State-related dysfunction

Bucala R, Model P, Cerami A (1984). Modification of DNA by reducing sugars A possible mechanism for nucleic acid aging and age-related dysfunction in gene expression. Proc. of the National Academy of Sciences of the United States of America, 81 105-109. 

The treatment of non-motor symptoms should be based on whether they are worse during an off state or if they could be related to other neurotransmitter dysfunction. 

There is ample support for the hypothesis of noradrenergic system dysfunction in depression however, the inconsistencies in findings rule out any simple model of increased or decreased noradrenergic activity. It is important to determine which noradrenergic system abnormalities relate specifically to the pathogenesis of mood disorders, and which are related to nonspecific effects of stress, homeostatic mechanisms, or comorbid psychopathology. More work is needed on the mood-state-depen-dence of noradrenergic function. 

An explanation for sleep EEG alterations in depression is provided by the well established monaminergic-cholinergic imbalance model [49] which includes monoaminergic dysfunction in depression. The result is a disturbance of the mutual interactions between the diverse nuclei which control the transitions between REM and nonREM states (see Fig. 7.5, right part). This concept was developed in close relation to the monamionergic-cholinergic imbalance model of depression [50] which is based on observations that inhibition of the aminergic system by re-... 

At present, the only brain manipulation that produces a clinical state behaviorally indistinguishable from schizophrenia is the blockade of brain NMDA receptors. The primary concept underlying glutamatergic models of schizophrenia, therefore, is that the dysfunction or dysregulation of NMDA receptor-mediated neurotransmission represents the common final mechanism underlying the symptom formation in schizophrenia. Although in some individuals, the NMDA dysfunction may be related to disturbances of the receptors themselves, for other individuals, these deficits may relate more to impairments of either upstream or downstream elements involving pre- and postsynaptic neural elements respectively. 

Persistent acute body zinc loss has resulted in many symptoms in addition to taste and smell dysfunction if losses continue at significant levels for periods of 14 days or more. These symptoms Include mental confusion, cerebellar dysfunction, including intention tremor and ataxia, an erythrematous, Intracrural rash, buccal epithelial lesions and ulcers, and acute toxic psychosis (,6). The altered mental state of these patients can be related to the rapid depletion of the relatively high zinc content in the limbic system of the brain (16.17), demonstrating that zinc can cross the blood brain barrier bidirectionally, dependent upon the gradient, and that it can be readily mobilized from brain tissue. 

A number of problems are associated with drinking alcohol, A biood alcohol concentration greater than 5.4 mM produces mild intoxication in nonalcoholics 22 mM may cause neurological dysfunctions. In the United States, intoxication i legally defined as a blood alcohol level greater than 21,7 mM, Concentrations above 109 mM may be fatal, because of respiratory failure. The major problem related to alcohol consumption is death from automobile accidents. About 50,000... 

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