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Edna Grünblatt,
Camelia Maria Monoranu,
Manuela Apfelbacher,
Daniela Keller,
Tanja M Michel,
Irina Alafuzoff,
Isidro Ferrer,
Safa Al-Saraj,
Kathy Keyvani,
Andrea Schmitt,
Peter Falkai,
Jens Schittenhelm,
Catriona McLean,
Glenda M Halliday, Clive Harper,
Jürgen Deckert,
Wolfgang Roggendorf,
Peter Riederer
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ABSTRACT: Postmortem human brain tissue is widely used in neuroscience research, but use of tissue originating from different brain bank centers is considered inaccurate because of possible heterogeneity in sample quality. There is thus a need for well-characterized markers to assess the quality of postmortem brain tissue. Toward this aim, we determined tryptophan (TRP) concentrations, phosphofructokinase-1 and glutamate decarboxylase activities in 119 brain tissue samples. These neurochemical parameters were tested in samples from autopsied individuals, including control and pathological cases provided by 10 different brain bank centers. Parameters were assessed for correlation with agonal state, postmortem interval, age and gender, brain region, preservation and freezing methods, storage conditions and storage time, RNA integrity, and tissue pH value. TRP concentrations were elevated significantly (p = 0.045) with increased postmortem interval; which might indicate increased protein degradation. Therefore, TRP concentration might be one useful and convenient marker for estimating the quality of human postmortem brain tissue.
Journal of Neurochemistry 07/2009; 110(5):1400-8. · 4.06 Impact Factor
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Camelia-Maria Monoranu,
Manuela Apfelbacher,
Edna Grünblatt,
Bernhard Puppe,
Irina Alafuzoff,
Isidro Ferrer,
Safa Al-Saraj,
Kathy Keyvani,
Andrea Schmitt,
Peter Falkai,
Jens Schittenhelm,
Glenda Halliday,
Jillian Kril, Clive Harper,
Catriona McLean,
Peter Riederer,
Wolfgang Roggendorf
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ABSTRACT: Abstract Aims: Most brain diseases are complex entities. Although animal models or cell culture experiments mimic some disease aspects, human postmortem brain tissue remains essential to advance our understanding of brain diseases using biochemical and molecular techniques. Postmortem artifacts must be properly understood, standardized, and either eliminated or factored into such experiments. Here we examine the influence of several pre- and postmortem factors on pH, and discuss the role of pH as a biochemical marker for brain tissue quality. Methods: We assessed brain tissue pH in 339 samples from 116 brains provided by 8 different European and 2 Australian brain bank centres. We correlated brain pH with tissue source, postmortem delay, age, gender, freezing method, storage duration, agonal state, or and brain ischaemia. Results: Our results revealed that only prolonged agonal state and ischaemic brain damage influenced brain tissue pH next to repeated freeze/thaw cycles. Conclusions: pH measurement in brain tissue is a good indicator of premortem events in brain tissue and it signals limitations for postmortem investigations.
Neuropathology and Applied Neurobiology 01/2009; · 3.80 Impact Factor
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ABSTRACT: Preliminary results from the immunohistochemical examination of the brainstems of chronic alcoholics, suggest that alcohol may have a role in damage to the principal serotonergic (5HT) nuclei. This view is reinforced by evidence from previous animal experiments which demonstrated a reduction in 5HT neurons in the brains of alcohol-preferring rats and selective neurotoxicity to 5HT neurons following 5,6-dihydroxytryptamine-induced increased ethanol intake. It is speculated that, like other neurotoxins, alcohol or its metabolites cause degeneration of 5HT axons and axon terminals. It is possible that if axonal damage is sufficiently severe and chronic, the eventual consequence is cell death. This could be due to insufficient opportunity for repair and regrowth under repeated and sustained insults of high alcohol consumption.
Metabolic Brain Disease 02/1995; 10(1):25-30. · 2.20 Impact Factor
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ABSTRACT: Two patients with acute Wemicke's encephalopathy, with the diagnosis confirmed pathologically at autopsy, showed substantial vacuolation and neuronal degeneration in discrete nuclei of the thalamus. Thalamic vacuolation has not been described previously in acute Wernicke's encephalopathy. The use of frozen sections to minimize processing artifact was fundamental in demonstrating this pathology. The pathogenic mechanism underlying this change appears to be different to that seen in the more typical periventricular, mamillary body and brainstem lesions. We hypothesize that a specific neural pathway may be involved and suggest that this pathway could be the ascending nitric oxide-containing cholinergic pathway from the brainstem.
Metabolic Brain Disease 01/1993; 8(2):107-113. · 2.20 Impact Factor
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ABSTRACT: The loss of noradrenergic locus coeruleus neurons has been identified as the possible critical lesion inducing amnesia in alcoholic patients with the Wernicke-Korsakoff syndrome. The present study aims to test this hypothesis by quantifying the number of pigmented locus coeruleus neurons in 4 alcoholics with the Wernicke-Korsakoff syndrome, 5 alcoholics with Wernicke's encephalopathy alone but no amnesia, and 1 alcoholic and 5 age-matched controls with no neurological disorders. Apart from an increased vascularity in the locus coeruleus of alcoholics, no significant differences in the number, morphology or distribution of pigmented locus coeruleus neurons was noted between any of the groups analysed. There was a significant correlation between the number of locus coeruleus neurons and brain weight. These data demonstrate that neither alcohol neurotoxicity nor thiamine deficiency result in a reduction in the number of pigmented cells in the locus coeruleus and refute the hypothesis that locus coeruleus cell loss is critical for the amnesia in the Wernicke-Korsakoff syndrome.
Brain Research 01/1993; · 2.73 Impact Factor
