Measurement of Glial Fibrillary Acidic Protein in Human Blood: Analytical Method and Preliminary Clinical Results

Mißler, U.; Wiesmann, Martin; Wittmann, Georg; Magerkurth, Olaf; Hagenström, H.

doi:10.1093/clinchem/45.1.138

Cited by 180 publications

(88 citation statements)

References 18 publications

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“…Interestingly, in one stroke study, GFAP concentration was used to differentiate between intracranial hemorrhage and ischemic stroke patients [68]. In 1999, Missler et al [69] demonstrated GFAP to be increased in the serum of patients suffering from severe head trauma. More recently, this protein has been confirmed as a specific marker for CNS damage [59,70,71] been demonstrated to be a potentially useful biomarker in predicting clinical outcome [50,59,70,72,73].…”

Section: Glial Fibrillary Acidic Protein (Gfap)mentioning

confidence: 99%

Biomarkers for the Clinical Differential Diagnosis in Traumatic Brain Injury-A Systematic Review

et al. 2013

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Rapid triage and decision-making in the treatment of traumatic brain injury (TBI) present challenging dilemma in "resource poor" environments such as the battlefield and developing areas of the world. There is an urgent need for additional tools to guide treatment of TBI. The aim of this review is to establish the possible use of diagnostic TBI biomarkers in (1) identifying diffuse and focal brain injury and (2) assess their potential for determining outcome, intracranial pressure (ICP), and responses to therapy. At present, there is insufficient literature to support a role for diagnostic biomarkers in distinguishing focal and diffuse injury or for accurate determination of raised ICP. Presently, neurofilament (NF), S100β, glial fibrillary acidic protein (GFAP), and ubiquitin carboxyl terminal hydrolase-L1 (UCH-L1) seemed to have the best potential as diagnostic biomarkers for distinguishing focal and diffuse injury, whereas C-tau, neuron-specific enolase (NSE), S100β, GFAP, and spectrin breakdown products (SBDPs) appear to be candidates for ICP reflective biomarkers. With the combinations of different pathophysiology related to each biomarker, a multibiomarker analysis seems to be effective and would likely increase diagnostic accuracy. There is limited research focusing on the differential diagnostic properties of biomarkers in TBI. This fact warrants the need for greater efforts to innovate sensitive and reliable biomarkers. We advocate awareness and inclusion of the differentiation of injury type and ICP elevation in further studies with brain injury biomarkers.

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Section: Glial Fibrillary Acidic Protein (Gfap)mentioning

confidence: 99%

Biomarkers for the Clinical Differential Diagnosis in Traumatic Brain Injury-A Systematic Review

et al. 2013

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“…Glial fibrillary acidic protein is a brain-specific protein that acts as the major integral component of the cell skeleton of astrocytes. After brain injury, GFAP releases the brain cells into the interstitial fluid in the environment and causes deterioration in the blood-brain barrier [23]. In many pathological con-ditions of the central nervous system and astrocytes, GFAP expression is increased.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of allopurinol on spinal cord injury in rats: a biochemical and immunohistochemical study

Baloğlu

Özkorkmaz

2019

Folia Morphol

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Background: Lesion in spinal cord causes a cascade of events such as the apoptosis of neurons and eventually, neurological dysfunction. Neurologic damage developing after acute spinal cord injury is also related with necrosis and free radical formation. Allopurinol, a xanthine oxidase inhibitor, was shown to have protective effects in several studies. B-cell lymphoma 2 (Bcl-2) family proteins regulate apoptosis. Apoptosis causes the death of neuronal cells, particularly neurons and oligodendrocytes in the spinal cord after lesion. Glial fibrillary acidic protein (GFAP) takes part in astrocyte and neuronal interconnection and synaptic transmission. Materials and methods: Male Sprague Dawley rats (n = 30) were divided as control, trauma, and trauma + allopurinol (i.p., 50 mg/kg of body weight) groups. Animals were applied a surgical procedure causing spinal cord injury and treated for 7 days then sacrificed under anaesthesia. The spinal cords were dissected, measurements of myeloperoxidase, malondialdehyde and glutathione were performed, remaining parts were fixed in 10% formaldehyde solution for histological and immunohistochemical evaluations. Results: Biochemical results exhibited an increase in myeloperoxidase levels in trauma group but a decrease in the allopurinol treatment group similar to malondialdehyde levels. Degenerative changes in multipolar and bipolar neurons together with apoptotic changes in some glial cells were observed in the trauma group whereas, mild degenerative changes were observed after allopurinol treatment. In the trauma group, negative GFAP expression in multipolar versus bipolar neuronal processes with a reduction in glial processes around blood vessels and positive GFAP expression were observed but, a regular and parallel positive GFAP expression of glial processes around blood vessels in the allopurinol treated group was apparent. Trauma group depicted a positive Bcl-2 expression in glial cells and in motor and bipolar neurons. On the contrary, negative Bcl-2 expression was noticed in the trauma + allopurinol group. Conclusions: This study is of importance to understand the effects of allopurinol in preventing degenerative changes in nerve and glial cells related to spinal cord injuries. (Folia Morphol 2019; 78, 4: 676-683)

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“…Following head trauma, serum concentrations of GFAP and S-100 concentrations correlate well during the rst 6 h (62). After the rst 6 h, however, the serum concentration of GFAP falls rapidly, whereas the serum concentration of protein S-100 remains increased for days.…”

Section: Comparisonsmentioning

confidence: 91%

Brain damage markers in children. Neurobiological and clinical aspects

Leviton

Dammann

2002

Acta Paediatrica

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Leviton A, Dammann O. Brain damage markers in children. Neurobiological and clinical aspects. Acta Paediatr 2002; 91: 9-13. Stockholm. ISSN 0803-5253The presence in blood of proteins normally con ned to the cytoplasm of brain cells is considered peripheral evidence of brain damage. Only recently have these proteins been measured in the blood of children at risk of brain damage. To show the value and limitations of measuring these proteins, we review their biology and the adult literature that has correlated the blood concentrations of these proteins with lesion size and dysfunction.Conclusion: We conclude that brain damage markers will increasingly be measured in the blood of newborns and other children at risk of brain damage.

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Measurement of Glial Fibrillary Acidic Protein in Human Blood: Analytical Method and Preliminary Clinical Results

Cited by 180 publications

References 18 publications

Biomarkers for the Clinical Differential Diagnosis in Traumatic Brain Injury-A Systematic Review

Biomarkers for the Clinical Differential Diagnosis in Traumatic Brain Injury-A Systematic Review

Neuroprotective effects of allopurinol on spinal cord injury in rats: a biochemical and immunohistochemical study

Brain damage markers in children. Neurobiological and clinical aspects

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