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- Neurodegeneration (2)
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- Cyclooxygenase (1)
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Articles 1 - 4 of 4
Full-Text Articles in Medicine and Health Sciences
Updates On And Advances In Therapeutic Strategies For Traumatic Brain Injury, Samantha M. Portis, Paul R. Sanberg
Updates On And Advances In Therapeutic Strategies For Traumatic Brain Injury, Samantha M. Portis, Paul R. Sanberg
Neurosurgery and Brain Repair Faculty Publications
No abstract provided.
Hippocampal Cholinergic Neurostimulating Peptide As A Possible Modulating Factor Against Glutamatergic Neuronal Disability By Amyloid Oligomers, Toyohiro Sato, Yoshiaki Ohi, Daisuke Kato, Masayuki Mizuno, Hiroshi Takase, Tetsuko Kanamori, Cesar V. Borlongan, Akira Haji, Noriyuki Matsukawa
Hippocampal Cholinergic Neurostimulating Peptide As A Possible Modulating Factor Against Glutamatergic Neuronal Disability By Amyloid Oligomers, Toyohiro Sato, Yoshiaki Ohi, Daisuke Kato, Masayuki Mizuno, Hiroshi Takase, Tetsuko Kanamori, Cesar V. Borlongan, Akira Haji, Noriyuki Matsukawa
Neurosurgery and Brain Repair Faculty Publications
Despite having pathological changes in the brain associated with Alzheimer's disease (AD), some patients have preserved cognitive function. A recent epidemiological study has shown that diet, exercise, cognitive training, and vascular risk monitoring interventions may reduce cognitive decline in at-risk elderly people in the general population. However, the details of molecular mechanisms underlying this cognitive function preservation are still unknown. Previous reports have demonstrated that enriched environments prevent the impairment of hippocampal long-term potentiation (LTP) through β2-adrenergic signals, when LTP is incompletely suppressed by synthetic amyloid-β (Aβ) oligomers. The cholinergic network from the medial septal nucleus (MSN) is also a …
Chronic Inflammation And Apoptosis Propagate In Ischemic Cerebellum And Heart Of Non-Human Primates, Sandra A. Acosta, Sherwin Mashkouri, Diana Nwokoye, Jea Y. Lee, Cesar V. Borlongan
Chronic Inflammation And Apoptosis Propagate In Ischemic Cerebellum And Heart Of Non-Human Primates, Sandra A. Acosta, Sherwin Mashkouri, Diana Nwokoye, Jea Y. Lee, Cesar V. Borlongan
Neurosurgery and Brain Repair Faculty Publications
The major pathological consequences of cerebral ischemia are characterized by neurological deficits commonly ascribed to the infarcted tissue and its surrounding region, however, brain areas, as well as peripheral organs, distal from the original injury may manifest as subtle disease sequelae that can increase the risks of co-morbidities complicating the disease symptoms. To evaluate the vulnerability of the cerebellum and the heart to secondary injuries in the late stage of transient global ischemia (TGI) model in non-human primates (NHP), brain and heart tissues were collected at six months post-TGI. Unbiased stereological analyses of immunostained tissues showed significant Purkinje cells loss …
Genetic And Histological Alterations Reveal Key Role Of Prostaglandin Synthase And Cyclooxygenase 1 And 2 In Traumatic Brain Injury–Induced Neuroinflammation In The Cerebral Cortex Of Rats Exposed To Moderate Fluid Percussion Injury, Hideki Shojo, Cesar V. Borlongan, Tadashi Mabuchi
Genetic And Histological Alterations Reveal Key Role Of Prostaglandin Synthase And Cyclooxygenase 1 And 2 In Traumatic Brain Injury–Induced Neuroinflammation In The Cerebral Cortex Of Rats Exposed To Moderate Fluid Percussion Injury, Hideki Shojo, Cesar V. Borlongan, Tadashi Mabuchi
Neurosurgery and Brain Repair Faculty Publications
After the initial insult in traumatic brain injury (TBI), secondary neurodegeneration occurs that is intimately associated with neuroinflammation. Prostaglandin (PG) synthases and cyclooxygenase (COX) 1 and 2 may contribute to inflammation in the brain. Temporal and spatial expression features of PG and COX1 and 2 following trauma may guide the development of antineuroinflammation strategies. Here, we examined PG synthase signaling and COX1 and 2 gene expression levels and COX-1- and 2-positive cell types and their temporal localization in TBI-induced brain in an effort to reveal their participation in the disease’s evolving neuroinflammation. Using brain samples from the cerebral cortex of …