Inflammatory Chemokines Expression Variations and Their Receptors in APP/PS1 Mice

Vallés, Soraya L; Aldasoro, Martı́n; Aldasoro, Constanza; Valles, Soraya L.

doi:10.3233/jad-210489

Cited by 7 publications

(7 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In APP/PS1 mice, increased expression of CCL2 and CCR2 produced amyloidosis. The deficiency of CCL2 and CCR2 is followed by reduced Aβ phagocytosis and amyloid clearance (Jorda et al, 2021). In the early stage of AD pathology, microglia also release insulin-degrading enzyme (IDE), proteins of the matrix metalloproteinase 9 (MMP9), plasminogen and neprilysin, which are involved in Aβ degradation and induce Aβ clearance (Gao et al, 2018;Corraliza-Gómez et al, 2022).…”

Section: Clearance or Aggravation Of Aβmentioning

confidence: 99%

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

Long

Zhou

Cheng

et al. 2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

Alzheimer’s disease (AD), the most common type of senile dementia, includes the complex pathogenesis of abnormal deposition of amyloid beta-protein (Aβ), phosphorylated tau (p-tau) and neuroimmune inflammatory. The neurodegenerative process of AD triggers microglial activation, and the overactivation of microglia produces a large number of neuroimmune inflammatory factors. Microglia dysfunction can lead to disturbances in iron metabolism and enhance iron-induced neuronal degeneration in AD, while elevated iron levels in brain areas affect microglia phenotype and function. In this manuscript, we firstly discuss the role of microglia in AD and then introduce the role of microglia in the immune-inflammatory pathology of AD. Their role in AD iron homeostasis is emphasized. Recent studies on microglia and ferroptosis in AD are also reviewed. It will help readers better understand the role of microglia in iron metabolism in AD, and provides a basis for better regulation of iron metabolism disorders in AD and the discovery of new potential therapeutic targets for AD.

show abstract

Section: Clearance or Aggravation Of Aβmentioning

confidence: 99%

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

Long

Zhou

Cheng

et al. 2022

Front. Aging Neurosci.

View full text Add to dashboard Cite

show abstract

“…Bijay ( 68 ) found that CCL11 significantly promoted the migration of glial cells and induced glial cells to produce reactive oxygen species by upregulating nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1), which eventually led to neuronal death. In addition, the study shows that the expression of CCL11/CCR3 is very likely to be an important factor involved in the inflammatory induction and demyelination of AD ( 6 ). In this present study, the content of CCL11 in the plasma and brain of the 5xFAD mice was detected for the first time, and it was found that QFY reversed the excessive level of CCL11 in the brain and plasma of the 5xFAD mice.…”

Section: Discussionmentioning

confidence: 99%

“…Through the genetic research on the families of patients with AD, the researchers found three main pathogenic genes, namely, β-amyloid precursor protein (APP) gene, presenilin 1 (PS1) gene, and presenilin 2 (PS2) gene, which laid the foundation for the formation of Aβ to play an important role in the pathogenesis of AD ( 5 ). Microglia are activated by Aβ and then release cytokines, chemokines, and other neurotoxic substances (such as NO and superoxide), which lead to neuroinflammation in the brain of AD patients ( 6 ). The 5xFAD mice express gene APP with mutation K670N/M671L (Swedish), I716V (Florida), and V717I (London) and PS1 with mutation M146L and L286V.…”

Section: Introductionmentioning

confidence: 99%

Qi-fu-yin attenuated cognitive disorders in 5xFAD mice of Alzheimer's disease animal model by regulating immunity

Yang

et al. 2023

Front. Neurol.

View full text Add to dashboard Cite

IntroductionCognitive impairment is the main symptom of Alzheimer's disease (AD). Accumulating evidence implicate that immunity plays an important role in AD. Here, we investigated the effect of Qi-fu-yin (QFY) on cognitive impairment and cytokine secretion of 5xFAD mice.MethodsWe used 2.5-month-old 5xFAD transgenic mice for behavioral tests to observe the changes in cognitive function after QFY treatment. After the behavioral experiment, the whole brain, cortex and plasma of each mouse were collected for soluble Aβ analysis, immunohistochemical experiment and cytokine analysis.ResultsHere we found that the treatment of QFY ameliorated the ability of object recognition, passive avoidance responses and the ability of spatial learning and memory in 5xFAD mice. The deposits of β1 − 42 and Aβ1 − 40 were alleviated and the ration of Aβ1 − 42/Aβ1 − 40 was decrease in the plasma and brain of 5xFAD mice administrated with QFY. The administration of QFY promoted the secretion of anti-inflammatory cytokines, IL-5, IL-10 and G-CSF, and reduced the content of proinflammatory cytokines IFN-γ in plasma of 5xFAD mice. Notably, we found that the treatment of QFY decreased the concentration of CCL11 in the brain and plasma of 5xFAD mice.ConclusionThis suggested that QFY improved cognition and reduced Aβ deposits in 5xFAD mice by regulating abnormal immunity in 5xFAD mice. QFY may be as a potential therapeutic agent for AD.

show abstract

“…Protein extracts from quadriceps were mixed with equal volumes of SDS buffer (0.125 M Tris-HCl, pH 6.8, 2% SDS, 0.5% (v/v) 2-mercaptoethanol, 1% protease inhibitors, 1% bromophenol blue and 19% glycerol) and then boiled for five minutes. Protein concentration was determined using a modified Lowry method [ 26 ]. Proteins were separated using SDS-PAGE gels and transferred to polyvinylidene difluoride membranes.…”

Section: Methodsmentioning

confidence: 99%

Protective action of ultrasound-guided electrolysis technique on the muscle damage induced by notexin in rats

et al. 2022

Self Cite

View full text Add to dashboard Cite

It is known that exercise can be one of the causes of muscular damage. In recent times, physiotherapists and medical professionals have been employing USGET techniques to stimulate muscle recovery to improve its performance after the injury. We pretend to analyse if the Ultrasound-guided electrolysis (USGET) technique could reduce muscle damage, inflammation, and pain in the present study. Female Wistar rats were assigned to one of three different groups: control (C), notexin (NOT) and notexin with USGET (electrolysis at 6mA) (NOT+USGET). We used the USGT technique, based on electrical stimulation with a continuous current of 4 pulses at an intensity of 6 mA for 5 seconds, conveyed to the muscle. The response was tested with motor function tests. In these tests, we could observe an increase in time and foot faults when crossing a beam in the NOT group compared to C group rats. On the other hand, a significant decrease in both variables was detected in the NOT+USGET compared to the NOT group. Muscle power was measured with a grip strength test, obtaining far better performances in NOT+USGET rats when compared to NOT rats. Moreover, the USGET technique prevented the increase of pro-inflammatory proteins IL-6 and chemokines CCL3 (Chemokine (C-C motif) ligand 3), CCL4 (Chemokine (C-C motif) ligand 4), and CCL5 (Chemokine (C-C motif) ligand 5) with their receptor CCR5 (C-C chemokine receptor type 5), induced by notexin in the quadriceps. At the same time, the study evidenced a decrease in both CCR8 (C-C chemokine receptor type 5,) and NF-ᴋB (nuclear factor- ᴋB) expressions after USGET treatment. On the other hand, we obtained evidence that demonstrated anti-inflammatory properties of the USGET technique, thus being the increase in IL-10 (Interleukin 10) and IL-13 (Interleukin 13) in the NOT+USGET group compared to the NOT group. Furthermore, when applying NSGET after damage, an increase in anti-inflammatory mediators and reduction of pro-inflammatory mediators, which, overall, promoted muscle regeneration, was observed. These results support the idea that the NSGET technique improves muscle recovery after toxic damages, which would justify its employment.

show abstract

Inflammatory Chemokines Expression Variations and Their Receptors in APP/PS1 Mice

Cited by 7 publications

References 75 publications

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

Qi-fu-yin attenuated cognitive disorders in 5xFAD mice of Alzheimer's disease animal model by regulating immunity

Protective action of ultrasound-guided electrolysis technique on the muscle damage induced by notexin in rats

Contact Info

Product

Resources

About