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Bladzijde 1 van 398 resultaten
Ventral root axonopathy and its relation to the neurofibrillary degeneration of lower motor neurons in aluminum-induced encephalomyelopathy.
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The injection of metallic aluminum (Al) into the cerebrospinal fluid of adult rabbits induces neurofibrillary degeneration of lower motor neurons. We studied the ventral roots and the corresponding motor neurons of Al-treated animals to clarify the modality and extent of reaction of the axon in
[Environmental factors in western Pacific foci of ALS and a possible pathogenetic role of aluminum (Al) in motor neuron degeneration].
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Recent decline in incidence rates of ALS in Guam and the Kii Peninsula of Japan strongly implicates environmental factors rather than inheritance in its causation. Environmental studies in Western Pacific foci showed identical mineral compositions in the soils and drinking water, i.e., extremely low
Induction of intestinal mucosal atrophy by difluoromethylornithine: a nonuremic model of enhanced aluminum absorption.
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The intestinal absorption of aluminum (Al) appears to be enhanced in the uremic rat. Since atrophic changes of the intestinal mucosa have been observed in uremia the present study investigated whether intestinal atrophy induced by difluoromethylornithine (DFMO), a specific inhibitor of ornithine
Reversal by desferrioxamine of tau protein aggregates following two days of treatment in aluminum-induced neurofibrillary degeneration in rabbit: implications for clinical trials in Alzheimer's disease.
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A clinical trial in patients with Alzheimer's disease has indicated that frequent intramuscular (i.m.) treatment with desferrioxamine (DFO) slows progression of the disease. Confirmatory trials have not been carried out, partly because of the rigors of twice daily intramuscular injections over a
Disrupted retention of the classically conditioned nictitating membrane response in rabbits with aluminum-induced neurofibrillary degeneration.
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Rabbits underwent classical conditioning of the nictitating membrane response (NMR) to a tone conditioned stimulus and an air puff unconditioned stimulus until they emitted 90 percent or greater conditioned responses (CRs) for two consecutive days. They then received intraventricular injection of
Chronic aluminum-induced motor neuron degeneration: clinical, neuropathological and molecular biological aspects.
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The monthly intracisternal inoculation of young adult New Zealand white rabbits with low-dose (100 micrograms) aluminum chloride induces aggregates of phosphorylated neurofilament that mimics the intraneuronal inclusions of amyotrophic lateral sclerosis. The chronic progressive myelopathy and
Progressing encephalomyelopathy with muscular atrophy, induced by aluminum powder.
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The injection of aluminum powder into the cerebrospinal fluid of adult rabbits induced a slowly progressing encephalomyelopathy characterized at first by alteration of posture and then by myoclonic jerks and muscle weakness. Neurofibrillary degeneration was the hallmark of the disease and involved
Biochemical and immunological characterization of neurofilaments in experimental neurofibrillary degeneration induced by aluminum.
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In order to identify the protein composition of 10 nm neuronal filaments, we prepared enriched fractions of rabbit spinal neurons undergoing experimental neurofilamentous degeneration induced by aluminum. Electron microscopy of the isolated perikarya showed well-preserved, large perinuclear masses
Neurofibrillary degeneration induced by systemic aluminum.
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Neurofibrillary degeneration was induced in brain of rabbits by repeated, subcutaneous administration of soluble aluminum salts. Atomic absorption spectroscopy showed brain aluminum levels to increase from 1.1+/0.3mug/g (dry weight) in uninjected animals to concentrations ranging from 2.5 to 47.9
Neuropathologic, neurochemical and immunocytochemical characteristics of aluminum-induced neurofilamentous degeneration.
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Inoculation of aluminum salts or metallic aluminum into the central nervous system of rabbits produces an encephalomyelopathy accompanied by widespread neurofibrillary degeneration (NFD) affecting restricted neuronal populations. Some investigators have suggested that this preparation may serve as
Central cholinergic activity in aluminum-induced neurofibrillary degeneration.
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Choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities were measured in spinal cord homogenates from rabbits with aluminum-induced neurofibrillary degeneration and a group of saline-treated, age-matched controls. All aluminum-treated animals showed neurofibrillary changes in the
[Effects of aluminum on the number of neurons granulovacuolar degeneration in rats].
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Effect of aluminum on neurobehavior and the number of neurons in different domains of brain as well as granulovacuolar degeneration (GVD) in hippocampus were observed in Sprague-Dawley rats by intraperitoneal injection with aluminum chloride for 60d. The injection of aluminum at the dosage of 4.0 or
Origin and resolution of the aluminum controversy concerning Alzheimer's neurofibrillary degeneration.
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Elevated concentrations of aluminum are found in regions of neurofibrillary change in brains with senile or presenile dementia of Alzheimer's type. The concentrations of aluminum found in the human disease are comparable to those found in experimental animals with aluminum-induced neurofibrillary
Results of immunocytochemical, neurochemical, and behavioral studies in aluminum-induced neurofilamentous degeneration.
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We undertook a series of experiments designed to further characterize behavioral, neurochemical and immunocytochemical features of aluminum neurotoxicity in the rabbit. Aluminum-exposed rabbits developed learning and memory deficits which were strongly correlated with the degree of whole brain
Tau immunoreactivity associated with aluminum maltolate-induced neurofibrillary degeneration in rabbits.
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Intracisternal administration of aluminum maltolate to rabbits produces a marked argyrophilic neurofibrillary degeneration (NFD) which is also immunoreactive for both phosphorylated and non-phosphorylated microtubule associated protein tau. Using tissue fixation in PBF, the monoclonal antibodies
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