scholarly journals Excitotoxicity-induced prostaglandin D2production induces sustained microglial activation and delayed neuronal death

2017 ◽  
Vol 58 (4) ◽  
pp. 649-655 ◽  
Author(s):  
Kensuke Iwasa ◽  
Shinji Yamamoto ◽  
Sosuke Yagishita ◽  
Kei Maruyama ◽  
Keisuke Yoshikawa
Keyword(s):  
Neuronal Death ◽  
Microglial Activation ◽  
Delayed Neuronal Death

scholarly journals Effects of Translocator Protein (18 kDa) Ligands on Microglial Activation and Neuronal Death in the Quinolinic-Acid-Injected Rat Striatum

2012 ◽  
Vol 3 (2) ◽  
pp. 114-119 ◽  
Author(s):  
Katherine R. Leaver ◽  
Aaron Reynolds ◽  
Sylvie Bodard ◽  
Denis Guilloteau ◽  
Sylvie Chalon ◽  
...  
Keyword(s):  
Quinolinic Acid ◽  
Neuronal Death ◽  
Microglial Activation ◽  
Translocator Protein ◽  
Rat Striatum ◽  
Translocator Protein 18 Kda

Accumulation of apolipoprotein E and β-amyloid-like protein in a trace of the hippocampal CA1 pyramidal cell layer after ischaemic delayed neuronal death

Neuroreport ◽  
1996 ◽  
Vol 7 (18) ◽  
pp. 3063-3068 ◽  
Author(s):  
Hirohisa Ishimaru ◽  
Koichi Ishikawa ◽  
Seiichi Haga ◽  
Mikio Shoji ◽  
Yoshihide One ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Pyramidal Cell ◽  
Neuronal Death ◽  
Cell Layer ◽  
Delayed Neuronal Death ◽  
Pyramidal Cell Layer ◽  
Hippocampal Ca1 ◽  
Β Amyloid

scholarly journals Effect of a New Calcium Entry Blocker, NB-818, on Delayed Neuronal Death in the Ischemic Gerbil Hippocampus.

1991 ◽  
Vol 56 (3) ◽  
pp. 279-286 ◽  
Author(s):  
Kazuo Kamei ◽  
Sonoko Tsuchida ◽  
Kazuhiro Taguchi ◽  
Masaru Nishikibe
Keyword(s):  
Neuronal Death ◽  
Calcium Entry ◽  
Delayed Neuronal Death ◽  
Calcium Entry Blocker ◽  
Entry Blocker

scholarly journals Induction of Caspase-3-Like Protease May Mediate Delayed Neuronal Death in the Hippocampus after Transient Cerebral Ischemia

1998 ◽  
Vol 18 (13) ◽  
pp. 4914-4928 ◽  
Author(s):  
Jun Chen ◽  
Tetsuya Nagayama ◽  
Kunlin Jin ◽  
R. Anne Stetler ◽  
Raymond L. Zhu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Death ◽  
Caspase 3 ◽  
Transient Cerebral Ischemia ◽  
Delayed Neuronal Death

scholarly journals Inflammation and JNK's Role in Niacin-GPR109A Diminished Flushed Effect in Microglial and Neuronal Cells With Relevance to Schizophrenia

2021 ◽  
Vol 12 ◽  
Author(s):  
Sabrina H. Ansarey
Keyword(s):  
Inflammatory Mediators ◽  
Neuronal Death ◽  
Microglial Activation ◽  
Negative Symptoms ◽  
Genome Wide Association Study ◽  
Genetic Mutation ◽  
Genome Wide ◽  
Ultra High Risk ◽  
Altered Proteins

Schizophrenia is a neuropsychiatric illness with no single definitive aetiology, making its treatment difficult. Antipsychotics are not fully effective because they treat psychosis rather than the cognitive or negative symptoms. Antipsychotics fail to alleviate symptoms when patients enter the chronic stage of illness. Topical application of niacin showed diminished skin flush in the majority of patients with schizophrenia compared to the general population who showed flushing. The niacin skin flush test is useful for identifying patients with schizophrenia at their ultra-high-risk stage, and understanding this pathology may introduce an effective treatment. This review aims to understand the pathology behind the diminished skin flush response, while linking it back to neurons and microglia. First, it suggests that there are altered proteins in the GPR109A-COX-prostaglandin pathway, inflammatory imbalance, and kinase signalling pathway, c-Jun N-terminal kinase (JNK), which are associated with diminished flush. Second, genes from the GPR109A-COX-prostaglandin pathway were matched against the 128-loci genome wide association study (GWAS) for schizophrenia using GeneCards, suggesting that G-coupled receptor-109A (GPR109A) may have a genetic mutation, resulting in diminished flush. This review also suggests that there may be increased pro-inflammatory mediators in the GPR109A-COX-prostaglandin pathway, which contributes to the diminished flush pathology. Increased levels of pro-inflammatory markers may induce microglial-activated neuronal death. Lastly, this review explores the role of JNK on pro-inflammatory mediators, proteins in the GPR109A-COX-prostaglandin pathway, microglial activation, and neuronal death. Inhibiting JNK may reverse the changes observed in the diminished flush response, which might make it a good therapeutic target.

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