Neuron-specific enolase as an effective immunohistochemical marker for injured axons after fatal brain injury

Abstract

Recently, it has been reported that a diagnosis of diffuse axonal injury in cases with a short survival period can be made with the use of immunolabelling for beta-amyloid precursor protein (APP). We examined whether immunostaining for neuron-specific enolase (NSE) can also be a useful marker for the detection of axonal injury in its early stages. Sections of the corpus callosum from 19 cases of head injury and from 9 cases of no head injury were immunostained for NSE and stained by the standard Holmes' silver method. For comparison, serial sections from several cases were immunostained for APP. Immunostaining for NSE as well as for APP, labelled injured axons in head injury cases with as early as 1.5 h survival where Holmes' staining failed to detect any changes of axons. Since NSE and APP labelled only injured axons but not normal axons, the results were readily interpretable. These findings indicate that NSE should be an effective marker for the detection of axonal injury in its early stages.

Rauwolfia vomitoria and Gongronema latifolium extracts influences cerebellar cortex

“…NSE is a cytosolic protein that functions as brain-specific glycolytic enzyme, and plays an important role in intracellular energy metabolism [48]. It is expressed by mature neurons and cells of neuronal origin, and thus regarded as a marker of the neuronal state [49,50], but becomes markedly expressed after brain injury [51]. It is reported that RV cause neuronal injury [20,22], and this may be a reason for the marked expression of the enolase, which may be deleterious to the normal function of the cerebellar cortical cells.…”

Serum biomarkers as predictors of long-term outcome in severe traumatic brain injury: analysis from a randomized placebo-controlled Phase II clinical trial

“…7,16,17,19,20 However, its specificity for neurons is limited by confounding factors like sepsis, hypoperfusion, extracranial trauma, bleeding, and liver or kidney damage, in which serum NSE level also increases, making it of less clinical relevance in patients with polytrauma. 7,20 The NSE levels in the first 72 hours postinjury have been more closely related with outcome, 21 probably because of its short half-life.…”

“…3,29,32 Due to the limitations of existing clinical and radiological evaluations for assessment and prognostication of TBI severity, there has been a considerable paradigm shift toward development and use of biochemical markers to delineate the extent of brain tissue damage and to independently predict global outcome. Neuronal (ubiquitin C-terminal hydrolase L1, neuron-specific enolase [NSE]) 4,7,[19][20][21] and glial (glial fibrillary acidic protein [GFAP], S100-B) 10,18,28,31,37 markers have been studied extensively over the past decade in various laboratory and clinical studies, with heterogeneous results. Similarly, the role of proinflammatory (interleukin [IL]-6, IL-1, tumor necrosis factor-a [TNF-a]) and antiinflammatory (IL-4, IL-10, transforming growth factor) cytokines has been validated in recent trials.…”

Two different immunostaining patterns of beta-amyloid precursor protein (APP) may distinguish traumatic from nontraumatic axonal injury

“…The details of the head injury cases and control cases are summarized in Tables 1 and 2, respectively. From each case, formalin-fixed, paraffin-embedded sections of corpus callosum were immunostained for APP as described previously [11,16]. Briefly, after deparaffinization and heating to 95°C in citrate buffer (10 mM, pH 6.0) for 20 min, the sections were immersed in 0.3 % H 2 O 2 -phosphate-buffered saline (PBS; pH 7.2) for 30 min to block endogenous peroxidase activity.…”

“…However, immunostaining for APP can detect axonal bulbs as early as 2-3 h after head injury [2][3][4][5][6][7][8][9]. Moreover, some axonal bulbs can be detected at 35 min [10] or 90 min [11] after head injury depending on the case.…”