scholarly journals Powerful beneficial effects of macrophage colony-stimulating factor on  -amyloid deposition and cognitive impairment in Alzheimer's disease

Brain ◽  
2008 ◽  
Vol 132 (4) ◽  
pp. 1078-1092 ◽  
Author(s):  
V. Boissonneault ◽  
M. Filali ◽  
M. Lessard ◽  
J. Relton ◽  
G. Wong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Amyloid Deposition ◽  
Colony Stimulating Factor ◽  
Beneficial Effects ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Amyloid β Protein Deposition in Osteopetrotic (op/op) Mice Is Reduced by Injections of Macrophage Colony Stimulating Factor

2005 ◽  
Vol 33 (6) ◽  
pp. 654-660 ◽  
Author(s):  
T Kawata ◽  
K Tsutsui ◽  
S Kohno ◽  
M Kaku ◽  
T Fujita ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Microglial Cell ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Colony Stimulating Factor ◽  
Β Protein ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

The deposition of amyloid β (Aβ) protein is a neuropathological change that characterizes Alzheimer's disease. Animals with the osteopetrosis (op/op) mutation suffer from a general skeletal sclerosis, a significantly reduced number of macrophages and osteoclasts in various tissues, and have no systemic macrophage colony stimulating factor (M-CSF). This study examined the effect that M-CSF injections had on Aβ deposition and microglial cell distribution in the brains of normal and op/op mice. Aβ-positive plaques were detected in the cerebral cortex of op/op mice, but not in normal mice. M-CSF reduced the numbers of Aβ-positive plaques in op/op mice. The microglial cell population was reduced in op/op mice compared with normal mice, and M-CSF increased the numbers to 65.8% of that observed in normal mice. Our results suggest that a clearer understanding of the role that microglial cells play in Aβ deposition may help determine the mechanisms involved in the pathogenesis of Alzheimer's disease.

scholarly journals Intracerebral GM-CSF contributes to transendothelial monocyte migration in APP/PS1 Alzheimer’s disease mice

2016 ◽  
Vol 36 (11) ◽  
pp. 1978-1991 ◽  
Author(s):  
De S Shang ◽  
Yi M Yang ◽  
Hu Zhang ◽  
Li Tian ◽  
Jiu S Jiang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Colony Stimulating Factor ◽  
Blood Brain ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
The Brain ◽  
Stimulating Factor

Although tight junctions between human brain microvascular endothelial cells in the blood–brain barrier prevent molecules or cells in the bloodstream from entering the brain, in Alzheimer’s disease, peripheral blood monocytes can “open” these tight junctions and trigger subsequent transendothelial migration. However, the mechanism underlying this migration is unclear. Here, we found that the CSF2RB, but not CSF2RA, subunit of the granulocyte-macrophage colony-stimulating factor receptor was overexpressed on monocytes from Alzheimer’s disease patients. CSF2RB contributes to granulocyte-macrophage colony-stimulating factor-induced transendothelial monocyte migration. Granulocyte-macrophage colony-stimulating factor triggers human brain microvascular endothelial cells monolayer tight junction disassembly by downregulating ZO-1 expression via transcription modulation and claudin-5 expression via the ubiquitination pathway. Interestingly, intracerebral granulocyte-macrophage colony-stimulating factor blockade abolished the increased monocyte infiltration in the brains of APP/PS1 Alzheimer’s disease model mice. Our results suggest that in Alzheimer’s disease patients, high granulocyte-macrophage colony-stimulating factor levels in the brain parenchyma and cerebrospinal fluid induced blood–brain barrier opening, facilitating the infiltration of CSF2RB-expressing peripheral monocytes across blood–brain barrier and into the brain. CSF2RB might be useful as an Alzheimer’s disease biomarker. Thus, our findings will help to understand the mechanism of monocyte infiltration in Alzheimer’s disease pathogenesis.

scholarly journals Granulocyte-macrophage colony-stimulating factor neuroprotective activities in Alzheimer’s disease mice

2018 ◽  
Vol 319 ◽  
pp. 80-92 ◽  
Author(s):  
Tomomi Kiyota ◽  
Jatin Machhi ◽  
Yaman Lu ◽  
Bhagyalaxmi Dyavarshetty ◽  
Maryam Nemati ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

A Cross-Sectional Exploration of Cytokine–Symptom Networks in Breast Cancer Survivors Using Network Analysis

2020 ◽  
pp. 084456212092753
Author(s):  
Ashley Henneghan ◽  
Michelle L. Wright ◽  
Garrett Bourne ◽  
Adam C. Sales
Keyword(s):  
Breast Cancer ◽  
Cognitive Impairment ◽  
Network Analysis ◽  
Breast Cancer Survivors ◽  
Interleukin 2 ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stress Fatigue ◽  
Stimulating Factor

Purpose The purpose of this study is to (a) visualize the symptom–cytokine networks (perceived stress, fatigue, loneliness, perceived cognitive impairment, daytime sleepiness, sleep quality, and 13 cytokines) and (b) explore centrality metrics of symptom–cytokine networks in breast cancer survivors who completed chemotherapy treatment. Methods Cross-sectional analysis of data collected from 66 breast cancer survivors who were on average three years post chemotherapy completion. Perceived stress, fatigue, loneliness, perceived cognitive impairment, daytime sleepiness, and sleep quality were measured with self-report instruments, and a panel of 13 cytokines was measured from serum using multiplex assays. Symptoms and cytokines were simultaneously evaluated with correlations, network analysis, and community analysis. Results Network analysis revealed the nodes with the greatest degree and closeness were interleukin-2, granulocyte-macrophage colony-stimulating factor, interleukin-13, and perceived cognitive impairment. Node betweenness was highest for perceived cognitive impairment and interleukin-2. Community analysis revealed two separate communities of nodes within the network (symptoms and the cytokines). Several edges connected the two communities including perceived cognitive impairment, stress, fatigue, depression, interleukin-2, granulocyte-macrophage colony-stimulating factor, interleukin-8, interleukin-13, and interleukin-10. Partial correlation analyses revealed significant negative relationships between interleukin-2 and fatigue, loneliness, stress, and perceived cognitive impairment ( rs = −.27 to −.37, ps < .05) and a significant negative relationship between perceived cognitive impairment and granulocyte-macrophage colony-stimulating factor ( r =  −.34, p <  .01). Conclusions Our analyses support that perceived cognitive impairment, stress, loneliness, depressive symptoms, and fatigue co-occur and extend the literature by suggesting that interleukin-2 may contribute to the underlying mechanistic pathway of these co-occurring symptoms. Our findings add to a growing body of literature that is shifting to study symptoms as they co-occur, or cluster, rather than individual symptoms.

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