Recommended Pages at jneuroinflammation.com
JNI | Abstract | Prenatal stress causes alterations in the morphology of microglia and the inflammatory response of the hippocampus of adult female mice
jneuroinflammation.com — “Stress during fetal life increases the risk of affective and immune disorders later in life. The altered peripheral immune response caused by prenatal stress may impact on brain function by the modification of local inflammation. In this study we have explored whether prenatal stress results in alterations in the immune response in the hippocampus of female mice during adult life.” View full resource at jneuroinflammation.com
Most Recently Shared on April 20, 2012 at 6:33 pm By:
Prenatal stress causes alterations in the morphology of microglia and the inflammatory response of the hippocamp... http://t.co/FkOeh0LX
JNI | Abstract | Therapeutic targeting of Kruppel-like factor 4 abrogates microglial activation
jneuroinflammation.com — “Neuroinflammation occurs as a result of microglial activation in response to invading micro-organisms or other inflammatory stimuli within the central nervous system. According to our earlier findings, Kruppel-like factor 4 (Klf4), a zinc finger transcription factor, is involved in microglial activation and subsequent release of proinflammatory cytokines, tumor necrosis factor alpha, macrophage chemoattractant protein-1 and interleukin-6 as well as proinflammatory enzymes, inducible nitric oxide” View full resource at jneuroinflammation.com
Most Recently Shared on March 19, 2012 at 12:35 pm By:
BioMed Central Medical Journal
Honokiol reduces inflammation in activated microglia http://t.co/QCy388Ab from #JournalofNeuroinflammation #neuroscience
JNI | Abstract | Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge
jneuroinflammation.com — “There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many diseases. However, long-term outcomes of chronic psychological stressors that elicit a neuroinflammatory response remain unknown.” View full resource at jneuroinflammation.com
Most Recently Shared on January 16, 2012 at 5:41 pm By:
BioMed Central Medical Journal
#Stressed out mice suffer from #neuroinflammation http://t.co/FH53x12X
JNI | Abstract | Wallerian degeneration: Gaining perspective on inflammatory events after peripheral nerve injury
jneuroinflammation.com — “In this review, we first provide a brief historical perspective, discussing how peripheral nerve injury (PNI) may have caused World War I. We then consider the initiation, progression, and resolution of the cellular inflammatory response after PNI, before comparing the PNI inflammatory response with that induced by spinal cord injury (SCI).” View full resource at jneuroinflammation.com
Most Recently Shared on August 31, 2011 at 10:49 am By:
Pete Shuster Promotional and Health Business Administrator
#journalofneuroinflammation Wallerian degeneration: Perspective on inflammatory events after peripheral nerve injury http://t.co/ffdVPfA
JNI | Full text | Subchronic infusion of the product of inflammation prostaglandin J2 models sporadic Parkinson's disease in mice
jneuroinflammation.com — “Chronic neuroinflammation is implicated in Parkinson's disease (PD). Inflammation involves the activation of microglia and astrocytes that release high levels of prostaglandins. There is a profound gap in our understanding of how cyclooxygenases and their prostaglandin products redirect cellular events to promote PD neurodegeneration. The major prostaglandin in the mammalian brain is prostaglandin D2, which readily undergoes spontaneous dehydration to generate the bioactive cyclopentenone prosta” View full resource at jneuroinflammation.com
Most Recently Shared on July 26, 2009 at 2:30 pm By:
Pete Shuster Promotional and Health Business Administrator
New pub on Parkinson's and inflammation: http://www.jneuroinflammation.com/content/6/1/18
