Increased expressions of TLR2 and TLR4 on peripheral blood mononuclear cells from patients with Alzheimer's disease

Zhang, Wei; Wang, Lizhu; Yu, Jin‐Tai; Chi, Zhen‐Ming; Tan, Lan

doi:10.1016/j.jns.2011.11.032

Cited by 65 publications

(33 citation statements)

References 36 publications

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“…Several groups have recently reported the study of TLRs mRNA levels [50][51][52]. These authors confirm that TLR2 and TLR4 mRNAs expression levels were positively correlated with both the levels of proteins and their function.…”

Section: Discussionsupporting

confidence: 53%

Retinoic acid receptor β deficiency reduces splenic dendritic cell population in a conditional mouse line

et al. 2012

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Section: Discussionsupporting

confidence: 53%

Retinoic acid receptor β deficiency reduces splenic dendritic cell population in a conditional mouse line

et al. 2012

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“…The important role conferred to Toll-like receptors (TLR2 and TLR4) in AD as peripheral biomarkers [75] of AD pathophysiology [75–77] is well studied. Notably, the part played by TLR receptors in AD progression addresses the importance of innate immune responses [78].…”

Section: Oxidative Stress Mediated Inflammation and Neuropsychiatrmentioning

confidence: 99%

ROS and Brain Diseases: The Good, the Bad, and the Ugly

Popa‐Wagner

Mitran

Sivanesan

et al. 2013

Oxidative Medicine and Cellular Longevity

346

222

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The brain is a major metabolizer of oxygen and yet has relatively feeble protective antioxidant mechanisms. This paper reviews the Janus-faced properties of reactive oxygen species. It will describe the positive aspects of moderately induced ROS but it will also outline recent research findings concerning the impact of oxidative and nitrooxidative stress on neuronal structure and function in neuropsychiatric diseases, including major depression. A common denominator of all neuropsychiatric diseases including schizophrenia and ADHD is an increased inflammatory response of the brain caused either by an exposure to proinflammatory agents during development or an accumulation of degenerated neurons, oxidized proteins, glycated products, or lipid peroxidation in the adult brain. Therefore, modulation of the prooxidant-antioxidant balance provides a therapeutic option which can be used to improve neuroprotection in response to oxidative stress. We also discuss the neuroprotective role of the nuclear factor erythroid 2-related factor (Nrf2) in the aged brain in response to oxidative stressors and nanoparticle-mediated delivery of ROS-scavenging drugs. The antioxidant therapy is a novel therapeutic strategy. However, the available drugs have pleiotropic actions and are not fully characterized in the clinic. Additional clinical trials are needed to assess the risks and benefits of antioxidant therapies for neuropsychiatric disorders.

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“…There is some conflict in the literature regarding the association of TLR2 genetic polymorphisms in AD (Yu et al, 2011a,b). In blood (PBMCs specifically) and brain tissue from AD patients, TLR2 and TLR4 are increased (Liu et al, 2005; Walter et al, 2007; Letiembre et al, 2009; Zhang et al, 2012). TLR activation leads to receptor dimerization at the plasma membrane with the adaptor protein MyD88, activation of the RIP1 kinase, and downstream signaling to NFκB and MAPK.…”

Section: Sterile Inflammationmentioning

confidence: 99%

Bioenergetic Dysfunction and Inflammation in Alzheimerâ€™s Disease: A Possible Connection

Wilkins

Carl

Greenlief

et al. 2014

Front. Aging Neurosci.

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Inflammation is observed in Alzheimer’s disease (AD) subject brains. Inflammation-relevant genes are increasingly implicated in AD genetic studies, and inflammatory cytokines to some extent even function as peripheral biomarkers. What underlies AD inflammation is unclear, but no “foreign” agent has been implicated. This suggests that internally produced damage-associated molecular pattern (DAMPs) molecules may drive inflammation in AD. A more complete characterization and understanding of AD-relevant DAMPs could advance our understanding of AD and suggest novel therapeutic strategies. In this review, we consider the possibility that mitochondria, intracellular organelles that resemble bacteria in many ways, trigger and maintain chronic inflammation in AD subjects. Data supporting the possible nexus between AD-associated bioenergetic dysfunction are discussed.

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Increased expressions of TLR2 and TLR4 on peripheral blood mononuclear cells from patients with Alzheimer's disease

Cited by 65 publications

References 36 publications

Retinoic acid receptor β deficiency reduces splenic dendritic cell population in a conditional mouse line

Retinoic acid receptor β deficiency reduces splenic dendritic cell population in a conditional mouse line

ROS and Brain Diseases: The Good, the Bad, and the Ugly

Bioenergetic Dysfunction and Inflammation in Alzheimerâ€™s Disease: A Possible Connection

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