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choline acetyltransferase/infarction
Врската е зачувана во таблата со исечоци
Страница 1 од 49 резултати
A comparison of brain choline acetyltransferase activity in Alzheimer's disease, multi-infarct dementia, and combined dementia.
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Brain choline acetyltransferase (ChAT) activity was determined in 43 patients with Alzheimer's disease (AD), 14 with multi-infarct dementia (MID), and 15 with combined dementia (CD) and in 53 age-matched controls. The activity of ChAT declined in the hippocampus, temporal and frontal cortex in
Substance P-like immunoreactivity, choline acetyltransferase activity and cholinergic muscarinic receptors in Alzheimer's disease and multi-infarct dementia.
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Substance P-like immunoreactivity, choline acetyltransferase (ChAT) activity and muscarinic cholinergic receptors were measured in brains from 9 individuals with senile dementia of the Alzheimer type (AD), 4 individuals with multi-infarct dementia (MID), 6 individuals with mixed type of dementia
Alterations in the cholinergic system after frontal cortical infarction in rat brain: pharmacological magnetic resonance imaging of muscarinic receptor responsiveness and stereological analysis of cholinergic forebrain neurons.
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Vascular cognitive impairment has been related to dysfunction of the central cholinergic system. Studies exploring the putative relationship between vascular cognitive impairment and cholinergic dysfunction have largely been aimed at symptomatic cholinergic treatment rather than focusing on
Heart-specific overexpression of choline acetyltransferase gene protects murine heart against ischemia through hypoxia-inducible factor-1α-related defense mechanisms.
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BACKGROUND
Murine and human ventricular cardiomyocytes rich in acetylcholine (Ach) receptors are poorly innervated by the vagus, compared with whole ventricular innervation by the adrenergic nerve. However, vagal nerve stimulation produces a favorable outcome even in the murine heart, despite
Subendocardial infarction produces epicardial parasympathetic denervation in canine left ventricle.
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Forty dogs underwent anterior descending coronary artery dissection with most having occlusion that was either maintained or reperfused. Study was performed 1-4 days later. Multiple electrodes placed in normal and ischemic zones were used to determine the depth of the epicardial rim overlying a
NGF prevents further atrophy of cholinergic cells of the nucleus basalis due to cortical infarction in adult post-hypothyroid rats but does not restore cell size compared to euthyroid [correction of euthroid] rats.
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We have tested the hypotheses that nerve growth factor treatment in adult post-hypothyroid rats can: (1) restore cross-sectional area of cholinergic cells of the nucleus basalis and (2) prevent further atrophy of these neurons following cortical infarction. In addition, we assessed the expression of
Paradoxical sleep insomnia and decreased cholinergic neurons after myocardial infarction in rats.
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OBJECTIVE
Acute myocardial infarction (MI) is followed, within a few hours, by neuronal loss in the central nervous system (CNS), including the limbic system, the hypothalamus, and the brainstem. Sleep before and after MI was investigated in the first experiment. In a parallel experiment, 2 weeks
Choline acetyltransferase activity in vascular dementia and stroke.
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OBJECTIVE
Alterations in cholinergic activity have not been systematically studied in types of cerebrovascular disease. We examined cholinergic function at postmortem, focussing on stroke and vascular dementia (VaD).
METHODS
Post-mortem brain tissue was studied from 61 patients with stroke or VaD
Muscarinic binding and choline acetyltransferase in postmortem brains of demented patients.
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Postmortem human brain samples were taken from non-neurological controls as well as demented subjects who died with Alzheimer's disease (AD), multi-infarct dementia (MID), or a combination of AD and MID dementia (MIXED). Choline acetyltransferase (ChAT) activity was measured radiometrically using
Long-term protective effects of human recombinant nerve growth factor and monosialoganglioside GM1 treatment on primate nucleus basalis cholinergic neurons after neocortical infarction.
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Neocortical infarction induces biochemical and morphological retrograde degenerative changes in cholinergic neurons of the rat nucleus basalis magnocellularis [Sofroniew et al. (1983) Brain Res. 289, 370-374]. In the present study, this lesion model has been reproduced in the non-human primate
Neocortical infarction in subhuman primates leads to restricted morphological damage of the cholinergic neurons in the nucleus basalis of Meynert.
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The aim of the present study was to investigate the long-term effect of cortical infarction on the subhuman primate (Cercopithecus aethiops) basal forebrain. The lesion, carried out by cauterizing the pial blood vessels supplying the left fronto-parieto-temporal neocortex, induced retrograde
[Effect of sailuotong capsule on intervening cognitive dysfunction of multi-infarct dementia in rats].
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OBJECTIVE
To study the effect of Sailuotong capsule (Sailuotong) on learning and memory functions of multi-infarct dementia (MID) rats and its mechanism.
METHODS
All SD rats were divided into five groups, namely the sham operation group, the model group, the positive group, the low dosage
Reduced epicardial vagal nerve density and impaired vagal control in a rat myocardial infarction-heart failure model.
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BACKGROUND
Autonomic remodeling, characterized by sympathetic activation and vagal withdrawal, contributes to heart failure (HF) progression. However, the exact mechanism(s) responsible for vagal withdrawal in HF remain(s) unclear, and whether HF causes epicardial autonomic nerve remodeling is
Tyrosine hydroxylase and choline acetyltransferase activities in ischemic canine heart.
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After coronary artery occlusion, enzymes involved in the synthesis of sympathetic and parasympathetic neurotransmitters may change disparately. We investigated this in the canine heart by measuring the activity of tyrosine hydroxylase (TH) and choline acetyltransferase (CAT) in normal and ischemic
Tragus Nerve Stimulation Suppresses Post-Infarction Ventricular Arrhythmia by Modulating Autonomic Activity and Heterogeneities of Cardiac Receptor Distribution
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BACKGROUND Imbalanced cardiac autonomic control and cardiac receptors redistribution contribute to the arrhythmogenic substrate under the myocardial infarction (MI) condition. Stimulating the auricular branch of vagus nerve (AB-VNS) has been proven to reduce post-infarction ventricular arrhythmia
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