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PubMed2004

Frontotemporal dementia with ubiquitinated neuronal inclusions presenting with primary lateral sclerosis and parkinsonism: clinicopathological report of an autopsy case.

We report a case displaying upper motor sign, parkinsonism, and behavioral abnormality, with marked degeneration of the precentral cortex, neostriatum and frontotemporal lobes, as well as ubiquitinated neuronal inclusions. The patient was a 66-year-old male at the time of death. At age 57, he noticed progressive difficulties in speaking and swallowing. At age 60, he was severely anarthric and displayed emotional lability and incontinence. Neurologically, very poor movement of tongue was observed, but without atrophy or fasciculation. Deep tendon reflexes were hyperactive. Grasp reflex and snout reflex were also positive. Needle electromyography revealed no abnormalities. A diagnosis of primary lateral sclerosis and character change was made. At age 62, he developed bradykinesia and rigidity of the neck and all extremities. Treatment with carbidopa-levodopa was initiated, but resulted in minimal improvement. At age 65, he was bed-ridden, and had repeated occurrences of aspiration pneumonia; he died of pneumonia. Neuropathological examination revealed marked atrophy of the frontal and temporal lobes with Betz cells completely absent and moderate atrophy of the neostriatum. The spinal cord and nerve roots appeared normal. Immunohistochemically, ubiquitin-positive but tau-negative intraneuronal inclusions were found in the frontal and temporal cortices, including the precentral cortex and the hippocampal dentate gyrus, and the neostriatum. This case could be included with inclusion-associated disorders such as frontotemporal dementia or amyotrophic lateral sclerosis with dementia, and furthermore, predominant upper motor sign and parkinsonism could represent phenotypes of clinical manifestations with such inclusions.

Cerebral Cortex↗

PubMed2006

The morphological basis of mental dysfunction in Parkinson's disease.

Mental dysfunction including dementia in Parkinson's disease (PD), the incidence of which averages 20-40%, is suggested to have six-fold lifetime risk compared to age-matched controls. It is caused by a variety of functional and pathological lesions ranging from damage to subcortical-cortical networks to cortical and limbic Lewy body and neuritic Alzheimer pathologies, the relationship and impact of which are still under discussion. Based on two consecutive autopsy series of PD, with prevalence of cognitive impairment of 33% to 35.7%, its essential morphological changes and their impact on the natural history (survival) are discussed. Whereas cortical Lewy body stages 5 and 6 without additional pathologies only rarely were associated with dementia, around 20% of demented PD cases were classified as dementia with Lewy bodies (DLB) with variable degrees of Alzheimer (AD) pathology, and around one third showed severe neuritic AD lesions which occurred in PD patients with later disease onset and significantly shorter survival. Frequent close relations in the severity between alpha-synuclein and tau-pathologies suggest synergistic reaction and common underlying pathogenesis of both lesions. Clinico-pathological studies in PD showed a significantly negative relation between cognitive impairment and neuritic AD lesions somewhat different from that in AD, suggesting that neuritic AD pathology, either alone or in combination with cortical and limbic Lewy bodies, are major causes of mental and cognitive dysfunction in PD.

Aged↗

PubMedDate not supplied

The roles of corneal mucopolysaccharides and water contents in post-mortem corneal clouding.

The quantitative changes in mucopolysaccharides (MPS) and water contents in post-mortem rabbit corneas were studied. On the basis of the results, the post-mortem periods were classified into 4 stages. The first stage was during the first day after death when the MPS and the corneal water contents were observed to have maintained their initial values and the cornea was "clear". The second was 1 to 3 days after death when the MPS remained at approximately their initial value, whereas the water contents were very pronounced. In this second stage the cornea was "a little clear" or "cloudy". The third was 3 to 6 days after death when the MPS were found to have decreased gradually, but the water contents maintained their high level. The cornea in this third stage was "cloudy" or "very cloudy". The fourth was 6 or more days after death when the two parameters were found to have decreased significantly, and the cornea was "very cloudy".

Animals↗

PubMedDate not supplied

[The morphofunctional changes in the air-blood barrier in hypostatic pneumonia].

An autopsy lung tissue was studied from former patients with hypostatic pneumonia following stroke. Two groups of patients were identified among the decreased: those having died within 4-24 hours after stroke (group I); those having died by day 4-6 after stroke (group II). The control was lung tissue from those persons having been killed in road-motoring accidents. General morphologic methods of investigation were employed together with a special method of immunofluorescent investigation according to Coon [correction of Kuns], using monospecific antibodies labelled with fluorescence isothiocyanate directed against heavy polypeptides of human immunoglobulins. The findings collected showed a significant increase in permeability of the constituent components of the blood-air barrier for native autogenous immunoglobulins recordable before the leucocytes' outgo into the alveolar cavities. The protective alterations are heterogeneous, varying with a section of focal pneumonia, their degree being related to the time spans during which the pathological process evolves. Under above conditions the bronchial barrier is acknowledged to be more stable since its permeability is not much changeable regardless of the stage of the illness.

Accidents, Traffic↗

PubMed2006

Post-mortem toxicology.

Studies examining post-mortem processes are difficult to conduct since changes will have already occurred when the body arrives at the mortuary. While control of collection site for blood can minimize changes in concentration it is very difficult to conduct experiments in humans aimed at understanding the mechanisms and determining the extent of such changes. The use of appropriate animal models can be useful in this regard providing the species and conditions are carefully chosen. Pharmacokinetic studies in humans are also very useful for understanding the changes in drug concentration with time in blood (and other fluids) and also for improving our understanding of drug effects. Unfortunately, doses of illicit drugs that can be given are relatively low to guarantee safety hence extrapolations are made to real life situations. Individual case studies can be useful to describe an unusual or particularly interesting circumstances but little useful information can be obtained when trying to ascertain the role of competing factors, e.g. role of individual drugs when multiple drugs are present, varying toxicity between route of administration, and the role of age or natural disease when drugs are also present. Epidemiological approaches by reviewing large numbers of related cases are the most powerful tool to obtain this information. All of these studies need to operate under the ethical and legal framework appropriate for a jurisdiction. This paper discusses the relative merits of scientific approaches to research in post-mortem toxicology and provides guidance on the most appropriate techniques for future studies.

Ethics, Research↗

PubMed1976

[Post mortem temperature equilibration of the structures of the head. I. Thermometric techniques and principal investigations (author's transl)].

Special thin and flexible thermometric probes showing a diameter of 1 mm and a sharp end were used for post mortem (p.m.) thermometric studies in several tissues. Brain temperatures were measured by inserting a double probe through the superior orbital fissura thus allowing to record the central and the peripheral brain regions separately. Another probe was inserted into the galea and a fourth into the liver. Temperature changes were recorded simultaneously. Many variables of the human head were measured. Sixteen corpses were investigated. The results were as follows: 1. Of all temperature curves registered those of the central brain regions showed the smallest variance. 2. The p.m. temperature curve of the brain shows a sigmoid shape with a rather short "plateau" in the beginning. 3. In the early p.m. phase there is an increasing difference of temperatures between central and peripheral brain regions amounting to 2-4, 6 degrees C in the time period between 78th and 128th minute. 4. The insertion of the thin probes does not cause visible damages. Thus it should be considered for use in forensic practice. 5. Some artificial "head models" were constructed and temperature decrease recorded after warming. The curves showed the same type of sigmoid shape as those obtained from the corpses. 6. Of the possible variables measured that could influence the temperature decrease only the density of the hair seems to be of interest.

Brain↗

PubMed1988

Spinal cord trauma: in search of the meaning of granular axoplasm and vesicular myelin.

The rapid appearance of selective axonal calcification following experimentally induced spinal cord impact injury has suggested that there is a sudden influx of intracellular calcium which mediates many of the pathological changes subsequent to the trauma. Granular dissolution of axoplasm and vesicular disruption of myelin are the most characteristic alterations in the affected white matter. These changes, which appear early and progress, are identical to those that can be induced by exposing myelinated axons to increased extracellular calcium or to calcium ionophores. These observations have led us to develop the hypothesis that calcium mediates the destruction of traumatized axons in the spinal cord by stimulating calcium-activated neutral proteinases (CANP), which in turn degrade axonal and myelin proteins. A rapid increase in CANP activity has been demonstrated in our experimental rat trauma model and a CANP has been isolated from rat spinal cord myelin which degrades both neurofilament and myelin proteins. However, the interpretation of the role of calcium has been complicated by the fact that granular axoplasm and vesicular myelin can be induced under conditions other than those favorable for CANP enhancement. The ultimate proof of the calcium hypothesis will depend on analyzing early intracellular ionic fluxes and correlating these with the localization of calcium-mediated enzymes and the evolution of pathological events.

Animals↗

PubMed1999

The effects of age and spontaneous adenoma formation on trophic activity in the rat pituitary gland: a comparison with trophic activity in the human pituitary and in human pituitary adenomas.

The effects of ageing on trophic activity in the pituitary gland and the molecular events that underlie pituitary tumour formation are poorly understood. In the present study we have used an extremely accurate system to analyse trophic activity in human pituitary tumours and compared our findings with trophic activity in spontaneous rat pituitary adenomas and with changes in basal rates of turnover as the animals age. Thin, hematoxylin and eosin-stained pituitary sections from groups of male Wistar rats aged 6 weeks to 16 months, killed at 90-min intervals after receiving a single intraperitoneal bolus of colchicine to block cellular passage through mitosis, were evaluated histologically. Extremely accurate quantification of small changes in the prevalence of trophic events, and thus the rate of cell turnover, was achieved using a dedicated computerized aid to manual cell counting. Results were compared with the prevalence of mitotic activity in 24 spontaneous rat pituitary adenomas and with a series of 97 archival human pituitary adenomas and 24 normal human pituitary glands obtained at autopsy. In rats, average basal pituitary cell turnover declined by over 95% between 6 weeks and 16 months of age. Concurrent with this decline was a marked increase in the prevalence of adenoma formation. The prevalence of mitotic activity in spontaneous rat pituitary adenomas averaged almost twice that seen in normal, young rat pituitary and exceeded 16 times that seen in the pituitary of aged animals. In contrast, when compared to normal human pituitary tissue, average trophic activity in human pituitary adenomas remained extremely low.

Adenoma↗

PubMed2005

Presymptomatic semantic impairment in a case of fronto-temporal lobar degeneration associated with the +16 mutation in MAPT.

We describe a patient who came to neurological attention because of his at-risk status for the +16 exon 10 splice mutation in the tau gene (microtubule associated protein tau, MAPT), which had given rise to progressive behavioural disturbances in two of his siblings. The patient began to exhibit early signs of behavioural disturbance at around the age of symptom onset in both of his siblings. Although he did not spontaneously complain of difficulties in the domain of language, he met clinical, radiological and neuropsychological criteria for semantic dementia. On the assumption that his illness is mediated by the same pathological process as those of his siblings, we propose that this clinical picture represents the earliest changes of a semantic impairment - a phase of the illness that is often retrospectively described by patients and their relations, but has never previously been documented at first hand. Although typical of semantic dementia in many respects, the illness had several interesting and atypical features that emerged on detailed testing: first, he exhibited no insight into his difficulties; secondly, progression over a twelve-month interval was unusually slow; thirdly, he evinced a striking and consistent advantage for nonliving over living concepts; fourthly, a differential impairment of distinctive over shared knowledge did not emerge except when items that he could still name were compared with those for which he was anomic. Finally, the availability of post mortem pathological analysis from the brains of both of his affected siblings allowed us to attribute his illness to a specific pathological process which is considered unusual for patients with this clinical phenotype.

Case-Control Studies↗

PubMed1981

Autopsy sampling and elemental analysis: errors arising from post-mortem changes.

The implication of post-mortem changes such as cell swelling, imbibition and autolysis on the elemental composition of body organs has been studied in rats. Liver has been chosen as an example. Retaining the liver inside the intact dead body for different periods of time at ambient temperature induced significant changes in its weight due to post-mortem tissue degeneration. Livers from animals that were frozen at -15 degrees C also showed significant decreases in weight when they were thawed on the third day. The effect of these changes on the concentrations of various elements depended on the association of the elements with extracellular fluid and intracellular components. For example, concentration of K+ was affected more by the lysis of the cell and sustained losses up to 30 per cent. in relation to the control values, while the total content was reduced by more than 40 per cent. as a result of both lysis and tissue liquefaction. For Na+, differences ranging from +10 to -20 per cent. in concentrations and +20 to -40 per cent. in total content were observed which could be explained by the movement of fluid in and out of the organ. Among trace elements, variation observed for iron ranged from -20 to +40 per cent., while both copper and zinc were found to fluctuate between -20 and +20 per cent. The loss observed in the total content in the liver for the five trace elements studied (Cu, Fe, Mn, Rb and Zn) was found to be about 20 to 40 per cent.

Animals↗

PubMed2005

Changes in nitric oxide levels in striated muscles of rats following different types of death.

BACKGROUND: Nitric oxide is a signal molecule regulating the organism functions in living bodies. The aim of this study was to investigate the NO levels of striated muscles after different types of death in rats. METHODS: Nitric oxide levels in the muscles of masseter, triceps, and quadriceps obtained from right and left sides of 24 Spraque-Dawley rats following death were investigated. The rats were divided into three groups as cervical dislocation (control) group, electric shock group, and drowning group. After applying a light anesthesia, the rats were killed by cervical dislocation, electric shock and drowning. The samples were taken immediately and 120 minutes after death. RESULTS: In all muscle types of all groups, NO concentrations were lower in samples obtained 120 minutes after death than in those obtained immediately after death. NO concentrations were lower in the electric shock and drowning group than in the control group for both times. CONCLUSION: We can conclude that the type of death may affect the occurrence of rigor mortis and NO measurement may give an important clue in evaluation the mode of death.

Animals↗

PubMed2000

Diagnosis of bovine spongiform encephalopathy: a review.

Cows affected with bovine spongiform encephalopathy (BSE) display chronic neurological signs consisting of behavioural changes, abnormalities of posture and movement, and/or hyperaesthesia. At present, there are no laboratory test available to diagnose BSE in the live animal. In this article, we describe the post-mortem diagnostic examination of brains from BSE-suspected cattle as currently performed at ID-Lelystad. The routine laboratory diagnosis of BSE consists of histopathological examination of the brain and detection of the modified prion protein, PrP(BSE), in brain tissue. These tests, however, have the disadvantage of being laborious and time consuming, so that results are available only after several days. Recently, at ID-Lelystad a new post-mortem test has been developed that enables screening of larger volumes of brain samples for PrP(BSE) within 1 day. This BSE test is especially suited for slaughterline monitoring. A preliminary validation study has shown that both sensitivity and specificity are 100% compared to the gold diagnostic standard of histopathology.

Animals↗

PubMedDate not supplied

Developmental changes in molecular forms of immunoreactive adrenocorticotropin in the anterior pituitary gland of humans.

In extracts of anterior pituitary tissue obtained at autopsy of fetal, infant, and adult humans, five molecular forms of immunoreactive ACTH (ACTHi) were detected that had apparent molecular weights of approximately 4044, 30-34, 24-28, 16-18, and 4.5 kilodaltons (K). The relative proportion of each molecular form of ACTHi was similar in tissues that were extracted at the time of autopsy and in tissues that were stored frozen (-20 degrees C) for up to 2 years prior to extraction. We found that 40-44K ACTHi comprised a significantly greater proportion of total ACTHi in fetuses (12.3+/-3.5%) than in adults (3.8+/-0.8%); intermediate amounts of this form of ACTHi (8.0+/-4.1%) were found in tissues obtained from infants. On the other hand, the proportion of 4.5 K ACTHi in fetal pituitaries (67 %) was less than that in those of adults (84 %). The ratio of 40-44/30-34K ACTHi was significantly greater (P<0.001) in fetuses (1.46+/-0.12) and infants (1.31+/-0.07) than in adults (0.52+/-0.07). The ontogenetic differences in molecular forms of pituitary ACTHi are thought to reflect alterations in the processing of proopiomelanocortin as a function of human development.

Adrenocorticotropic Hormone↗

PubMed2005

Post mortem degradation of nucleosides in the brain: comparison of human and rat brains for estimation of in vivo concentration of nucleosides.

There is an increasing attention paid for nucleoside metabolism and changes of nucleoside concentrations in human brain because of its pathological and physiological relevance. In order to determine the post mortem degradation of nucleosides and nucleoside metabolites, the concentrations of four nucleosides and three nucleobases were measured in rat and neurosurgical human cerebral cortical samples with 30s to 24h post mortem delay. Adenosine degradation coefficient (a multiplying factor for calculating concentrations of investigated substances for the living state) was 0.886 for human brain at 2 h post mortem time, while it was 1.976 for rats. Hypoxanthine, an adenosine degradation product had coefficients 0.564 for human brain and 0.812 for the rat brain. We provide data and degradation coefficients for the concentrations of adenosine, guanosine, inosine, uridine, uracil, hypoxanthine and xanthine with 2, 4, 6 and 24 h post mortem delay. We also report a method how to validate human neurosurgical brain samples in terms of sample preparation and statistical analysis.

Aged↗

PubMed2003

Dihydropyrimidinase related protein-2 as a biomarker for temperature and time dependent post mortem changes in the mouse brain proteome.

Proteome analysis in the central nervous system area represents a large and important challenge in drug discovery. One major problem is to obtain representative and well characterized tissues of high quality for analysis. We have used brain tissues from normal mice to study the effect of post mortem time (up to 32 h) and temperature (4 degrees C and room temperature) on protein expression patterns. A number of proteins were identified using mass spectrometry and potential markers were localized. One of the proteins identified, dihydropyrimidinase related protein-2 (DRP-2), occurs as multiple spots in two-dimensional electrophoresis gels. The ratio between the truncated form of DRP-2 (fDRP-2) and full length DRP-2 is suggested as an internal control that can be used as a biomarker of post mortem time and post mortem temperature between unrelated brain protein samples. Results of this study may be useful in future efforts to detect disease specific alterations in proteomic studies of human post mortem brain tissues.

Animals↗

PubMed1979

Effects of post-mortem storage on synaptic 5-HT binding and uptake in mammalian brain.

Synaptosomes and synaptic membranes were isolated from rat brain after various storage times and temperatures of the tissue. Synaptosomal 5-HT uptake was diminished by about 20% within the first hour after decapitation. No significant change in the incorporation rate was observed for the seven proceeding hours if the brains were stored at room temperature. After an initial decrease of about 15%, 5-HT incorporation remained constant for at least 24 hours if the tissue was stored at 4 degrees C. Electron micrographs showed that nerve endings were highly disrupted by freezing and thawing of the brains.--The capacity of high affinity 5-HT binding to the microsomal synaptic membrane fraction decreased with the first hour by about 13% to 120--130 fmoles 5-HT/mg protein and remained almost constant for the next eight hours. Freezing at --80 degrees C of whole brain or of isolated membranes did not affect 5-HT receptor interaction.--The capacity of specific 5-HT binding to membranes isolated from human post-mortem brain was comparable to that found with synaptic membranes from rat brain. In contrast to the control values, a significant decrease in 5-HT binding was observed in membrane fractions isolated from brain after cerebral insult.

Animals↗

PubMed1987

Regional differences in the changes in rat brain GABA concentrations post mortem and following inhibition of the synthesis and metabolism.

Experimentally induced changes in the concentration of GABA were studied in regions where GABA is present, predominantly in nerve terminals (substantia nigra, pituitary gland) or outside nerve terminals (corpus callosum). Some other regions (cerebellum, cuneate nucleus, corpus striatum, hippocampus) were included where the cellular localization of GABA is less certain. The post mortem increase in GABA was about equal percentage-wise in all regions indicating that it occurs in all locations where GABA is present. The increase in GABA following the GABA alpha-ketoglutaric acid aminotransferase inhibitor gamma-acetylenic GABA was much greater in the corpus callosum than in the other regions indicating that this enzyme is more important for the GABA present outside than inside the GABA nerve terminals. The glutamic acid decarboxylase inhibitor 4-deoxypyridoxine decreased the endogenous concentration of GABA and it inhibited the increase in GABA induced by gamma-acetylenic GABA in the substantia nigra and in the pituitary gland, but not in the corpus callosum, indicating that this compound inhibits the decarboxylase mainly in the GABA nerve terminals.

Alkynes↗

PubMed2004

Increased caveolin-1 expression in Alzheimer's disease brain.

Increasing evidence suggests that cholesterol plays a central role in the pathophysiology of Alzheimer's disease (AD). Caveolin is a cholesterol-binding membrane protein involved in cellular cholesterol transport. We investigated the changes in the protein amount of hippocampal caveolin of autopsy-confirmed AD and aged-matched control subjects. Our results demonstrate that caveolin protein levels in the hippocampus and caveolin mRNA in the frontal cortex are up-regulated in AD by approximately two-fold, compared to control brains. These results suggest a relationship between caveolin-1 expression levels and a dysregulation of cholesterol homeostasis at the plasma membrane of brain cells. In support of this hypothesis, a significant increase in caveolin protein levels has also been observed in hippocampal tissue from ApoE-deficient (knockout) and aged wild-type mice; two situations associated with modifications of transbilayer distribution of cholesterol in brain synaptic plasma membranes. These results indicate that caveolin over-expression is linked to alterations of cholesterol distribution in the plasma membrane of brain cells and are consistent with the notion of a deterioration of cholesterol homeostasis in AD.

Aged↗