Inflammation and Alzheimer’s disease

Lee, Young-Jung; Han, Sang Bae; Nam, Sang-Yoon; Oh, Ki‐Wan; Hong, Jin Tae

doi:10.1007/s12272-010-1006-7

Cited by 352 publications

(234 citation statements)

References 200 publications

(164 reference statements)

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“…Some studies showed benefits of certain NSAIDs in the improvement of cognitive functions or delaying onset of AD. However, other studies showed no improvement (19). Intriguingly, while neuroinflammation, which accompanies development of AD, has been the primary reason for testing NSAIDs, several studies have suggested that the positive effects of this class of drugs are not related to inflammation (or A␤ processing, see below) (20,21).…”

Section: Discussionmentioning

confidence: 99%

Identification of Small Molecule Inhibitors of Neurite Loss Induced by Aβ peptide using High Content Screening

Ofengeim

Shi

Miao

et al. 2012

Journal of Biological Chemistry

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Background: Amyloid-␤-induced degeneration of neurites is a key event in Alzheimer disease. Results: We describe NeuriteIQ high content screening platform for analysis of neurite degeneration. Conclusion: We identified multiple cyclooxygenase inhibitors and agonists of PPAR␥ as suppressors of A␤-induced neurite loss. Significance: Our study demonstrates the feasibility of using NeuriteQ to discover inhibitors of neurite loss and provide a new insight into neurite degeneration.

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Section: Discussionmentioning

confidence: 99%

Identification of Small Molecule Inhibitors of Neurite Loss Induced by Aβ peptide using High Content Screening

Ofengeim

Shi

Miao

et al. 2012

Journal of Biological Chemistry

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“…Research has suggested that mitochondrial dysfunction [12,18,19] , metal accumulation [12,20,21] , hyperphosphorylated tau [22,23] , inflammation [24,25] , and β-amyloid (Aβ) accumulation [12,19] are the basic mechanisms underlying the induction of oxidative stress. Deficiency or destruction of components of the antioxidant system such as SOD in the mitochondria (Mn-SOD or SOD2) and cytosol (Cu-Zn-SOD or SOD1), [14,17,26] .…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress in Alzheimer’s disease

2014

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Oxidative stress plays a significant role in the pathogenesis of Alzheimer's disease (AD), a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons (lipids, proteins, and nucleic acids) can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, infl ammation, and β-amyloid (Aβ) peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment.Keywords: Alzheimer's disease; oxidative stress; β-amyloid; tau; metals; antioxidants ·Review· IntroductionThe human brain, although it constitutes only 2% of the body weight, consumes ~20% of the oxygen supplied by the respiratory system [1] . The high energy-consumption of the brain means that it is more susceptible to oxidative stress than any other organ. As the basic functional unit of the brain, the neuron is particularly vulnerable to oxidative damage because it has a higher metabolic rate than other cells [2] . The oxidation of lipids, proteins, and nucleic acids in neurons is a common pathological feature of Alzheimer's disease (AD) [3] . Neurons contain a large amount of polyunsaturated fatty acids (PUFAs) that can interact with reactive oxygen species (ROS), leading to a selfpropagating cascade of lipid peroxidation and molecular destruction [4] . Furthermore, neurons contain low levels of glutathione, an essential antioxidant for eliminating free radicals [5] . Therefore, neurons are highly susceptible to oxidative stress.An increased oxidative burden has been reported in the brains of non-demented elderly and/or sporadic AD patients [6,7] . Increased levels of oxidative stress biomarkers in the blood reflect such stress in the brain [8,9] . Currently, many blood markers of oxidative stress have been identified in AD patients or related animal models, including protein carbonyls and 3-nitrotyrosine [10,11] , , malondialdehyde (MDA) [12] , 4-hydroxynonenal (4-HNE), and F2-isoprostanes (F2-IsoPs) [13][14][15][16] . Apart from the intracellular accumulation of free radicals, changes in the activities or expressions of antioxidant enzymes, such as superoxide dismutase (SOD) and catalase, have also been described in both the central nervous system and peripheral tissues of AD patients [14,17] . Thus, oxidative stress is an important pathological feature in AD.However, how and where the oxidative stress originates in AD are open questions. Research has suggested that mitochondrial dysfunction [12,18,19] , metal accumulation [12,20,21] , hyperphosphorylated tau [22,23] , inflammation [24,25] , and β-amyloid (Aβ) accumulation [12,19] are the basic mechanisms underlying the induction of oxidative stress. Deficiency or destruction of components of the antioxidant system such as SOD in the mi...

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“…Moreover, recent evidence suggests that 15d-PGJ2 may exert a protective effect on the CNS under pathological conditions, as well as antiviral effects (11). Thus, current research interests for the treatment of neurodegenerative diseases are focused primarily on PPARγ agonists such as 15d-PGJ2, which is being clinically evaluated for potential improvement of cognition (12,13). Recently, only minimal information is available regarding the effects of 15d-PGJ2 on HIV-1 Tat-induced cytotoxicity in the hippocampus, as well as the possible molecular pathways impinged upon by this process, despite of the intense research conducted to characterize the various biological activities of 15d-PGJ2.…”

Section: Human Immunodeficiency Virus-1 (Hiv-1) Infection Canmentioning

confidence: 99%

HIV-1 Tat Protein-dependent Cytotoxicity is Attenated by 15-deoxy-Delta^12,14-Prostaglandin J2 in Rat Hippocampal Slices: Involvement of the ERK1/2 Signaling Pathway

et al. 2013

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Inflammation and Alzheimer’s disease

Cited by 352 publications

References 200 publications

Identification of Small Molecule Inhibitors of Neurite Loss Induced by Aβ peptide using High Content Screening

Identification of Small Molecule Inhibitors of Neurite Loss Induced by Aβ peptide using High Content Screening

Oxidative stress in Alzheimer’s disease

HIV-1 Tat Protein-dependent Cytotoxicity is Attenated by 15-deoxy-Delta^12,14-Prostaglandin J2 in Rat Hippocampal Slices: Involvement of the ERK1/2 Signaling Pathway

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Inflammation and Alzheimer’s disease

Cited by 352 publications

References 200 publications

Identification of Small Molecule Inhibitors of Neurite Loss Induced by Aβ peptide using High Content Screening

Identification of Small Molecule Inhibitors of Neurite Loss Induced by Aβ peptide using High Content Screening

Oxidative stress in Alzheimer’s disease

HIV-1 Tat Protein-dependent Cytotoxicity is Attenated by 15-deoxy-Delta12,14-Prostaglandin J2 in Rat Hippocampal Slices: Involvement of the ERK1/2 Signaling Pathway

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HIV-1 Tat Protein-dependent Cytotoxicity is Attenated by 15-deoxy-Delta^12,14-Prostaglandin J2 in Rat Hippocampal Slices: Involvement of the ERK1/2 Signaling Pathway