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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormally high brain aluminum concentrations have been detected in hemodialysis patients who died of an unexplained encephalopathy. As a result, this study was undertaken to examine whether the ingestion of aluminum produces behavioral aberrations in non-dialysed human subjects and rats with ostensibly normal renal function. Rats were fed AlCl3 by intubation in varying doses, and tests measuring learning ability, visual temporal acuity, motor coordination and activity were administered. It was found that orally ingested aluminum is absorbed by rats and deposited in the brain. High brain aluminum levels are associated with rapid general activity, decreased ability to maintain roto-rod activity, and increased sensitivity to flicker. Behavioral tests were also given to elderly human subjects and performance correlated with serum aluminum level. High serum levels of aluminum in elderly humans are associated with impaired visuo-motor coordination, poor long-term memory, and increased sensitivity to flicker.
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PMID:Behavioral effects of aluminum ingestion on animal and human subjects. 46 80

A previous study reported that the intracranial injection of a soluble aluminum salt induced an encephalopathy which may serve as a useful animal model of dementia. An early sign of the encephalopathy in cats was a progressive decrement in both the performance of a short-term visual retention task and acquisition of a conditioned avoidance response in the presence of normal visual discrimination. This study reports that 10 days following the application of aluminum (AlCl3) there was an absence in cat visual cortex of neurons with spontaneous frequencies between 7 and 12 spikes/sec. The loss was associated with neurofibrillary degeneration and aluminum concentrations in lateral gyrus between 4 and 6 mug/g dry weight. The remaining neurons decreased their variability of response to identical visual stimuli and increased their probability of response and frequency of discharge.
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PMID:Neuronal correlates of an encephalopathy associated with aluminum neurofibrillary degeneration. 123 66

Aluminum (Al) is believed to exert a primary role in the neurotoxicity associated with dialysis encephalopathy and has been suggested to be involved in a number of other neurological disorders, including Alzheimer's disease. Al, complexed with fluoride to form fluoroaluminate (AlF4-), can activate the GTP-binding (G) proteins of the adenylate cyclase and retinal cyclic GMP phosphodiesterase systems. Since an involvement of G-proteins with cerebral phosphoinositide (PtdIns) metabolism has also been suggested, in this study we investigated the interaction of the stable GTP analogue GTP(S), Al salts and NaF with this system. In rat cerebral cortical membranes, GTP(S) dose-dependently stimulated [3H]inositol phosphates ([3H]InsPs) accumulation. This effect was potentiated by carbachol and was partially prevented by the GTP-binding antagonist GDP(S), indicating that CNS muscarinic receptor activation is coupled to PtdIns hydrolysis via putative G-protein(s). GTP(S) stimulation was also inhibited by phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, which is known to exert a negative feedback control on agonist-stimulated PtdIns metabolism. Both Al salts and NaF mimicked the action of GTP(S) in stimulating PtdIns turnover. Their actions were highly synergistic, suggesting that AlF4- could be the active stimulatory species. However, the stimulatory effects of AlCl3 and/or NaF were not potentiated by carbachol and were not inhibited by GDP(S) and PMA, suggesting that separate sites of action might exist for GTP(S) and AlF4-. In the nervous tissue, activation of PtdIns hydrolysis by Al (probably as AlF4-) may be mediated by activating a regulatory G-protein at a location distinct from the GTP-binding site or by a direct stimulation of phospholipase C.
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PMID:Interaction of aluminum ions with phosphoinositide metabolism in rat cerebral cortical membranes. 194 39

Intracellular recordings in 'in vitro' hippocampal slices, prepared from intracisternally AlCl3-intoxicated rabbits, were obtained from 43 CA1 pyramidal neurons. The experiments were performed 12-20 days after aluminum administration. The electrotonic length was significantly shorter than that of 33 control neurons, in agreement with morphological evidence of an Al-induced dendritic impairment. Both postsynaptic and Ca2(+)-dependent K+ hyperpolarizing potentials were also found to be significantly decreased, with reciprocal enhancement of excitatory postsynaptic potentials and depolarizing after-potentials. The former finding is ascribed to a selective neurotoxic effect of aluminum on GABAergic interneurons; the latter can be accounted for by an Al-induced increase in cyclic AMP, which is known to block the Ca2(+)-activated K+ conductance responsible for after-hyperpolarizing potentials. It is concluded that aluminum can exert its epileptogenic effect through multiple neurotoxic mechanisms involving membrane electrotonic properties, K+ conductances, and synaptic influences, thus resulting in a neuronal hyperexcitable state. Such changes are detectable in the early stages of the Al-induced encephalopathy, when there is only slight evidence of cytoskeleton alterations (i.e., neurofibrillary degeneration).
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PMID:Changes in excitability of CA1 pyramidal neurons in slices prepared from AlCl3-treated rabbits. 235 54