Immunohistochemistry of neuron-specific enolase in neurons of the medulla oblongata from human autopsies

Nogami, Makoto; Takatsu, Akihiro; Endo, Noriko; Ishiyama, Ikuo

doi:10.1016/s0065-1281(98)80034-2

Cited by 14 publications

(11 citation statements)

References 13 publications

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“…DAT and COMT expression were unchanged, and therefore DA recycling may not be affected. We also measured the protein and mRNA levels of neuron specific enolase (NSE), as a marker of neuronal cells and can be used to measure postmortem tissue integrity in the absence of acute injury [49, 50]. The difference in NSE protein and mRNA levels were insignificant between control and AD groups.…”

Section: Discussionmentioning

confidence: 99%

Disturbed Neurotransmitter Transporter Expression in Alzheimer’s Disease Brain

Chen

Reese²,

Kim³

et al. 2011

JAD

111

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Alzheimer disease (AD) is a neurodegenerative disorder characterized by memory loss and behavioral and psychological symptoms of dementia. An imbalance of different neurotransmitters – glutamate, acetylcholine, dopamine, and serotonin - has been proposed as the neurobiological basis of behavioral symptoms in AD. The molecular changes associated with neurotransmission imbalance in AD are not clear. We hypothesized that altered reuptake of neurotransmitters by vesicular glutamate transporters (VGLUTs), excitatory amino acid transporters (EAATs), the vesicular acetylcholine transporter (VAChT), the serotonin reuptake transporter (SERT), or the dopamine reuptake transporter (DAT)) are involved in the neurotransmission imbalance in AD. We tested this hypothesis by examining protein and mRNA levels of these transporters in postmortem prefrontal cortex from 10 AD patients and 10 matched non-AD controls. Compared with controls, protein and mRNA levels of VGLUTs, EAAT1–3, VAChT, and SERT were reduced significantly in AD. Expression of DAT and catechol O-methyltransferase (COMT) was unchanged. Reduced VGLUTs and EAATs may contribute to an alteration in glutamatergic recycling, and reduced SERT could exacerbate depressive symptoms in AD. The reduced VAChT expression could contribute to the recognized cholinergic deficit in AD. Altered neurotransmitter transporters could contribute to the pathophysiology of AD and are potential targets for therapy.

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Section: Discussionmentioning

confidence: 99%

Disturbed Neurotransmitter Transporter Expression in Alzheimer’s Disease Brain

Chen

Reese²,

Kim³

et al. 2011

JAD

111

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“…NSE immunostaining in the brain is useful for evaluating brain damage from various cases. This also supports the notion that NSE immunoreactivity is spared in less necrotic neurons (Nogami et al, 1998a). The present findings, which showed an increase in NSE immunoreactivity and nissl staining in the single dose PTZ-treated group, were correlated with the results of Nogami et al (1998a).…”

Section: Discussionsupporting

confidence: 88%

“…This also supports the notion that NSE immunoreactivity is spared in less necrotic neurons (Nogami et al, 1998a). The present findings, which showed an increase in NSE immunoreactivity and nissl staining in the single dose PTZ-treated group, were correlated with the results of Nogami et al (1998a). In another study that quantified NSE (+) neurons in the frontal cortex and hippocampus of the rat brain after systemic administration of kainic acid, while the concentrations of NSE remained unaffected in the frontal cortex, NSE levels were found to be significantly decreased in the hippocampus (Ding et al, 2000).…”

Section: Discussionsupporting

confidence: 88%

Cellular and Molecular Mechanisms Underlying Epilepsy: An Overview with Our Findings

Yardımoğlu¹,

İlbay²,

Dalçįk³

et al. 2012

Epilepsy - Histological, Electroencephalographic and Psychological Aspects

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“…In these cases NSE-positive neurons indicate vital reaction after TBI. 27,28 Also, NSE has been defined as an effective marker of axonal injury within the CNS in its early stages 29 and of brain stress in general. 30 Both S100 and NSE are clinical biomarkers used in patients with TBI.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Investigation of S100 and NSE in Cases of Traumatic Brain Injury and Its Application for Survival Time Determination

Krohn

Dreßler

Bauer

et al. 2015

Journal of Neurotrauma

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The availability of markers able to provide insight into protein changes in the central nervous system after fatal traumatic brain injury (TBI) is limited. The present study reports on the semi-quantitative assessments of the immunopositive neuroglial cells (both astrocytes and oligodendrocytes) and neurons for S100 protein (S100), as well as neuronal specific enolase (NSE), in the cerebral cortex, hippocampus, and cerebellum with regard to survival time and cause of death. Brain tissues of 47 autopsy cases with TBI (survival times ranged between several minutes and 34 d) and 10 age- and gender-matched controls (natural deaths) were examined. TBI cases were grouped according to their survival time in acute death after brain injury (ABI, n = 25), subacute death after brain injury (SBI, n = 18) and delayed death after brain injury (DBI, n = 4). There were no significant changes in the percentages of S100-stained astrocytes between TBI and control cases. The percentages of S100-positive oligodendrocytes in the pericontusional zone (PCZ) in cases with SBI were significantly lower than in controls (p < 0.05) and in the ABI group (p < 0.05). In the hippocampus, S100-positive oligodendrocytes were significantly lower in cases with ABI and SBI (both, p < 0.05), compared with controls. It is of particular interest that there were also S100-positive neurons in the PCZ and hippocampus in TBI cases after more than 2 h survival but not in ABI cases or controls. The percentages of NSE-positive neurons in the hippocampus were likewise significantly lower in cases with ABI, compared with controls (p < 0.05) but increased in cases with SBI in PCZ (p < 0.05). In conclusion, the present findings emphasize that S100 and NSE-immunopositivity might be useful for detecting the cause and process of death due to TBI. Further, S100-positivity in neurons may be helpful to estimate the survival time of fatal injuries in legal medicine.

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Immunohistochemistry of neuron-specific enolase in neurons of the medulla oblongata from human autopsies

Cited by 14 publications

References 13 publications

Disturbed Neurotransmitter Transporter Expression in Alzheimer’s Disease Brain

Disturbed Neurotransmitter Transporter Expression in Alzheimer’s Disease Brain

Cellular and Molecular Mechanisms Underlying Epilepsy: An Overview with Our Findings

Immunohistochemical Investigation of S100 and NSE in Cases of Traumatic Brain Injury and Its Application for Survival Time Determination

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