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PubMed1988

[Status of the ventricular system and dynamics of the cerebrospinal fluid changes in chronic brain diseases].

Using noninvasive (echoventriculometry (Echo-VM), REG and invasive (planimetric PEG, graphic recording of the CSF pressure) methods of examination, the authors determined the size of cerebral ventricles and the status of the cerebral hemo- and CSF dynamics in 606 patients with various chronic diseases of the brain (consequences of craniocerebral injury, epilepsy, discirculatory encephalopathy, etc.). According to PEG and Echo-VM findings, two groups of patients were distinguished. In moderate dilatation of cerebral ventricles the most significant finding was an increase in the pulse pressure of the CSF, whereas its mean pressure was normal or slightly elevated. In patients with pronounced hydrocephaly the pulse and mean pressure of the CSF tended to decrease. The progress of hydrocephaly was parallelled by increasing disorders of the cerebral hemodynamics expressed in hindered venous outflow from the cranial cavity and elevated peripheral vascular resistance. Four CSF-related syndromes have been identified (normotension, total CSF hypertension, intraventricular tension, total CSF hypotension) differing in their diagnostic and prognostic significance and in the pathogenesis of disorders of the hemo- and CSF dynamics.

Adolescent↗
PubMed2003

Channels formed with a mutant prion protein PrP(82-146) homologous to a 7-kDa fragment in diseased brain of GSS patients.

A major prion protein (PrP) mutant that forms amyloid fibrils in the diseased brain of patients with Gerstmann-Sträussler-Scheinker syndrome (GSS) is a fragment of 7 kDa spanning from residues 81-82 to 144-153 of PrP. Analysis of ionic membrane currents, recorded with a lipid bilayer technique, revealed that the wild-type fragment PrP(82-146) WT and the partially scrambled PrP(82-146) (127-146) SC are capable of forming heterogeneous ion channels that are similar to those channels formed with PrP(106-126). In contrast, PrP(82-146) peptides in which the region from residue 106 to 126 had been scrambled (SC) showed a reduction in interaction with lipid membranes and did not form channels. The PrP(82-146) WT- and PrP(82-146) (127-146) SC-formed cation channels with fast kinetics are Cu2+ sensitive and rifampicin (RIF) insensitive, whereas the time-dependent inactivating channels formed by these same peptides are both Cu2+ and RIF insensitive. The presence of RIF in the solution before the addition of PrP(82-146) WT or PrP(82-146) (127-146) SC affected their incorporation into the lipid bilayers. PrP(82-146) WT and PrP(82-146) (127-146) SC fast cation channels formed in the presence of RIF appeared in an electrically semisilent state or an inactivated state. Increasing [Cd2+]cis enhanced the incorporation of PrP(82-146) WT and PrP(82-146) (127-146) SC channels formed in the presence of RIF. We conclude that the major PrP mutant fragment in the diseased brain of GSS patients is prone to form channels in neuronal membranes, causing their dysfunction. We propose that Cd2+ may accentuate the neurotoxicity of this channel-forming PrP fragment by enhancing its incorporation into the membrane.

Brain↗
PubMed1977

Treatment of brain disease with dietary precursors of neurotransmitters.

A growing number of brain diseases are characterized by decreased levels of one or more of the neurotransmitters. Recent experimental evidence indicates that nutritional factors strongly influence the regulation of two of these neurotransmitters, serotonin and acetylcholine. As a result, attempts are now being made to treat diseases associated with low levels of serotonin or acetylcholine by administering their dietary precursors, tryptophan and choline, respectively. This treatment may increase the amount of the deficient neurotransmitter at synapses and produce clinical benefit. Such efforts to elevate brain neurotransmitter levels with a naturally occurring precursor represent a new approach in medical therapeutics and will probably continue. We review the scientific basis for such treatment and show that brain levels of serotonin and acetylcholine depend upon the amounts of tryptophan and choline available to the brain; these, in turn, fluctuate according to dietary factors.

Acetylcholine↗
PubMed1977

Resting tremor in alcoholic brain disease.

Two patients with signs of alcoholic brain disease of the Wernicke-Korsakoff type were found to have an unusual movement disorder manifested basically as a resting tremor. Electrographic recording showed that the tremor wave comprised multiple elements, though the rate of the basic tremor was stable. Though the tremor was qualitatively similar to documented rubral tremor, a mesencephalic lesion could be defined in only 1 patient.

Alcohol Amnestic Disorder↗
PubMedDate not supplied

Analysis of message expression in single neurons of Alzheimer's disease brain.

Because many cell types and disease states exist in the sample of cells in even a very small region of Alzheimer's disease (AD) brain tissue, optimal understanding of disease mechanisms requires study at the level of the single cell. Our Golgi studies of single neurons in the AD brain have revealed reduced dendritic extent in many, but not all, brain regions. This reduced dendritic extent is interpreted as reduced capacity of neurons in AD to proliferate new dendritic material. Studies of message expression in single neurons reveal that neurons containing neurofibrillary tangles (NFTs) show reduced expression of messages for proteins related to growth of neuronal processes and to synapses. Neighboring neurons free of NFTs express these messages at levels approximating the levels expressed by single neurons from control brain. This reduction of expression of messages related to growth of neuronal processes and to synapses is selective, because expression of message for the lysosomal enzyme, cathepsin D, is increased in neurons containing NFTs. Simultaneous analysis of the expression of multiple genes by single neurons using an aRNA technique offers powerful capacity to profile message expression as a function of disease state of single cells.

Alzheimer Disease↗
PubMed1997

Transglutaminase activity is increased in Alzheimer's disease brain.

Transglutaminase is a calcium-activated enzyme that crosslinks substrate proteins into insoluble, often filamentous aggregates resistant to proteases. Because the neurofibrillary tangles in Alzheimer's disease have similar characteristics, and because tau protein, the major component of these tangles is an excellent substrate of transglutaminase in vitro, transglutaminase activity and levels were measured in control and Alzheimer's disease brain. Frozen prefrontal cortex and cerebellum samples from Alzheimer's disease and control cases matched for age and postmortem interval were used in the analyses. Total transglutaminase activity was significantly higher in the Alzheimer's disease prefrontal cortex compared to control. In addition the levels of tissue transglutaminase, as determined by quantitative immunoblotting, were elevated approximately 3-fold in Alzheimer's disease prefrontal cortex compared to control. To our knowledge, this is the first demonstration that transglutaminase is increased in Alzheimer's disease brain. There were no significant differences in transglutaminase activity or levels in the cerebellum between control and Alzheimer's disease cases. Because the elevation of transglutaminase in the Alzheimer's disease samples occurred in the prefrontal cortex, where neurofibrillary pathology is usually abundant, and not in the cerebellum, which is usually spared in Alzheimer's disease, it can be suggested that transglutaminase could be a contributing factor in neurofibrillary tangle formation.

Aged↗
PubMed2005

Mitochondrial damage and histotoxic hypoxia: a pathway of tissue injury in inflammatory brain disease?

The immunological mechanisms leading to tissue damage in inflammatory brain diseases are heterogeneous and complex. They may involve direct cytotoxicity of T lymphocytes, specific antibodies and activated effector cells, such as macrophages and microglia. Here we describe that in certain inflammatory brain lesions a pattern of tissue injury is present, which closely reflects that found in hypoxic conditions of the central nervous system. Certain inflammatory mediators, in particular reactive oxygen and nitrogen species, are able to mediate mitochondrial dysfunction, and we suggest that these inflammatory mediators, when excessively liberated, can result in a state of histotoxic hypoxia. This mechanism may play a major role in multiple sclerosis, not only explaining the lesions formed in a subtype of patients with acute and relapsing course, but also being involved in the formation of diffuse "neurodegenerative" lesions in chronic progressive forms of the disease.

Brain Diseases↗
PubMed1996

Degenerative brain disease.

Inherited degenerative diseases of the brain are chronically progressive and often lead to severe debilitation. The cerebellum is particularly susceptible to degenerative processes. For lysosomal storage disorders, the metabolic defect is often known and diagnostic tests are available. For other abiotrophies, the inborn error of metabolism is not known and diagnosis is made on postmortem. Pathogenesis of brain dysfunction is not well understood in a majority of the neurodegenerative diseases.

Animals↗
PubMed1990

Minding the need for specialists in brain diseases.

A recent call for a new speciality in biologically based brain diseases is questioned on historical, empirical, and theoretical grounds. Psychiatry has oscillated between biological and psychosocial explanations for mental illness since its inception. Training in the biological basis of mental illness is and should be incorporated into psychiatric training, along with a balanced appreciation of the utility of psychotherapeutic and social intervention. Emphasis on only one aspect resurrects Cartesian dualism. Any disease, however biological in origin, is best treated by a clinician adept at multiple levels of understanding and intervention.

Biological Psychiatry↗
PubMed2004

[Depression and organic brain diseases in the elderly].

Depressive symptoms are observed in many organic brain diseases in the elderly, particularly in stroke, degenerative or vascular dementias and Parkinson's disease. In many cases, an accurate estimation of the respective part of neurobiological abnormalities, adjustment disorders, disability and narcissistic wounds related to the disease appears very difficult for the practitioner. Specific data on the therapeutical aspects of secondary depressive disorders remains quite scarce. The efficacy of antidepressant drugs may be less important in geriatric depression with cerebral disorders or "secondary depressions" than in primary ones. Consequently, electroconvulsive-therapy may appear as an interesting therapeutical option for these patients.

Aged↗
PubMed2000

Neuroengineering models of brain disease.

The techniques of computational simulation have begun to be applied to modeling neurological disease and mental illness. Such neuroengineering models provide a conceptual bridge between molecular/cellular pathology and cognitive performance. We consider models of Alzheimer's disease, Parkinson's disease, and schizophrenia. Each of these diseases involves a disorder of neuromodulation coupled with underlying neuronal pathology. Parallels arising between these models suggests that a common set of computational mechanisms may account for functional loss across a spectrum of brain diseases. In particular, we focus on attractor-based network dynamics and how they arise from neural architectures, on mechanisms for linking sequences of attractor states and their role in cognition, and on the role of neuromodulation in controlling these processes. These studies suggest new approaches to understanding the forebrain circuits underlying cognition, and point toward a new tool for dissecting the pathophysiology of brain disease.

Alzheimer Disease↗
PubMed2005

[Influence of heart and brain disease on multifractal singularity spectrum of synchronous 12-lead ECG signals].

We analyzed the multifractal singularity spectrum of synchronous 12-lead ECG (electrocardiogram) signals from heart and brain disease patients, and found that multifractal curves of different leads do not overlap each other. After calculating the scope of the singularity strength, we noticed that the averages of scope are not the same in different subjects,and the dispersing degree is also different in someone's different leads. Both the deltaalpha, the average of the deltaalpha, and the dispersing degree deltaalpha (be defined as standard deviation) of the deltaalpha of every one's 12-lead ECG were computed. Then, a comparison was made between the spectrum of the healthy subjects and the heart disease patients. The results showed that their deltaalpha are close, but their deltaalpha are markedly different. Also the healthy subjects and brain disease patients were compared, we found that their deltaalpha are close, but their deltaalpha are markedly different. These indicate that the character of multifractal spectrum is controlled by both the neurosystem of body and the self-syntonic property of cardiac structures. Furthermore, the deltaalpha is related with the neuroautonomic control of people's body on the ECG, and the deltaalpha is related with the anisotropy of the heterogeneous tissue and the electric signal propagation in heart.

Aged↗
PubMedDate not supplied

The significance of hemispheric localization of ischemic brain lesion for the early prognosis of ischemic brain disease.

The possibility of early prediction of ischemic brain disease (IBD) is extremely significant for the creation of the individually designed treatment program. The aim of this study was to determine the significance of hemispheric localization of ischemic brain lesion as possible factor for the early prediction of IBD outcome. The study included 170 patients with IBD, whose score of neurologic and functional impairment was determined after admission by using the standard scales. The values of hemorrheological parameters-erythrocyte sedimentation rate (ESR), fibrinogen and alpha 2 globulin were also determined, so as the extensity of ischemic lesion by CT and MR brain examinations. After the treatment, the score of neurologic and functional impairment was also determined and the degree of ischemic disturbance was estimated-transitory ischemic attack (TIA), reversible ischemic attack (RIA) and cerebral infarction. The lower scores were noticed for neurologic and functional impairment, meaning the more severe degree of ischemic disorder with ischemic lesion localization in right cerebral hemisphere (RCH), in acute stage and at the end of treatment. The higher values of ESR, slightly less of fibrinogen and alpha 2 globulin were revealed in the case of ischemic lesion localization in RCH, so as the higher frequency of RCH lesions in percentages connected with the more severe ischemic disorders. It was concluded that the ischemic lesion localization in RCH might be the predictor of poorer IBD outcome.

Blood Sedimentation↗
PubMed2000

Agrin binds to beta-amyloid (Abeta), accelerates abeta fibril formation, and is localized to Abeta deposits in Alzheimer's disease brain.

Agrin is an extracellular matrix heparan sulfate proteoglycan (HSPG) well known for its role in modulation of the neuromuscular junction during development. Although agrin is one of the major HSPGs of the brain, its function there remains elusive. Here we provide evidence suggesting a possible function for agrin in Alzheimer's disease brain. Agrin protein binds the amyloidogenic peptide Abeta (1-40) in its fibrillar state via a mechanism that involves the heparan sulfate glycosaminoglycan chains of agrin. Furthermore, agrin is able to accelerate Abeta fibril formation and protect Abeta (1-40) from proteolysis, in vitro. Supporting a biological significance for these in vitro data, immunocytochemical studies demonstrate agrin's presence within senile plaques and cerebrovascular amyloid deposits, and agrin immunostained capillaries exhibit pathological alterations in AD brain. These data therefore suggest that agrin may be an important factor in the progression of Abeta peptide aggregation and/or its persistence in Alzheimer's disease brain.

Agrin↗