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PubMed2001

The neuronal calcium sensor protein VILIP-1 is associated with amyloid plaques and extracellular tangles in Alzheimer's disease and promotes cell death and tau phosphorylation in vitro: a link between calcium sensors and Alzheimer's disease?

To investigate whether the observed association of intracellular neuronal calcium sensor (NCS) proteins with amyloid plaques and neurofibrillar tangles in Alzheimer brains is linked to a possible neuroprotective or neurotoxic activity of the protein, we performed cytotoxicity tests in PC12 cells transfected with the calcium sensor protein VILIP-1 (visinin-like protein) and the calcium buffer protein calbindin-D28K. Whereas VILIP-1 expression enhanced the neurotoxic effect of ionomycin already at low ionophore concentrations, calbindin-D28K protected against ionomycin-induced cytotoxicity only at high ionomycin and therefore calcium concentrations. However, in double-transfected cells calbindin-D28K rescued VILIP-1-mediated cytotoxicity at low ionomycin concentrations. Since VILIP-1 was found to be associated with fibrillar tangles in Alzheimer brains, we tested whether VILIP-1 has an influence on tau hyperphosphorylation. VILIP-1 expression enhanced hyperphosphorylation of tau protein compared to nontransfected or calbindin-D28K-transfected cells. These results raise the possibility that the observed reduction in VILIP-1-expressing cells may indicate a selective vulnerability of these neurons and that the calcium sensor protein is involved in the pathophysiology of Alzheimer's disease. The calcium sensor protein may influence tau phosphorylation and have a role in calcium-mediated neurotoxicity opposed to the previously discovered protective effect of calcium buffer proteins.

Alzheimer Disease↗

PubMed1989

Effects of chronic in vivo replacement of choline with a false cholinergic precursor.

Chronic administration to rats of a diet in which all choline is replaced by NADe, an unnatural choline analog, results in a classical hypocholinergic syndrome characterized by progressive loss of learning and memory, hyperkinesis, hyperreactivity and hyperalgesia. Discontinuation of the artificial diet results in rapid elimination of NADe from both free and phospholipid-bound pools in all tissues studied, but the behavioral effects recede more slowly and incompletely. These results are consistent with a model in which choline and NADe compete in both acetylcholine and phospholipid synthesis, resulting in selective vulnerability of cholinergic neurons. Histological studies are in progress to determine whether microanatomical changes are also consistent with this model.

Animals↗

PubMed2006

The effect of neuromelanin on the proteasome activity in human dopaminergic SH-SY5Y cells.

In Parkinson's disease (PD), the selective depletion of dopamine neurons in the substantia nigra, particular those containing neuromelanin (NM), is the characteristic pathological feature. The role of NM in the cell death of dopamine neurons has been considered either to be neurotoxic or neuroprotective, but the precise mechanism has never been elucidated. In human brain, NM is synthesized by polymerization of dopamine and relating quinones, to which bind heavy metals including iron. The effects of NM prepared from human brain were examined using human dopaminergic SH-SY5Y cells. It was found that NM inhibits 26S proteasome activity through generation of reactive oxygen and nitrogen species from mitochondria. The mitochondrial dysfunction was also induced by oxidative stress mediated by iron released from NM. NM accumulated in dopamine neurons in ageing may determine the selective vulnerability of dopamine neurons in PD.

Blotting, Western↗

PubMed2006

Iron and Friedreich ataxia.

Friedreich ataxia is due to insufficient levels of frataxin, a mitochondrial iron chaperone that shields this metal from reactive oxygen species (ROS) and renders it bioavailable as Fe II. Frataxin participates in the synthesis of iron-sulfur clusters (ISCs), cofactors of several enzymes, including mitochondrial and cytosolic aconitase, complexes I, II and III of the respiratory chain, and ferrochelatase. It also plays a role in the maintenance of ISCs, in particular for mitochondrial aconitase. A role of frataxin in heme synthesis has been postulated, but is controversial. Insufficient frataxin leads to deficit of ISC enzymes and energy deficit. Iron levels increase in mitochondria. Oxidative stress may result from respiratory chain dysfunction and from direct reaction between iron and ROS. Stress pathways are activated that may lead to apoptosis or other forms of cell death. The basis for the selective vulnerability of specific neurons, like sensory neurons, is still unknown.

Animals↗

PubMed2004

The natural course of lesion development in brain ischemia.

Histopathologic and NMR imaging studies show that focally ischemic brain lesions tend to increase in size over time. In animal models of stroke as well as in patients presenting with hemispheric stroke, considerable lesion growth was observed. In focal cerebral ischemia, lesions predominantly enlarge early (<12 hrs postinsult) and show complete ischemic injury due to pan necrosis in the vast majority of affected tissue. In global cerebral ischemia--a condition that is present after cardiac arrest--lesions appear late (>12 hrs) in selectively vulnerable brain regions and neurons are damaged by apoptosis. The short resuscitation time of the brain explains why periods of global ischemia result in widespread and global loss of energy metabolites combined with diffuse brain edema and global damage. Mechanisms involved in lesion growth include excitotoxicity, peri-infarct depolarizations, lactacidosis, microcirculatory disturbances, and flow-metabolism uncoupling among others. Problems involved in the subject under focus are related to maturation phenomena of injury and the different imaging modalities (metabolic imaging, NMR imaging, positron emission tomography) that require a subtly differentiated interpretation of the alterations observed.

Animals↗

PubMed2003

Evaluation of neuronal cell death after a new global ischemia model in infant mice.

For the first time we set up a new model for global ischemia in the infant mice, and time-dependent changes of the blood-brain barrier (BBB) disruption and neuronal cell death were investigated in detail. Infant C57/B16 mice (postnatal 13 days) were anesthetized with inhalation of sevoflurane in N2O/O2 (70/30%) and were subjected to global ischemia by bilateral common carotid artery occlusion (CCAO) for 25 minutes. Disruption of BBB was noted at 4 hours and increased up to 24 hours after the injection of 2% Evan's Blue in the transient CCAO (tCCAO) model. Evaluation of neuronal cell death was determined with toluidine blue staining. Morphological changes of neurons after tCCAO were clearly observed in the hippocampal CA1 region but were slightly detected in the CA3 region. However, there were no morphological changes in the hippocampal dentate gyrus, the neocortex, the striatum and the hypothalamus. The number of survival neurons in the CA1 was significantly decreased at 2 days and sustained up to 4 days after tCCAO. These data indicate that this method is very useful to induce selective vulnerability in mouse hippocampus, and it provides a reliable ischemic model in infant mice.

Animals↗

PubMed2003

Cécile & Oskar Vogt: the significance of their contributions in modern neuroscience.

A) By introducing and propagating the use of multidisciplinary approaches, Cécile and Okar Vogt played a decisive role in establishing brain research as a distinct branch of science, and thus laid the foundations for modern Neuroscience. B) The Vogts' and Brodmann's monumental work on brain cytoarchitectonics, supplemented with electrical stimulation of the exposed cerebral cortex, demonstrated correlations between evoked functional responses and the topography of brain regions endowed with distinct cytoarchitectonic structure (topistic units). This opened the field of functional brain mapping, a subject hotly pursued at the present time. C) One of the most important aspects of Pathoclisis is that the Vogts based their theory on molecular genetics. They envisaged that in any topistic unit the neurons had a different specific, molecular ("physico-chemical") composition, accounting for differences observed in the dynamics of neuronal development and involution. In sublethal injury, the induced genomic reactivity varies according to the selective vulnerability of various topistic units. Thus, in cerebral ischemia, the fluctuating genomic reactivity may play a significant role in designing therapeutic strategies, which would include enhancing regenerative expressions and suppressing harmful ones. D) The pathoclisis theory may be of assistance in analyzing the nature of various genetic disorders, which could be considered for the application of gene therapy.

Germany↗

PubMed1999

Mechanism and consequences of nerve cell death in Parkinson's disease.

The etiology of Parkinson's disease remains unknown, making it difficult to develop therapeutical approaches to stop the progression of the disease. The best known treatment to date is based on the use of L-DOPA or dopaminergic agonists. These are merely substitutive therapies and have limitations because of their side effects. Thus, the development of new therapeutical strategies will require a far better knowledge of the mechanism and the consequences of nerve cell death in Parkinson's disease. Parkinson's disease is characterized by a selective vulnerability of sub-populations of dopaminergic neurons in the mesencephalon. The fact that the neurons which degenerate in Parkinson's disease are already sensitive to oxidative stress in control subjects and the reported increased production of oxygen free radicals in Parkinson's disease suggest that oxidative stress may be involved in the mechanism of nerve cell death. Furthermore, oxygen free radicals are also involved in an oxygen-dependent pro-apoptotic pathway stimulated by the inflammatory reaction observed in Parkinson's disease. These data suggest that anti-oxidant or anti-inflammatory treatments may slow down the progression of the disease. On the other hand, new substitutive therapies may be developed by trying to restore the activity of the neurons located downstream from the nigrostriatal pathway. Indeed, the nigrostriatal denervation induces a hyper-activity of the output structures of the basal ganglia (internal segment of the globus pallidus and substantia nigra pars reticulata), as demonstrated in various animal models of the disease. These changes in the activity of the output structures of the basal ganglia seem to be directly induced by the hyperactivity of the glutamatergic afferent fibers from the subthalamic nucleus. The fact that L-DOPA treatment or a reduction in the activity of the subthalamic nucleus alleviate the symptoms of the disease and restore the activity of the output structures of the basal ganglia in parkinsonism suggests that these structures play a key role in the pathophysiology of the disease and could represent a potential therapeutic target.

Animals↗

PubMed1999

Role and mechanisms of secondary mitochondrial failure.

Ischemia is accompanied by mitochondrial dysfunction, as assessed by measurements of mitochondrial respiratory activities in vitro. Following brief periods of ischemia, mitochondrial function is usually normalized during reperfusion. However, particularly after ischemia of longer duration, reperfusion may be accompanied by secondary mitochondrial failure. After short periods of ischemia this is observed in selectively vulnerable areas and, after intermediate to long periods of ischemia, in other areas as well. However, it has remained unsettled if the mitochondrial dysfunction is the result or the cause of cell death. Although it has been commonly assumed that such failure is secondary to cell injury by other mechanisms, recent results suggest that mitochondrial dysfunction may be the cause of cell death. Indirect evidence for this postulate is provided by experiments showing that cyclosporin A (CsA), when allowed to cross the blood-brain barrier, is a potent neuroprotectant. CsA is a virtually specific blocker of the mitochondrial permeability transition (MPT) pore, a voltage-gated channel allowing molecules and ions with a mass < 1500 Daltons to pass the inner mitochondrial membrane. Experiments on isolated cells in vitro demonstrate that cell calcium accumulation or oxidative stress triggers the assembly of an MPT pore, which leads to collapse of the mitochondrial membrane potential, to ATP hydrolysis, to enhanced production of reactive oxygen species (ROS), and to cell death. The beneficial effect of CsA could thus be related to its ability to block the MPT pore. Longer periods of ischemia, such as occurs after transient middle cerebral artery (MCA) occlusion, lead to pan-necrotic lesions (infarction). In the rat, recirculation following 2 h of MCA occlusion leads to partial normalization of the bioenergetic state but this is followed within 4-6 h by secondary bioenergetic failure. The latter seems unrelated to blockade of the microcirculation, but correlates to secondary mitochondrial failure. The brain damage incurred is ameliorated by the spin trap alpha-phenyl-N-butyl nitrone (PBN) and by the immunosuppressant FK506 even when given 1-3 h after the start of recirculation. The two drugs also prevent the secondary mitochondrial failure during early recirculation, suggesting that such failure is pathogenetically important. Probably, though, the mitochondrial dysfunction involves not only the assembly of an MPT pore but also other mechanisms. Since recirculation is associated with release of mitochondrial proteins it is not unlikely that such proteins, e.g. cytochrome c, trigger cascades of events leading to cell death.6.

Animals↗

PubMed2002

Temporal and regional profile of neuronal and glial cellular injury after induction of kaolin hydrocephalus.

AIM: To study regional and temporal pattern of glial and neuronal reaction to induction of kaolin hydrocephalus in adult rats. Enzyme- and immunohistochemistry was performed in 20 adult rats with kaolin-hydrocephalus after 2, 4, 6 and 8 weeks to glial glutamatergic transmission activity (GLDH) and neuronal nitrous oxide synthetic activity (nNOS). Also, glial fibrillary acidic protein (GFAP), 68 kd neurofilament protein (NF68) and synaptophysin (SYN38) and basic fibroblastic growth-factor (bFGF) were stained. Results were quantified by imaging analysis (SCION IMAGE) and expressed as relative immunopositive area. After 2 weeks, nNos-activity increased in cortical and hippocampal neurones (CA1 and CA3) and GLDH-activity also showed increases, most significant in periventricular white matter (25.7 +/- 3.8 vs. 15.5 +/- 4.9; p < 0.001) and hippocampus (p < 0.01). After 4 or 6 weeks, global cortical GLDH-activity showed further marked increases (25.7 +/- 3.9 vs. 11.3 +/- 1.5; p < 0.05), while sustained structural changes have occurred: GFAP decreased in periventricular (3.3 +/- 0.5 vs. 6.3 +/- 1.2; p < 0.01), hippocampal and cortical astrocytes (0.9 +/- 0.34 vs. 5.0 +/- 0.7%; p < 0.01), whereas NF68 in cortical efferent neurones increased (6.5 +/- 1.5% vs. 4.7 +/- 0.1; p < 0.01) followed by a decrease in cortical and hippocampal (CA1) SYN 38 (p < 0.05). Acute glial and neuronal reactions were almost functional and in chronic stages sustained structural changes predominated. Since neuronal reactions were pronounced in selective vulnerable areas glial reaction was not restricted to periventricular astrocytes.

Animals↗

PubMed1997

Leukocyte-endothelium interactions in global cerebral ischemia.

A closed cranial window was implanted in male Mongolian Gerbils to investigate leukocyte-endothelium interactions (LEI) at the brain surface in global cerebral ischemia (GCI) by intravital fluorescence microscopy. Four days after 15 min of bilateral common carotid artery occlusion the ischemic tissue damage was histologically analysed in selectively vulnerable areas of the brain. The frequency of Rhodamine 6G labeled leukocytes rolling along ("roller") and firmly attached ("sticker") to postcapillary endothelium was assessed before and up to 180 min after GCI. As compared to the sham operated control animals induction of LEI was found in animals with GCI, following a steady increase up to a significant level attained at 60 min (rollers) or at 120 min of reperfusion (sticker), respectively (p < 0.05). In animals with cerebral ischemia histological assessment revealed a significant decrease of viable neurons in the CA1-sector of hippocampus (neurons/mm2 +/- SEM: 1308 +/- 71 vs. 829 +/- 106), in parietal neocortex (727 +/- 17 vs. 542 +/- 49), and in striatum (547 +/- 26 vs. 352 +/- 49; p < 0.01), respectively. A significant correlation between the extent of irreversible neuronal damage and the frequency of leukocyte adherence to the endothelium could not be established. Nevertheless a direct correlation between the number of surviving neurons and of rolling leukocytes was observed, which may be suggestive of a protective potential of leukocyte rolling.

Animals↗

PubMed1997

Selective impairments of mitochondrial respiratory chain activity during aging and ischemic brain damage.

Cumulative oxidative damage to mitochondrial deoxyribonucleic acid (DNA) with subsequent defects in oxidative phosphorylation may reduce the capacity of the aging brain to cope with metabolic stress. This may contribute to the age related increase in cerebral infarct size that has been documented following permanent middle cerebral artery occlusion (MCAO) in the rat. This hypothesis was evaluated by assessing mitochondrial respiratory chain complex activity in both ischemic and non ischemic brain tissue of adult (10 month) and aged (28 month) male Wistar rats, six hours after occlusion of the left middle cerebral artery. Aging was associated with a significant decline in cerebral mitochondrial function with impairment of the activities of complexes I. II and IV. The individual respiratory chain complexes also exhibited selective vulnerability to a focal cerebral ischemic lesion, with significant impairment of complex I activity in the lesioned hemisphere of both age groups. The age related decline in complex I activity may be important in the enhanced susceptibility of the aging brain to ischemic neuronal damage.

Aging↗

PubMed1996

Neuroprotective efficacy of microvascularly-localized versus brain-penetrating antioxidants.

The 21-aminosteroid (lazaroid) tirilazad mesylate has been demonstrated to be a potent inhibitor of lipid peroxidation and to reduce traumatic and ischemic damage in a number of experimental models. Currently, tirilazad is being actively investigated in phase III clinical trials in head and spinal cord injury, ischemic stroke and subarachnoid hemorrhage. This compound acts in large part to protect the microvascular endothelium and consequently to maintain normal blood-brain barrier (BBB) permeability and cerebral blood flow autoregulatory mechanisms. However, due to its limited penetration into brain parenchyma, tirilazad has generally failed to affect delayed neuronal damage to the selectively vulnerable hippocampal CA1 and striatal regions. Recently, we have discovered a new group of antioxidant compounds, the pyrrolopyrimidines, which possess significantly improved ability to penetrate the BBB and gain direct access to neural tissue. Several compounds in the series, such as U-101033E, have demonstrated greater ability to protect the CA1 region in the gerbil transient forebrain ischemia model with a post-ischemic therapeutic window of at least four hours. In addition, U-101033E has been found to reduce infarct size in the mouse permanent middle cerebral artery occlusion model in contrast to tirilazad which is minimally effective. These results suggest that antioxidant compounds with improved brain parenchymal penetration are better able to limit certain types of ischemic brain damage compared to those which are localized in the cerebral microvasculature. On the other hand, microvascularly-localized agents like tirilazad appear to have better ability to limit BBB damage.

Animals↗

PubMed1991

Spatial-frequency-dependent changes in the human pattern electroretinogram after acute acetyl-L-carnitine administration.

Acetyl-L-carnitine (LAC) is a neuroactive compound that is thought to be involved in cholinergic transmission. The effects of acute intravenous LAC administration (30 mg/kg) on pattern-evoked electroretinograms (P-ERGs) were evaluated in nine healthy volunteers ranging in age between 21 and 27 years. Nine age-matched, normal subjects treated with a placebo served as controls. Steady-state (8 Hz) P-ERGs recorded in response to counterphased sinusoidal gratings of variable spatial frequency (0.6-4.8 cycles/degree) were obtained before and at 20, 50 and 80 min after LAC or placebo administration. The amplitude and phase of the Fourier-analysed P-ERG second harmonic were measured. As compared with placebo-treated controls, LAC-treated subjects showed a selective P-ERG amplitude increase (Mann-Whitney rank test: P less than 0.05), which was found 80 min posttreatment at a spatial frequency of 4.8 cycles/degree. For the same stimulus a significant (P less than 0.05) P-ERG phase shortening (at 50 min after drug administration) was also found. The spatial frequencies of other stimuli did not show a significant difference between the LAC- and placebo-treated groups. These results indicate that acute LAC administration induces a spatial-frequency-dependent enhancement of the human P-ERG. This is compatible with a cholinergic excitatory effect and suggests a therapeutic role for this compound in retinal dysfunctions with selective vulnerability to medium-high spatial frequencies.

Acetylcarnitine↗

PubMed1992

The microglial reaction in the rat hippocampus following global ischemia: immuno-electron microscopy.

Transient arrest of the cerebral circulation leads to neuronal cell death in selectively vulnerable regions of the central nervous system. It has recently been shown at the light microscopical level that neuronal necrosis is accompanied by a rapid microglial reaction in ischemia (Gehrmann et al. (1992) J. Cereb. Blood Flow Metab. 12:257-269). In the present study we have examined the postischemic microglial reaction in the dorsal rat hippocampus at the ultrastructural level using immuno-electron microscopy. Global ischemia was produced by 30 min of four-vessel occlusion and the microglial reaction then studied after 8, 24 and 72 h. In sham-operated controls microglial cells were not phagocytic; they were randomly distributed throughout the neuropil and occasionally made contacts with other structures such as dendrites in CA1. Ultrastructural signs of activation were observed from 1 day postlesion onward. Reactive microglial cells were consistently seen to phagocytose degenerating neurons particularly in the CA1 stratum pyramidale and in the CA4 sector. They were sometimes interposed between two morphologically distinct types of CA1 neurons, i.e., "dark" (degenerating) and "pale" (surviving) types of neurons. Phagocytic microglial cells also became positive for major histocompatibility complex (MHC) class II antigens at these locations from 1 day after ischemia onward. Furthermore, activated microglial cells were frequent along degenerating dendrites in the stratum radiatum of CA1. After survival times of up to 72 h microglial cells, but not astrocytes, were occasionally observed to undergo mitosis. In addition to their random distribution across the neuropil, microglial cells were frequently observed in a perivascular position under normal conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Differential distribution of 68 Kd and 200 Kd neurofilament proteins in the gerbil hippocampus and their early distributional changes following transient forebrain ischemia.

The distribution of neurofilament (NF) proteins was studied immunohistochemically in the gerbil hippocampus with antibodies against NF68 (68 Kd molecular weight) and NF200 proteins, and changes in the distribution of NF proteins after transient ischemia were observed in order to investigate the temporal correlation between NF and delayed neuronal death. In the normal hippocampus, NF68-like immunoreactivity (NF68-LI) was densely distributed in nerve processes in CA2, CA3 and the hilus of the dentate gyrus but was less intense in CA1. In contrast, processes with NF200-LI appeared to be evenly distributed in CA1, CA2, CA3 and the dentate gyrus. Mongolian gerbils were subjected to transient ischemia for 5 min by bilateral carotid occlusion and subjected to immunohistochemistry 1, 2, 3 and 4 days after ischemia. Following transient ischemia, prior to neuronal cell death, the intensity of both NF68-LI and NF200-LI decreased in the whole hippocampal formation. This decrease was more obvious in the case of NF68-LI than NF200-LI. Four days after ischemia, when neuronal death of CA1 pyramidal cells had occurred, processes in CA1, particularly 68 Kd components, showed marked decreases in number and staining intensity, although processes in most layers of CA2, CA3 and the dentate gyrus appeared to be stained similarly to normal brain. Since NF68 protein is considered to be the major component of NF proteins and NF200 is an associated accessory protein, the current observations suggest that the poor distribution of NF68 in CA1 and the early loss of NF proteins may be closely related to selective vulnerability of CA1 pyramidal cells and delayed neuronal death.

Animals↗

PubMed1995

The recovery function of paired somatosensory evoked potentials in cerebral ischemic rabbits.

In cerebral ischemia of different degrees, the amplitudes of somatosensory evoked potentials (SEPs) are facilitated or depressed. Different mechanisms might be responsible for the explanation of the contradictory phenomena. SEPs obtained using the paired stimulation method were employed in trying to find out the role of the functional changes of the inhibitory system in the brain during ischemia. Eight rabbits were used for recording the amplitude recovery curve of paired SEPs in the normal state, and the other ten were used for recording the recovery curve in different cerebral ischemic degrees. Cerebral ischemia was induced by the iron particle injection method. The attenuation of the depressed recovery function of the paired SEP amplitudes was detected during cerebral ischemia when SEP amplitudes were either facilitated or depressed. The results indicate that the function of the inhibitory system in the brain is selectively vulnerable during cerebral ischemia.

Animals↗

PubMed1989

Cytomegalovirus (CMV) disease of the brain in AIDS and connatal infection: a comparative study by histology, immunocytochemistry and in situ DNA hybridization.

Brain tissues from 45 patients with AIDS and two brains with connatal cytomegalic inclusion body disease were investigated for a cytomegalovirus (CMV) etiology of encephalitic lesions. Nineteen brains showed evidence of CMV infection by histology, immunocytochemistry (ICC) using two different antibodies (mono- and polyclonal), and in situ hybridization (ISH). Fourteen cases with typical cytomegalic cells in conventional histology [eight with focally necrotizing encephalitis/ventriculitis including the two connatal infections and six with nodular encephalitis (NE)] revealed CMV with any method. In 5 of 15 AIDS cases of NE without cytomegalic cells, CMV infection was established by ISH, whereas ICC remained negative in these cases. Typical lesions of human immunodeficiency virus (HIV)-induced multi-focal giant cell encephalitis (HIV encephalitis) in 13 brains were never labeled for CMV. In necrotizing encephalitis/ventriculitis, cell types which labeled for CMV, with and without cytomegalic change, comprised neurons, astrocytes, oligodendrocytes, ependyma, choroid plexus, endothelia, and cells in peri- and endoneurium, and in leptomeninges. Both ISH and ICC were able to detect widespread non-cytomegalic CMV-infected cells in normal parenchyma, well beyond the necrotizing lesions, in two AIDS cases. Labeling patterns of nuclei versus cytoplasms varied between the three methods for CMV detection. We conclude that in CNS tissues with cytomegalic cells, ICC and ISH are of comparable sensitivity; however, a diagnosis of CMV disease is possible in such cases by conventional histology. For an in situ diagnosis of CMV infection in NE without cytomegalic cells in AIDS, ISH is the method of choice. A selective vulnerability to CMV infection of any specific cell type of the human CNS is absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗