
DOI . ORG {
}
Title[redir]:
Neuroinflammatory processes in Alzheimerās disease | Journal of Neural Transmission
Description:
Generation of neurotoxic amyloid β peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimerās disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or, more likely, in concert account for the epidemiologically observed protection.
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Keywords {š}
google, scholar, pubmed, cas, article, disease, alzheimers, brain, neurosci, expression, amyloid, microglia, receptor, alzheimer, mice, neurol, nitric, oxide, heneka, antiinflammatory, transgenic, inflammation, inflammatory, cell, betaamyloid, activation, microglial, neurochem, beta, neurobiol, protein, res, astrocytes, cells, synthase, sci, peroxisome, neuronal, model, receptors, role, neurons, cyclooxygenase, human, aging, obanion, mouse, rat, interleukin, drugs,
Topics {āļø}
peroxisome proliferator-activated receptor-gamma g-protein-coupled receptor mfpr2 tumor-necrosis-factor-alpha stimulate tumor necrosis factor-alpha/lipopolysaccharide peroxisome proliferator-activated receptors beta-catenin/t-cell factor bone-marrow-derived cells contribute month download article/chapter beta-amyloid-induced glial expression beta-amyloid-stimulated proinflammatory responses tumor-necrosis-factor-alpha tumor necrosis factor-alpha tumor necrosis factor-alpha long-term potentiation nonsteroidal anti-inflammatory drug oxidative stressāmediated neuroinflammation steroidal anti-inflammatory drugs nonsteroidal anti-inflammatory drugs oligomeric beta-amyloid peptide widespread peroxynitrite-mediated damage amyloid-beta-induced chemokine production ischemia-induced oxidative damage anti-inflammatory cyclopentenone prostaglandins amyloid-beta peptide-receptor nitric oxide-mediated apoptosis ischaemia-induced hippocampal lesions nmda-induced neuronal injury bind monomeric beta-amyloid flurbiprofen target gamma-secretase lack abeta-activated neurotoxicity beta1 integrin-dependent mechanism prostaglandin e2-mediated neuroprotection neuron-astrocyte cross-talk experimental autoimmune encephalomyelitis a-beta amyloid plaque cxc chemokine-mediated angiogenesis macrophage-colony stimulating factor macrophage colony-stimulating factor cholinergic anti-inflammatory pathway inflammation-mediated neurodegenerative diseases pro-amyloidogenic alpha1-antichymotrypsin app[v717i] transgenic mice tumor necrosis factor {beta}-stimulated microglial activation beta-amyloid-mediated inhibition microglia kill amyloid-beta disease amyloid beta-protein microglial-produced nitric-oxide alzheimer beta-amyloid peptides inflammatory cytokines ifn-gamma
Questions {ā}
- Breitner JC, Zandi PP (2001) Do nonsteroidal antiinflammatory drugs reduce the risk of Alzheimerās disease?
- Davis S, Laroche S (2003) What can rodent models tell us about cognitive decline in Alzheimerās disease?
- Feinstein DL, Spagnolo A, Akar C, Weinberg G, Murphy P, Gavrilyuk V, Russo CD (2005) Receptor-independent actions of PPAR thiazolidinedione agonists: is mitochondrial function the key?
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headline:Neuroinflammatory processes in Alzheimerās disease
description:Generation of neurotoxic amyloid β peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimerās disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or, more likely, in concert account for the epidemiologically observed protection.
datePublished:2010-07-15T00:00:00Z
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Alzheimerās disease
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Amyloid beta
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Neurology
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headline:Neuroinflammatory processes in Alzheimerās disease
description:Generation of neurotoxic amyloid β peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimerās disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or, more likely, in concert account for the epidemiologically observed protection.
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Alzheimerās disease
Neuroinflammation
Amyloid beta
Peroxisome proliferator activated receptor gamma
Cytokines
Locus ceruleus
Neurology
Psychiatry
Neurosciences
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