Brain dysfunction adults

Wender, P.H., Wood, D.R., and Reimherr, EW. (1985) Pharmacological treatment of attention deficit disorder, residual type (ADDRT, minimal brain dysfunction , hyperactivity ) in adults. Psycho-pharmacol Bull 21 222-232. 

Adults require 1-2 mg of copper per day, and eliminate excess copper in bile and feces. Most plasma copper is present in ceruloplasmin. In Wilson s disease, the diminished availability of ceruloplasmin interferes with the function of enzymes that rely on ceruloplasmin as a copper donor (e.g. cytochrome oxidase, tyrosinase and superoxide dismutase). In addition, loss of copper-binding capacity in the serum leads to copper deposition in liver, brain and other organs, resulting in tissue damage. The mechanisms of toxicity are not fully understood, but may involve the formation of hydroxyl radicals via the Fenton reaction, which, in turn initiates a cascade of cellular cytotoxic events, including mitochondrial dysfunction, lipid peroxidation, disruption of calcium ion homeostasis, and cell death. 

The over-production of bilirubin to the point at which the liver s capacity to metabolize is exceeded or if there is dysfunction of the liver itself due to damage or metabolic immaturity, can lead to a yellow discolouration of tissues called jaundice. The accumulation of unconjugated bilirubin in neonates, often as a result of antibody-mediated destruction of the baby s red cells is dangerous as serious and irreversible brain damage can occur. Acute or chronic damage to the adult liver (hepatitis) may cause jaundice but not brain damage. 

Cellular therapy is the replacement of lost or dysfunctional tissues with new ones. Various cell types have been evaluated and considered for therapy. In the CNS, fetal neuronal tissue has been particularly evaluated for its merit in treating neurological diseases and injuries [1]. While numerous experimental and clinical transplantation studies showed that fetal neuronal transplants improve functional deficits in models of CNS diseases [2-5], others reported less positive outcomes [6, 7]. In addition, the rate of survival of fetal neuronal cells transplanted into the adult brain is relatively low, requiring large quantities of tissue, generally from several fetuses, for therapy. Researchers are looking at other opportunities for cellular therapy, particularly in the CNS. 

If schizophrenia is caused by abnormal early brain development (cf. Figs. 10—15 and 10—16), it may be virtually impossible to reverse such abnormalities in adulthood. On the other hand, some day it may be possible to compensate for such postulated neurodevelopmental difficulties by other mechanisms or to interrupt an ongoing mechanism still present in the symptomatic patient. Therefore, it will be critical to learn what neurodevelopmental abnormalities may exist in schizophrenia in order to devise strategies for reducing their potential impact. It may even be possible to identify such abnormalities in presymptomatic individuals or to exploit the plasticity of adult neurons to compensate for neurodevelopmentally endowed dysfunction. These are bold and unsubstantiated theoretical extrapolations based on... 

Nonallergic hyperreactivity corresponds to the traditional notion of food intolerance. It is a syndrome in which dysfunctions are similar to those observed in the course of allergic diseases, induced by various mechanisms, excluding immunology-related factors. Nonallergic hyperreactivity occurs more frequently than allergy. Morbidity rate in children is approximately 20%-50%, while in adults it is estimated to be approximately 20%. Attention is drawn to the fact that the enzymatic system in children is less mature, so the capacity to bind chemical compounds by plasma proteins is poorer, and so is the blood-brain barrier permeability by low molecular weight compounds. 

The animals had a reduced ability to experience pleasure and reward, particularly when it was measured by sensitivity to cocaine. In addition, they found that the animals exposed to Ritalin during pre-adolescence were more prone to express despair-like behaviors in stressful situations (such as swim tests) as adults. Overall, the animals showed more evidence of dysfunctional brain reward systems and depressive-like behaviors in adulthood. 

Of particular interest is that the A6 oligomers implicated in AD were shown to reduce PAKl and PAK3 expression levels and activities in the hippocampus and temporal cortex, resulting in a loss of drebrin from the spines and synaptic dysfunctions (Zhao et al., 2006 Ma et al., 2008). Drebrin is localized at spines in adult brains and is required for active clustering and synaptic targeting of PSD95... 

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