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tetrahydroaminoacridine/atròfia

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Oral tetrahydroaminoacridine treatment of Alzheimer's disease evaluated clinically and by regional cerebral blood flow and EEG.

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Neurochemical evidence indicates that cognitive impairment in dementia of Alzheimer type (DAT) is related to degeneration of cholinergic neurons in the brain. A pharmacological approach is treatment with a cholinesterase inhibitor such as tetrahydroaminoacridine (THA). THA treatment of 17 patients

Effects of tetrahydroaminoacridine and nicotine in nucleus basalis and serotonin-lesioned rats.

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The present study was designed to investigate the hypothesis that concurrent degeneration of serotonin and acetylcholine cells may decrease the therapeutic effects of cholinergic drugs on cognitive functioning in Alzheimer dementia. Therefore, we compared the effects of pretraining injections of a

Tetrahydroaminoacridine improves the recency effect in Alzheimer's disease.

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We investigated the effects of a single administration of tetrahydroaminoacridine (25 and 50 mg, orally), a cholinesterase inhibitor, on memory function in Alzheimer's disease patients. The recall of memory items from the end of the word list (recency effect) was improved in a subgroup of

Effects of tetrahydroaminoacridine on spatial navigation of nucleus-basalis- and frontal-cortex-lesioned rats.

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The present study investigates the effects of tetrahydroaminoacridine (THA: 1 and 3 mg/kg) on water maze (WM) spatial learning performance of intact, nucleus-basalis- (NB) lesioned, frontal-cortex- (FR) lesioned, or NB + FR-lesioned rats. NB lesions did not impair WM learning and had no effect on
The present study examines whether tetrahydroaminoacridine (THA) can improve the deterioration in passive avoidance (PA) retention performance induced by medial septal (MS) and fimbria-fornix (FF) lesions in young rats or by aging. Retention of young MS-lesioned rats was improved by pretraining

Tetrahydroaminoacridine alleviates medial septal lesion-induced and age-related spatial reference but not working memory deficits.

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This study examined the effects of tetrahydroaminoacridine (THA, an anticholinesterase) on water-maze (WM) spatial reference (stable platform location during training) and spatial working memory (reversal of platform location) learning in young intact/medial septal (MS)-lesioned and aged rats. THA

Hippocampal atrophy, acute THA treatment and memory in Alzheimer's disease.

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We designed the present study to investigate the hypothesis that progression of hippocampal pathology may decrease the therapeutic effects of anti-cholinesterase drug, tetrahydroaminoacridine, on memory functioning in Alzheimer's disease (AD) patients. Memory, visuoconstructive, executive and
The nicotinic alpha7 agonist dimethoxybenzilidene anabaseine (DMXB) and cholinesterase inhibitor tetrahydroaminoacridine (THA) were investigated in a trans-synaptic model for neocortical atrophy and degeneration following nucleus basalis lesions. Bilateral lesions reduced parietal neuronal density
We have investigated whether 9-amino-1,2,3,4-tetrahydroacridine (THA), a drug with potential antidementia activity, has a trophic action on differentiating cerebellar granule cells by using the method of [3H]inositol incorporation into inositol-containing phospholipid. Addition of THA (30-50 microM)

Cholinergic therapies for Alzheimer's disease. Palliative or disease altering?

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Loss of cholinergic function in the neocortex and hippocampus arising from death or atrophy of basal forebrain cholinergic neurons is a consistent feature of the Alzheimer brain at autopsy or biopsy. Replacement of lost cholinergic function, therefore, may be of therapeutic benefit to the

Alzheimer's disease and THA: a review of the cholinergic theory and of preliminary results.

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The cholinergic theory is based on the assumption that acetylcholine (ACh) metabolism plays an important role in memory processes and that the deterioration of memory and other cognitive functions in Alzheimer's disease (AD) is directly related to degeneration of cerebral presynaptic cholinergic

Tacrine, a drug with therapeutic potential for dementia: post-mortem biochemical evidence.

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A review of biochemical findings is presented which support the idea that Alzheimer's disease represents a condition for which tetrahydroaminoacridine (tacrine) may have a beneficial effect. There is evidence that clinical and histopathologic hallmarks of the disease relate to cholinergic and

No interaction of memantine with acetylcholinesterase inhibitors approved for clinical use.

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The loss of cholinergic neurons within the basal forebrain of patients with Alzheimer's disease (AD) may underlie aspects of the dementia. Excessive activation of N-methyl-D-aspartate (NMDA) receptors may underlie the degeneration of cholinergic cells. New drug therapies have been designed to either

THA improves word priming and clonidine enhances fluency and working memory in Alzheimer's disease.

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We investigated the effects of a single administration of a cholinesterase inhibitor, tetrahydroaminoacridine (THA, 25 and 50 mg, orally), and an alpha 2-agonist, clonidine (0.5 and 2 micrograms/kg, orally), on neuropsychologic performance in two groups of patients with Alzheimer's disease (AD).

Therapy of Alzheimer disease: symptomatic or neuroprotective?

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Therapeutic strategies aimed to treat Alzheimer disease (AD) may either produce an attenuation of symptoms or slow down deterioration by attenuating progression of the disease. Presently, cholinesterase inhibitors (ChEI) have shown the most promising therapeutical effects. The best documented
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