Cytokines Mediate the Adverse Effects of Social Stress in an Animal Model of Multiple Sclerosis

2008 ◽  
Author(s):  
Mary W. Meagher ◽  
C. Jane R. Welch
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Adverse Effects ◽  
Social Stress

The Voltage-Gated Sodium Channel Nav1.2 Contributes to Neurodegeneration in an Animal Model of Multiple Sclerosis

2016 ◽  
Vol 47 (S 01) ◽  
Author(s):  
W. Fazeli ◽  
B. Schattling ◽  
B. Engeland ◽  
M. Friese ◽  
D. Isbrand
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Sodium Channel ◽  
Voltage Gated Sodium Channel ◽  
Voltage Gated

scholarly journals Social stress and risk of declining cognition: a longitudinal study of men and women in the United States

2021 ◽  
Author(s):  
Jutta Lindert ◽  
Kimberley C. Paul ◽  
E. Lachman Margie ◽  
Beate Ritz ◽  
Teresa Seeman
Keyword(s):  
United States ◽  
Adverse Effects ◽  
Executive Functioning ◽  
Episodic Memory ◽  
Social Status ◽  
Social Stress ◽  
The United States ◽  
Subjective Social Status ◽  
Linear Regression Models ◽  
Men And Women

AbstractLimited research is available on the relationship between social stress and risk of declining cognition. We sought to examine whether social stress has adverse effects on risk of declining episodic memory and executive functioning in aging individuals. We used data from the MIDUS study, a national probability sample of non-institutionalized, English speaking respondents aged 25–74 living in the 48 contiguous states of the United States. The initial wave (1995) included 4963 non-institutionalized adults aged 32–84 (M = 55, SD = 12.4). We used an analytic sample from MIDUS-II (1996/1997) and MIDUS-III (2013) (n = 1821). The dependent variables are episodic memory and executive functioning, which were assessed with the Brief Test for Cognition (BTACT). The independent variables were social stress variables (subjective social status, family and marital stress, work stress and discrimination). To evaluate episodic memory and executive functioning changes over a time period of 10 years, we estimated adjusted linear regression models. Women report significantly lower subjective social status and more discrimination stress than men across all age groups. Controlling for education and income, age, and baseline episodic memory and executive functioning, lower subjective social status had additional adverse effects on declines in episodic memory in men and women. Marital risk had adverse effects on episodic memory in men but not in women. Daily discrimination had adverse effects on executive functioning on all individuals. Public health strategies should focus on reducing social stress in a socio-ecological perspective. Especially, subjective social status and discrimination stress might be a target for prevention efforts.

Current Treatment Strategies for Multiple Sclerosis - Efficacy Versus Neurological Adverse Effects

2012 ◽  
Vol 18 (2) ◽  
pp. 209-219 ◽  
Author(s):  
Martin S. Weber ◽  
Til Menge ◽  
Klaus Lehmann-Horn ◽  
Helena C. Kronsbein ◽  
Uwe Zettl ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Adverse Effects ◽  
Treatment Strategies ◽  
Current Treatment

The brain 3β-HSD up-regulation in response to deteriorating effects of background emotional stress: an animal model of multiple sclerosis

2021 ◽  
Author(s):  
Sogol Meknatkhah ◽  
Monireh-Sadat Mousavi ◽  
Pouya Sharif Dashti ◽  
Leila Azizzadeh Pormehr ◽  
Gholam Hossein Riazi
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
Emotional Stress ◽  
The Brain

AIM2 inflammasome activation in astrocytes occurs during the late phase of EAE

2021 ◽  
Author(s):  
William E. Barclay ◽  
M. Elizabeth Deerhake ◽  
Makoto Inoue ◽  
Toshiaki Nonaka ◽  
Kengo Nozaki ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Animal Model ◽  
Cell Death ◽  
Nervous System ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Inflammasome Activation ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
Experimental Autoimmune

ABSTRACTInflammasomes are a class of innate immune signaling platforms that activate in response to an array of cellular damage and pathogens. Inflammasomes promote inflammation under many circumstances to enhance immunity against pathogens and inflammatory responses through their effector cytokines, IL-1β and IL-18. Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are such autoimmune conditions influenced by inflammasomes. Despite work investigating inflammasomes during EAE, little remains known concerning the role of inflammasomes in the central nervous system (CNS) during the disease. Here we use multiple genetically modified mouse models to monitor activated inflammasomes in situ based on ASC oligomerization in the spinal cord. Using inflammasome reporter mice, we found heightened inflammasome activation in astrocytes after the disease peak. In contrast, microglia and CNS-infiltrated myeloid cells had few activated inflammasomes in the CNS during EAE. Astrocyte inflammasome activation was dependent on AIM2, but low IL-1β expression and no significant signs of cell death were found in astrocytes during EAE. Thus, the AIM2 inflammasome activation in astrocytes may have a distinct role from traditional inflammasome-mediated inflammation.SIGNIFICANCE STATEMENTInflammasome activation in the peripheral immune system is pathogenic in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, inflammasome activity in the central nervous system (CNS) is largely unexplored. Here, we used genetically modified mice to determine inflammasome activation in the CNS during EAE. Our data indicated heightened AIM2 inflammasome activation in astrocytes after the disease peak. Unexpectedly, neither CNS-infiltrated myeloid cells nor microglia were the primary cells with activated inflammasomes in SC during EAE. Despite AIM2 inflammasome activation, astrocytes did not undergo apparent cell death and produced little of the proinflammatory cytokine, IL-1β, during EAE. This study showed that CNS inflammasome activation occurs during EAE without associating with IL-1β-mediated inflammation.

RON-regulated innate immunity is protective in an animal model of multiple sclerosis

2005 ◽  
Vol 57 (6) ◽  
pp. 883-895 ◽  
Author(s):  
Shigeki Tsutsui ◽  
Farshid Noorbakhsh ◽  
Andrea Sullivan ◽  
Andrew J. Henderson ◽  
Kenneth Warren ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Innate Immunity ◽  
Animal Model
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