[The significance of collateral cerebral circulation in organic brain diseases for their neurosurgical treatment].
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Brain Diseases↗
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Early and progressive accumulation of reactive microglia in the Huntington disease brain.
Microglia may contribute to cell death in neurodegenerative diseases. We studied the activation of microglia in affected regions of Huntington disease (HD) brain by localizing thymosin beta-4 (Tbeta4), which is increased in reactive microglia. Activated microglia appeared in the neostriatum, cortex, and globus pallidus and the adjoining white matter of the HD brain, but not in control brain. In the striatum and cortex, reactive microglia occurred in all grades of pathology, accumulated with increasing grade, and grew in density in relation to degree of neuronal loss. The predominant morphology of activated microglia differed in the striatum and cortex. Processes of reactive microglia were conspicuous in low-grade HD, suggesting an early microglia response to changes in neuropil and axons and in the grade 2 and grade 3 cortex, were aligned with the apical dendrites of pyramidal neurons. Some reactive microglia contacted pyramidal neurons with huntingtin-positive nuclear inclusions. The early and proximate association of activated microglia with degenerating neurons in the HD brain implicates a role for activated microglia in HD pathogenesis.
Adult↗
[Leukocyte cytochemical indices in brain diseases].
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Brain Diseases↗
Heterogeneity of melanized neurons expressing neurotensin receptor messenger RNA in the substantia nigra and the nucleus paranigralis of control and Parkinson's disease brain.
We have recently cloned the neurotensin receptor from human substantia nigra. Using in situ hybridization techniques, with an 35S-labeled antisense RNA probe complementary to this receptor complementary DNA, we studied the expression of the human neurotensin receptor in the brain from control and Parkinson's disease subjects. We also performed an analogous study with rat brain. Neurotensin receptor messenger RNA was present in high levels in melanized neurons of the substantia nigra pars compacta and the nucleus paranigralis (the ventral tegmental area for rat brain). Background levels of signals for neurotensin receptor messenger RNA were detected in the nucleus ruber, the colliculus inferior and the striatal subdivisions (the nucleus caudatus, the putamen and the nucleus accumbens) of both human and rat brain. All these areas, except the nucleus ruber and the collicus inferior, contain very high to high levels of neurotensin receptor binding sites. Additionally, Parkinson's disease brains had markedly fewer melanized (possibly dopaminergic) neurons, as expected, and correspondingly very low or background levels of messenger RNA for neurotensin receptor. We have also demonstrated heterogeneity among the melanized cells expressing messenger RNA encoding the neurotensin receptor in the substantia nigra and the nucleus paranigralis of human brain. The neurons in the nucleus paranigralis had lower melanin pigmentation and higher expression of neurotensin receptor messenger RNA. In general, the expression of the messenger RNA within the highly and evenly melanized neurons was lower than that found in low or unevenly pigmented neurons. The neurons in the nucleus paranigralis had lower melanin pigmentation and higher expression of neurotensin receptor messenger RNA. The low pigmented neurons in the ventral tier of the substantia nigra had relatively high expression. On the other hand, highly and evenly melanized neurons in these regions of the brain had low expression of neurotensin receptor messenger RNA. Together with the previous binding data, it is suggested that not only in rat brain, but also in human brain, melanized (possibly dopaminergic) neurons in the substantia nigra and the nucleus paranigralis (ventral tegmental area of rat brain) synthesize neurotensin receptors and express them in their perikarya and the terminal regions. Additionally, the heterogeneity of the melanized neurons in human brain may play a role in the normal function of dopaminergic systems and probably in the etiology of some neurological and psychiatric disorders.
Aged↗
Collagen XVIII: a novel heparan sulfate proteoglycan associated with vascular amyloid depositions and senile plaques in Alzheimer's disease brains.
Heparan sulfate proteoglycans (HSPGs) may play a role in the formation and persistence of senile plaques and neurofibrillary tangles in Alzheimer's disease brains. Recently, it has been demonstrated that the human extracellular matrix-associated molecule collagen XVIII is the first collagen carrying heparan sulfate side-chains. Two variants of collagen XVIII with both different signal peptides and N-terminal domains have been described and are referred to as the short and long form. To investigate the distribution of these variants we performed an immunohistochemical analysis by using specific well-characterized polyclonal antibodies. Anti-long huXVIII, a polyclonal antibody directed against the long variant of collagen XVIII, weakly stained large cortical and leptomeningeal vessels, whereas small cortical vessels remained unstained. Interestingly, all amyloid-laden vessels and classic senile plaques were strongly stained. Anti-all huXVIII, a polyclonal antibody directed against an epitope common to both collagen XVIII variants, intensely stained all types of cerebral blood vessels, cerebral amyloid angiopathy-affected vessels and classic senile plaques. Collagen XVIII expression was absent in neurofibrillary tangles. We conclude that collagen XVIII is a novel heparan sulfate proteoglycan associated with vascular A beta and classic senile plaques and that at least the long form of collagen XVIII accumulates in amyloid-laden vessels and classic senile plaques.
Aged↗
Altered expression of protein p42IP4/centaurin-alpha 1 in Alzheimer's disease brains and possible interaction of p42IP4 with nucleolin.
The protein p42IP4 (centaurin-alpha1) is a brain-specific InsP4/PtdIns3 (PIP)-binding protein, whish is localized in neurons of the human brain. In Alzheimer's disease (AD) the intraneuronal expression of the protein was shown to be elevated. In addition, p42IP4 immunostaining decorated neuritic plaques. Attempting to explain the putative role of the protein in AD, we have concentrated on its well-known interactions with casein kinase I, which is known to be prominently involved in AD pathophysiology. Meanwhile, specific interaction of p42IP4 with nucleolin, another player in AD pathology, has been revealed. Based on these data, we propose alternative concepts of how p42IP4 might act in AD pathomechanisms.
Adaptor Proteins, Signal Transducing↗
Increased titer of anticardiolipin antibodies represents the risk for the development of ischemic brain disease in persons below 50.
The aim of this paper was to investigate the frequency of increased ACLA titer in patients with ischemic brain disease (IBD) and to define their clinical profile. The group consisted of 162 IBD patients of both sexes, aged 39-81 years, with 50 healthy volunteers and 23 patients with other neurological diseases as control. Increased ACLA titer (above 0.9 GPL U/l IgG and 0.5 MPL U/l IgM) was registered in 17.9% IBD patients, and more frequently in patients with transitory ischemic attacks (TIA)-32.6%; slightly increased titer predominated (0.9-20 GPL U/l IgG and 0.5-15 MPL U/l IgM) in 69% IBD patients, while moderately increased (20-80 GPL U/l and 15-50 MPL U/l IgM) was present in 21% IBD patients, while highly increased titer (above 80 GPL U/l IgG and above 50 MPL U/l IgM) was present in 10.3%; IgG class was most frequently increased (9.2%), than IgM-5%, while increase of both classes was present in 3.7%. All patients with increased ACLA titer were below 50 years of age, had history of previous IBD attacks, more often TIA, irregularity of at least one coagulation test and fewer risk factors for IBD. Hence, increased ACLA titer was present in IBD patients of both sexes, below 50 years of age with previous history of IBD attacks and fewer atherosclerosis risk factors.
Adult↗
Diagnosis and prognosis of behavior disorder associated with organic brain disease in children.
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Behavior↗
Somatic expansion of the (CAG)n repeat in Huntington disease brains.
The mutation causing Huntington disease (HD) has been identified as an expansion of a polymorphic (CAG)n repeat in the 5' part of the huntingtin gene. The specific neuropathology of HD, viz. selective neuronal loss in the caudate nucleus and putamen, cannot be explained by the widespread expression of the gene. Since somatic expansion is observed in affected tissue in myotonic dystrophy, we have studied the length of the (CAG)n repeat in various regions of the brain. Although we have not found clear differences when comparing severely and mildly affected regions, we have observed a minor increase in repeat length upon comparison of affected brain samples with cerebellum or peripheral blood. Hence, although further somatic amplification seems to occur in affected areas of the brain, the differences between affected and unaffected regions are too small to make this mechanism an obvious candidate for the cause of differential neuronal degeneration in HD.
Aged↗
[Intrauterine fetal death in brain diseases of the mother involving the hypothalamus].
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Adult↗
Immunohistochemical evidence for a possible somatostatin-containing amygdalostriatal pathway in normal and Alzheimer's disease brain.
Somatostatin (SOM) immunohistochemistry was used to map SOM-containing fibers, perikarya and terminal-like structures in the human forebrain of 8 control and 8 Alzheimer's diseased patients. Immunohistochemically processed tissue revealed a somatostatin-immunoreactive amygdalostriatal fiber pathway apparently originating from SOM-positive neurons of the central amygdaloid nucleus. This pathway coursed dorsomedially between the optic tract and the internal segment of the globus pallidus within the ansa peduncularis-ventral amygdalofugal fiber system en route to the substantia innominata-nucleus basalis complex, the bed nucleus of the stria terminalis, the medial preoptic hypothalamic area, the nucleus accumbens and the olfactory tubercle. Somatostatin fibers associated with this pathway appeared as coarse heavily stained 'wooly fibers'. At the light microscopic level, there was no apparent difference in this somatostatin containing amygdalostriatal pathway between neurologically normal and Alzheimer's diseased brains.
Adolescent↗
Temporal orientation in patients with brain disease.
A brief schedule of questions, based on empirically derived norms, disclosed significant inaccuracy in temporal orientation in 24% of a groups of nonaphasic patients with brain disease. Conventional neurological examination detected temporal disorientation in only 15%. Patients with bilateral lesions showed a higher frequency of temporal disorientation than did those with inilateral lesions. In a group of 15 aphasic patients, 5 (33%) showed evidence of temporal disorientation according to the test while only 3 (20%) were detected on clinical examination. It is suggested that a schedule of questions scored on the basis of empirically derived norms should be incorporated into the neurological examination to assess temporal orientation.
Aphasia↗
[Aneurysm carriers and aneurysmic brain disease].
Bifurcational failure of the brain arterial circle is a combination of congenital and acquired structural changes in the apical angles of the brain arteries branching. Their combination with hemodynamic changes (stress) produced by various diseases creates aneurysmogenic situation which is probably exclusive property of the circulus arteriosus Willisii. Bifurcational--hemodynamic (so-called congenital) aneurysms are not more than anatomical phenomenon underlying two conditions; aneurysm carriage and aneurysmic disease. Each of them should be distinguished as a separate nosological entity.
Circle of Willis↗
The value of proton MR spectroscopy in pediatric metabolic brain disease.
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Brain↗
Impaired G-protein-stimulated adenylyl cyclase activity in Alzheimer's disease brain is not accompanied by reduced cyclic-AMP-dependent protein kinase A activity.
Previous studies have shown that the regulation of adenylyl cyclase activity is disrupted in Alzheimer's disease postmortem brain. In the present study, we determined whether disrupted adenylyl cyclase is accompanied by altered cAMP-dependent protein kinase activity in Alzheimer's disease superior temporal cortex and cerebellum. GTP gamma S-stimulated adenylyl cyclase activity was significantly lower in Alzheimer's disease superior temporal cortex, but not cerebellum, compared to values from a series of matched control cases. Neither basal or forskolin-stimulated adenylyl cyclase activities were significantly different between the Alzheimer's disease and control brain regions. No significant differences were seen in either particulate or soluble fraction cAMP-dependent protein kinase activities between the Alzheimer's disease and control brain regions. It is concluded that disrupted adenylyl cyclase signalling in Alzheimer's disease brain occurs specifically at the level of Gs-protein-enzyme interactions and is not accompanied by an altered cAMP-dependent protein kinase activity.
Adenylyl Cyclases↗
Sporadic inclusion-body myositis and its similarities to Alzheimer disease brain. Recent approaches to diagnosis and pathogenesis, and relation to aging.
Sporadic inclusion-body myositis (s-IBM) is the most common, debilitating and progressive muscle disease beginning at the age 50 or later. The most characteristic pathologic feature is vacuolar degeneration of muscle fibers accompanied by intrafiber congophilia and clusters ("tangles") of paired-helical filaments, containing phosphorylated tau. An unusual feature of sporadic inclusion-body myositis is accumulation within its abnormal muscle fibers of several proteins that are characteristic of Alzheimer disease brain, including epitopes of beta-amyloid precursor protein (betaAPP), phosphorylated tau, alpha-1-antichymotrypsin, apolipoprotein E, and presenilin-1. Indicators of oxidative stress are also present within abnormal s-IBM muscle fibers. In this review, we describe new advances seeking the pathogenic mechanism of sporadic inclusion-body myositis. We hypothesize on the possible pathogenic role of abnormally accumulated proteins, and we propose that important contributory factors leading to inclusion-body myositis are the milieu of muscle-fiber aging and oxidative stress. In addition, we present evidence that overexpression of adenovirus-transferred betaAPP gene in cultured human muscle fibers induces aspects of the inclusion-body myositis phenotype, and suggest that betaAPP-overexpression is an early event in the pathogenic cascade causing inclusion-body myositis.
Alzheimer Disease↗
[Clinical polymorphism of neoplastic and vascular brain diseases: pathogenetic characteristics].
Using evidence on 533 patients with an atypical course of brain tumors and vascular diseases, the author discusses the role of the vascular factor in polymorphism of clinical manifestations of tumors and metastases to the brain. It is shown that in 55.4% of cases brain tumors simulated CNS affections. Of these most frequent was the picture of cerebral circulatory disturbances. Mechanisms causing cerebral circulation impairment in various tumors and metastases to the brain are considered. It is found that pathologically changed circulation and angioarchitecture of the tumors may contribute to a wide spectrum of clinical signs typical for vascular brain diseases. The conclusions are based on the analysis of the results obtained with present-day techniques of angio- and neurovisualization and postoperative as well as autopsy examinations of the tumors.
Biopsy↗
MRS of ischemic/hypoxic brain disease.
Significant increases in magnetic field strengths and improvements in magnetic field homogeneity have made combined high-resolution magnetic resonance imaging (MRI) and multinuclear spectroscopy (MRS) feasible for investigating the relationship between biochemical and structural changes induced by ischemic brain disease. Magnetic resonance spectroscopy is the only noninvasive technique capable of measuring concentrations of high-energy phosphate metabolites, lactate, and other metabolically relevant compounds. Anticipated advances in localization of the volume of tissue from which spectra are obtained will enhance the clinical potential of MRS in the diagnosis of ischemic disease.
Animals↗