Immunological aspects of microglia: relevance to Alzheimer's disease

Benveniste, Etty N.; Nguyen, Vince T.; O'Keefe, George M

doi:10.1016/s0197-0186(01)00045-6

Cited by 175 publications

(110 citation statements)

References 109 publications

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“…This leads to an increased production of proinflammatory cytokines, iNOS, and NO, which have been proposed to play a pathological role in several neurodegenerative disorders, including AD (Akiyama et al, 2000;Benveniste et al, 2001). In the current study, we examined the activation of microglia in the CA1 area of the hippocampus after thrombin injection in vivo.…”

Section: Thrombin Induces Neurodegeneration and Microglial Activationmentioning

confidence: 99%

“…A number of studies have demonstrated that microglial activation is found in the brains of AD patients (Benveniste et al, 2001) and in the hippocampus of animal models of AD caused by administration of ␤-amyloid (Stepanichev et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…This leads to the increased production of ROS and resulting oxidative insult (Benveniste et al, 2001;Coraci et al, 2002), which plays a key role in neurodegeneration (Gao et al, 2003a,b;Wu et al, 2003;Zhang et al, 2004). NADPH oxidase is a multicomponent enzyme, and its activation is responsible for generating ROS in microglia (Babior, 1999;Cross and Segal, 2004;Patel et al, 2005).…”

mentioning

confidence: 99%

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Thrombin-Induced Oxidative Stress Contributes to the Death of Hippocampal NeuronsIn Vivo: Role of Microglial NADPH Oxidase

Choi¹,

Lee²,

Kim³

et al. 2005

J. Neurosci.

147

138

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The present study investigated whether thrombin, a potent microglial activator, can induce reactive oxygen species (ROS) generation through activation of microglial NADPH oxidase and if this may contribute to oxidative damage and consequent neurodegeneration. Seven days after intrahippocampal injection of thrombin, Nissl staining and immunohistochemistry using the neuronal-specific nuclear protein NeuN revealed a significant loss in hippocampal CA1 neurons. In parallel, thrombin-activated microglia, assessed by OX-42 and OX-6 immunohistochemistry, and ROS production, assessed by hydroethidine histochemistry, were observed in the hippocampal CA1 area in which degeneration of hippocampal neurons occurred.

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Section: Thrombin Induces Neurodegeneration and Microglial Activationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Thrombin-Induced Oxidative Stress Contributes to the Death of Hippocampal NeuronsIn Vivo: Role of Microglial NADPH Oxidase

Choi¹,

Lee²,

Kim³

et al. 2005

J. Neurosci.

147

138

View full text Add to dashboard Cite

show abstract

“…The pathological hallmarks of AD are cortical atrophy with accumulation of extracellular deposits of amyloid (A ) in senile plaques and intracellular neurofibrillary tangles (NFT) of hyperphosphorylated tau in the cerebral cortex (De Strooper and Annaert, 2000). It is known that A serves as a microglial activator and leads to production of various inflammatory mediators (Benveniste et al, 2001). On the other hand, a neuroprotective role of microglia was found in AD.…”

Section: Regenerative Approachesmentioning

confidence: 99%

Perspectives of Stem Cell-Derived Microglia for Medicine

Roy¹,

Beutner²,

Neumann³

2011

Embryonic Stem Cells - Recent Advances in Pluripotent Stem Cell-Based Regenerative Medicine

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“…Infl ammation mediated by activated microglia is an important component of AD pathophysiology (9) and neuritic plaques are the foci of the local infl ammatory response (10). Aβ neuritic plaques are surrounded by activated microglia, cytokines, and complement components, which are called "inflammatory foci".…”

mentioning

confidence: 99%

Immunological Aspects and Anti-Amyloid Strategy for Alzheimer’s Dementia

Liščić

2013

Archives of Industrial Hygiene and Toxicology

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Alzheimer's dementia (AD) is the most common form of dementia among the elderly, accounting for at least two-thirds of all dementia cases. It represents a costly burden, since its global prevalence is estimated at 24 million cases. Amyloid beta or Aβ plaques and neurofi brillary tangles defi ne AD pathologically but do not fully explain it, because dementia may also be caused by infl ammation resulting in neuronal, axonal synaptic loss and dysfunction. An important component of AD pathophysiology are amyloid plaques surrounded by activated microglia, cytokines, and complement components, suggesting infl ammation. In the diagnosis of AD, cerebrospinal fl uid markers, especially in vivo amyloid measurements, contribute to an accurate assessment of AD pathology and differential diagnosis. Aβ levels are a very good marker for the presence of amyloid deposits in the brain, while total tau and phosphorylated tau are useful for the detection of neurodegeneration. The implementation of anti-amyloid therapy and other disease-modifying interventions may have immense clinical impact if initiated at an early or presymptomatic stage of AD, before signifi cant brain damage occurs. This paper briefl y reviews the abovementioned topics and provides recommendations for future studies.

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Immunological aspects of microglia: relevance to Alzheimer's disease

Cited by 175 publications

References 109 publications

Thrombin-Induced Oxidative Stress Contributes to the Death of Hippocampal NeuronsIn Vivo: Role of Microglial NADPH Oxidase

Thrombin-Induced Oxidative Stress Contributes to the Death of Hippocampal NeuronsIn Vivo: Role of Microglial NADPH Oxidase

Perspectives of Stem Cell-Derived Microglia for Medicine

Immunological Aspects and Anti-Amyloid Strategy for Alzheimer’s Dementia

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