proliferators-activated receptors (PPARs), as well as cytokines and chemokines. Both the microglia and astrocytes have been shown to generate beta-amyloid protein (Abeta), one of the main pathologic features of AD. Abeta itself has been shown to act as a pro-inflammatory agent causing the activation of many of the inflammatory components. Further substantiation for the role of neuroinflammation in AD has come from studies that demonstrate patients who took non-steroidal anti-inflammatory drugs had a lower risk of AD than those who did not. These same results have led to increased interest in pursuing anti-inflammatory therapy for AD but with poor results. On the other hand, increasing amount of data suggest that AChRs and PPARs are involved in AD-induced neuroinflammation and in this regard, future therapy may focus on their specific targeting in the AD brain.

Subfields: Biological Psychiatry, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/56db388e14a1d15fedf1ef3c9d8abf7cf4b156fc

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Citations in the corpus

Neuroinflammation Induces Neurodegeneration (2016, background): “Microglia and astrocytes generate Aβ that can activate proinflammatory pathways in AD [34].”
Inflammatory processes in Alzheimer's disease. (2007, positive): “In contrast to animal models, nearly all cytokines that have been studied in AD, including IL-1α/β, IL-6, TNF-α, IL-8, and TGF-β, seem to be upregulated in AD compared to control individuals (Akiyama et al., 2000; Tuppo and Arias, 2005).”
A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “Their production is increased in inflammatory states and they function by regulating the intensity and duration of the immune response [13].”
Expression of Nrf2 in Neurodegenerative Diseases (2007, positive): “Because there is a pronounced inflammatory component to amyloid plaques (55), one possibility is that Nrf2 translocation is inhibited by inflammatory signaling molecules such as cytokines, chemokines, and neurotrophic factors.”
Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “In this review we briefly examined the evidence of environmental etiologies related to two of the most common neurodegenerative diseases, AD and PD, from epidemiological as well as experimental studies.”
Nanoparticle-mediated brain drug delivery: Overcoming blood-brain barrier to treat neurodegenerative diseases. (2016, background): “Microglia and astrocytes are also main players in controlling the levels of Aβ load and boosting Aβ production when activated [115].”
Insulin and insulin-like growth factor expression and function deteriorate with progression of Alzheimer's disease: Link to brain reductions in acetylcholine (2005, positive): “The AD Braak Stage associated increases in the AIF-1 and IBA-1 microglial markers are of interest with respect to the inflammatory hypothesis of AD neurodegeneration, particularly since previous studies demonstrated that microglial cells and astrocytes contribute to Aβ accumulation and neurotoxicity”
Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function (2009, background): “These drugs may impart therapeutic benefit in neurodegenerative diseases of aging, including reduced risk of age-related dementia (2, 173, 178, 216, 289, 454, 470).”
Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease. (2014, background): “However there is also evidence that microglia can have neurotoxic effects in the brain [212], likely via the release of potent pro-inflammatory molecules [213] and other immunomodulatory molecules which lead to the recruitment of monocytes and lymphocytes through the blood-brain barrier (BBB) [214,2”
A review on Alzheimer’s disease pathophysiology and its management: an update (2015, background): “The discharged glutamate activates the extrasynaptic NMDARs of the astrocytes’ partner neurons [20,22].”
The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide (2010, positive): “Alargebody of data supports a central role for neuroinflammation in AD neuropathology [55].”