The role of inflammation in Alzheimer's disease

Tuppo, Ehab; Arias, Hugo R.

doi:10.1016/j.biocel.2004.07.009

Cited by 643 publications

(486 citation statements)

References 170 publications

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“…In the brains of both AD individuals and transgenic animal models, it was found that Ab plaques are surrounded by activated glial cells (Bauer et al 1991;Cagnin et al 2001;Fillit et al 1991;Liu et al 2013;Varnum and Ikezu 2012). Activated microglia and astrocytes strongly secrete inflammatory components such as pro-inflammatory cytokines, chemokines, complement, macrophage inflammatory proteins, monocyte chemoattractant proteins, reactive oxygen species (ROS), nitric oxide (NO) prostaglandins, leukotrienes, thromboxanes and so on (Akiyama et al 2000;Griffin et al 1998;Mrak et al 1995;Town et al 2005;Tuppo and Arias 2005). The released inflammatory molecules, especially some cytokines such as interleukin (IL)-18, IL-1b and tumor necrosis factor (TNF)-a, impair the balance of normal neurophysiologic condition that correlates with cognition and learning and memory (Fillit et al 1991;Gemma and Bickford 2007;Jankowsky and Patterson 1999;Liu et al 2013;Varnum and Ikezu 2012).…”

Section: Inflammation In Admentioning

confidence: 99%

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Zhang

et al. 2015

Arch. Immunol. Ther. Exp.

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Alzheimer's disease (AD) is a complex agerelated neurodegenerative disorder of the central nervous system. Since the first description of AD in 1907, many hypotheses have been established to explain its causes. The inflammation theory is one of them. Pathological and biochemical studies of brains from AD individuals have provided solid evidence of the activation of inflammatory pathways. Furthermore, people with long-term medication of anti-inflammatory drugs have shown a reduced risk to develop the disease. After three decades of genetic study in AD, dozens of loci harboring genetic variants influencing inflammatory pathways in AD patients has been identified through genome-wide association studies (GWAS). The most well-known GWAS risk factor that is responsible for immune response and inflammation in AD development should be APOE e4 allele. However, a growing number of other GWAS risk AD candidate genes in inflammation have recently been discovered. In the present study, we try to review the inflammation in AD and immunity-associated GWAS risk genes like HLA-DRB5/DRB1, INPP5D, MEF2C, CR1, CLU and TREM2.

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Section: Inflammation In Admentioning

confidence: 99%

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Zhang

et al. 2015

Arch. Immunol. Ther. Exp.

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“…This neuroinflammatory process manifests as an increase of reactive astrocytes and activated microglia 35 . To determine the effect of cigarette smoke in AD-associated microglial activation, we immunostained microglial cells using Iba1 antibody ( Fig.…”

Section: Enhancement Of Neuroinflammation By Cigarette Smokingmentioning

confidence: 99%

Smoking exacerbates amyloid pathology in a mouse model of Alzheimer’s disease

Moreno-González

Estrada²,

Sánchez-Mejías

et al. 2013

Nat Commun

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“…81,85 Most of the complement proteins found in blood are also expressed in the brain, mainly by microglia and to a lesser extent by stressed or damaged astrocytes and neurons. 81,86,87 C1q, C3, C4, C5, C6, C9, CR1, C1qRp, CR3, CR4, Factor H and others have been shown to be upregulated in brain in humans and experimental animals with infection, ischemia and stroke, Alzheimer's disease, prion disease, Huntington's chorea and many other CNS diseases. 81,85,86 C1q-deficient mice have less injury following cerebral ischemia and have less neuropathology in transgenic mouse models of Alzheimer's disease.…”

Section: Role Of Complement In the Brainmentioning

confidence: 99%

A proteomic study of serum from children with autism showing differential expression of apolipoproteins and complement proteins

Corbett

Kantor²,

Schulman³

et al. 2006

Mol Psychiatry

164

113

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Modern methods that use systematic, quantitative and unbiased approaches are making it possible to discover proteins altered by a disease. To identify proteins that might be differentially expressed in autism, serum proteins from blood were subjected to trypsin digestion followed by liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) on time-of-flight (TOF) instruments to identify differentially expressed peptides. Children with autism 4-6 years of age (n = 69) were compared to typically developing children (n = 35) with similar age and gender distributions. A total of 6348 peptide components were quantified. Of these, five peptide components corresponding to four known proteins had an effect size > 0.99 with a P < 0.05 and a Mascot identification score of 30 or greater for autism compared to controls. The four proteins were: Apolipoprotein (apo) B-100, Complement Factor H Related Protein (FHR1), Complement C1q and Fibronectin 1 (FN1). In addition, apo B-100 and apo A-IV were higher in children with high compared to low functioning autism. Apos are involved in the transport of lipids, cholesterol and vitamin E. The complement system is involved in the lysis and removal of infectious organisms in blood, and may be involved in cellular apoptosis in brain. Despite limitations of the study, including the low fold changes and variable detection rates for the peptide components, the data support possible differences of circulating proteins in autism, and should help stimulate the continued search for causes and treatments of autism by examining peripheral blood.

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The role of inflammation in Alzheimer's disease

Cited by 643 publications

References 170 publications

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

Smoking exacerbates amyloid pathology in a mouse model of Alzheimer’s disease

A proteomic study of serum from children with autism showing differential expression of apolipoproteins and complement proteins

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