Microglial AGE-albumin is critical for neuronal death in Parkinson&amp;#39;s disease: a possible implication for theranostics

Bayarsaikhan, Enkhjargal; Bayarsaikhan, Delger; Lee, Jaesuk; Son, Myeongjoo; Oh, Seyeon; Moon, Jeongsik; Park, Hye-Jeong; Arivazhagan, Roshini; Kim, Seung Up; Song, Byoung–Joon; Jo, Seung-Mook; Byun, Kyunghee; Lee, Bong-Hee

doi:10.2147/ijn.s95077

Cited by 29 publications

(16 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Advanced glycation end products (AGEs) are potent noxious molecules that induce host cell death and contributing to organ damage. AGEs can induce neurodegenerative diseases [ 60 ] and associate with inflammation and oxidative stress [ 61 , 62 ]. Elevated levels of AGEs ( Fig 4A ) leads to the formations of reactive oxygen and nitrogen species which in turn elicit further AGEs formation [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

et al. 2020

View full text Add to dashboard Cite

Background Neuroinflammation causes neurodegenerative conditions like Alzheimer's disease (AD). Ipriflavone (IP), therapeutic compound to postmenopausal osteoporosis, has limited estrogenic activity and is accounted as AChE inhibitor. The developing of drug delivery systems to enable drug targeting to specific sites increases the drug therapeutic effect. Objective The aim of the present study was to formulate and evaluate ipriflavone loaded albumin nanoparticles (IP-Np) along with free ipriflavone against lipopolysaccharide (LPS) induced neuroinflammation in rats. Methods Neuroinflammation was induced by intra-peritoneal (i.p) injection of LPS (250 μg/kg rat body weight) then treatments were conducted with (1) ipriflavone at two doses 50 mg/kg and 5 mg/kg, (2) IP-Np (5 mg ipriflavone/kg) or (3) IP-Np coated with polysorbate 80 (IP-Np-T80) (5 mg ipriflavone/kg). The alteration of the inflammatory response in male adult Wistar rats' brain hippocampus was investigated by examining associated indices using biochemical and molecular analyses. Results A significant upsurge in inflammatory mediators and decline in antioxidant status were observed in LPS-induced rats. In one hand, ipriflavone (50 mg/kg), IP-Np and IP-Np-T80 ameliorated LPS induced brain hippocampal inflammation where they depreciated the level

show abstract

Section: Discussionmentioning

confidence: 99%

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Another form of soluble RAGE (sRAGE) (Figure 4) stems from proteolytic cleavage of the native RAGE expressed on the cell surface, both may act as decoys protecting from excessive ligand binding to RAGE and its consequent inflammatory cascades (Leonardis et al, 2012; Raposeiras-Roubín et al, 2010; Vazzana et al, 2009; Yan et al, 2010b). Further, the protective effect of esRAGE against dopaminergic neuronal death through inhibition of AGE-albumin build-up suggests the direct link between AGE-RAGE interaction and neurodegeneration (Bayarsaikhan et al, 2016). …”

Section: Pathways Underlying Age-mediated Effects On Aging and Age-rementioning

confidence: 99%

“…The RAGE interaction with the secreted AGE-albumin complexes has been shown to mediate an apoptotic cascade leading to the death of human dopaminergic neurons. Elevated AGE-albumin accumulation from activated microglia has been suggested as potential biomarkers for neurodegenerative diseases (Bayarsaikhan et al, 2016). Activation of macrophages leads to an exacerbated release of AGE-albumin complexes, a major AGE derivative that drives shared pathways resulting in the progression of neurodegeneration (Byun et al, 2017).…”

Section: Modeling the Influence Of Ages In Neurodegenerative Diseasesmentioning

confidence: 99%

The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality

et al. 2018

View full text Add to dashboard Cite

Accumulation of advanced glycation end products (AGEs) on nucleotides, lipids, and peptides/proteins are an inevitable component of the aging process in all eukaryotic organisms, including humans. To date, a substantial body of evidence shows that AGEs and their functionally compromised adducts are linked to and perhaps responsible for changes seen during aging and for the development of many age-related morbidities. However, much remains to be learned about the biology of AGE formation, causal nature of these associations, and whether new interventions might be developed that will prevent or reduce the negative impact of AGEs-related damage. To facilitate achieving these latter ends, we show how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGE-adduct development.

show abstract

“…Many studies have demonstrated AGEs are considered as potent toxic molecules that produce several non-communicable diseases such as T2D, CRC, cardiovascular diseases, Parkinson disease, AD (63)(64)(65)(66)(67)(68). Epidemiological evidence has reported that elevated AGEs were associated with CRC (69).…”

Section: Ligands Advanced Glycation End-productsmentioning

confidence: 99%

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

et al. 2020

View full text Add to dashboard Cite

Receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein taken in diverse chronic inflammatory conditions. RAGE behaves as a pattern recognition receptor, which binds and is engaged in the cellular response to a variety of damage-associated molecular pattern molecules, as well as HMGB1, S100 proteins, and AGEs (advanced glycation end-products). The RAGE activation turns out to a formation of numerous intracellular signaling mechanisms, resulting in the progression and prolongation of colorectal carcinoma (CRC). The RAGE expression correlates well with the survival of colon cancer cells. RAGE is involved in the tumorigenesis, which increases and develops well in the stressed tumor microenvironment. In this review, we summarized downstream signaling cascade activated by the multiligand activation of RAGE, as well as RAGE ligands and their sources, clinical studies, and tumor markers related to RAGE particularly in the inflammatory tumor microenvironment in CRC. Furthermore, the role of RAGE signaling pathway in CRC patients with diabetic mellitus is investigated. RAGE has been reported to drive assorted signaling pathways, including activator protein 1, nuclear factor-κB, signal transducer and activator of transcription 3, SMAD family member 4 (Smad4), mitogen-activated protein kinases, mammalian target of rapamycin, phosphoinositide 3-kinases, reticular activating system, Wnt/β-catenin pathway, and Glycogen synthase kinase 3β, and even microRNAs.

show abstract

Microglial AGE-albumin is critical for neuronal death in Parkinson's disease: a possible implication for theranostics

Cited by 29 publications

References 39 publications

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

Contact Info

Product

Resources

About