Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233794 (memory impairment)
 7,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A double-blind study of the effect of CDP-choline on memory impairment following bilateral ECT was performed on 22 inpatients suffering from endogenous depression. 2. Memory scores were checked after 2 and 4 ECT sessions, and the length of the post-ECT confusional state was also measured. 3. The results show no statistically significant differences between the reduced memory scores obtained by both groups. Our findings do not support the hypothesis that CDP-choline affords protection against ECT-induced memory dysfunction in depression cases.
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PMID:The value of cytidine-5-diphosphate-choline in the prevention of impairment of memory function after electric convulsive therapy. A double-blind study. 675 60

An examination of cortex of area 46 in the floor of the principal sulcus in the frontal lobe of the rhesus monkey has been carried out using three young (4-6 years of age), one middle-aged (12 years of age), and five old (25-32 years of age) rhesus monkeys. Light microscopic examination revealed no age-related change in the thickness of the cortex, and no changes in the frequency of profiles of neurons displaying nuclei and contained in 250-micron-wide strips of 1-micron-thick sections. Since the diameters of the nuclei of the neurons were found to be the same in the young and old monkeys, it was concluded that there was no change in the numbers of neurons beneath similar areas of cortical surface of area 46 with age. This conclusion was reinforced by an electron microscopic examination, since there was no suggestion of degeneration of the cell bodies of the neurons, which accumulated but little lipofuscin in the old monkeys. However, there were signs of degeneration in some of the dendrites in the upper layers of the cortex in the old monkeys, especially in layer 1, in which many of the dendrites had lost organelles from their cytoplasm. The other notable change was a degeneration of myelinated axons in the deep layers and white matter in some of the old monkeys. In contrast to the neurons, the effects of aging on the neuroglial cells and pericytes were very obvious, since in the old monkeys each type of neuroglial cell accumulated large inclusions within its cytoplasm. Prior to fixation, these monkeys had been behaviorally tested using a series of spatial and visual recognition tasks, which revealed that relative to the young monkeys, the old monkeys as a group displayed memory impairment. On one task, the extent of the impairment for each old monkey correlated well with the extent of degeneration of myelinated fibers in the cortex and white matter. Consequently, it is suggested that age-related cognitive changes are unlikely to be a result of a loss of neurons, but might be due to an alteration in connections between the cortex and other brain structures.
Cereb Cortex
PMID:The effects of aging on area 46 of the frontal cortex of the rhesus monkey. 770 88

The effects of cytidine diphosphate choline (CDP-choline, CAS 987-78-0) on learning and memory in rats with memory deficits were examined using behavioral methods of active avoidance with punishment reinforcement (shuttle-box), passive avoidance with punishment reinforcement (step-through and step-down), and active avoidance with positive (alimentary) reinforcement (staircase-maze). In the majority of experiments CDP-choline was applied orally at doses of 10-50 or 100 mg/kg daily for 7 days before the training session. The experiments were carried out on young-adult (aged 5 months) and old (aged 22 months) rats and on rats with a low capability for retention of learned behavior. Memory deficits were induced by the muscarinic cholinoceptor antagonist scopolamine (in young and old rats and mice), by the alpha 2-adrenoceptor agonist clonidine, by electroconvulsive shock, and by hypoxy. Memory deficits were also induced in rats offspring of dams that had been exposed to alcohol during pregnancy and lactation. The results suggest that CDP-choline acts as a memory-enhancing drug and that its effect is particularly pronounced in animals with memory deficits.
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PMID:Effects of cytidine diphosphate choline on rats with memory deficits. 821 35

Correlational analysis of regional cerebral glucose metabolism (rCMRglc) obtained by high-resolution positron emission tomography (PET) has demonstrated reduced neocortical rCMRglc interactions in mildly/moderately demented patients with probable Alzheimer's disease (AD). Thus, identification of individual differences in patterns of rCMRglc interactions may be important for the early detection of AD, particularly among individuals at greater risk for developing AD (e.g., those with a family history of AD). Recently, a statistical procedure, using multiple regression and discriminant analysis, was developed to assess individual differences in patterns of rCMRglc interdependencies. We applied this new statistical procedure to resting rCMRglc PET data from mildly/moderately demented patients with probable AD and age/sex-matched controls. The aims of the study were to identify a discriminant function that would (a) distinguish patients from controls and (b) identify an AD pattern in an individual at risk for AD with isolated memory impairment whose initial PET scan showed minor abnormalities, but whose second scan showed parietal hypometabolism, coincident with further cognitive decline. Two discriminant functions, reflecting interactions involving regions most involved in reduced correlations in probable AD, correctly classified 87% of the patients and controls, and successfully identified the first scan of the at-risk individual as AD (probability > 0.70). The results suggest that this statistical approach may be useful for the early detection of AD.
J Cereb Blood Flow Metab 1993 May
PMID:Early detection of Alzheimer's disease: a statistical approach using positron emission tomographic data. 847 2

Alzheimer's disease (AD) causes progressive deterioration of cognition and behavior. Memory dysfunction is the hallmark, but there are also changes in behavior, emotion and autonomic functions, which cannot be explained simply as a consequence of memory impairment. These observations suggest that the natural disease process of AD involves not only memory-related neural structures, but also specific neural systems related to other behaviors, emotion and autonomic functions. Since recent evidence has indicated a primary role for ventromedial frontal (VMF) cortex in such functions, we examined laminar distribution of neurofibrillary tangles and Alz 50 immunoreactive neurons in subdivisions of VMF cortex in 20 AD patients and seven age-matched controls. The densities of pathological changes were: (i) highest in the posteromedial mesocortical regions, particularly Brodmann's area 25 (A25), posterior orbitofrontal cortex (POF) and anterior insula (AI); (ii) of comparable severity between posteromedial mesocortical regions and most temporal cortices, excluding only the entorhinal cortex and temporal pole; and (iii) located predominantly in layer III and especially layer V. Further analysis demonstrated selective pathology in layer V of A25, POF and AI that would disrupt direct cortico-autonomic projections. This is the first study to detail severe AD pathology in these autonomic-related cortices, which could contribute to the behavioral changes, emotional disturbance and autonomic dysregulation that often accompany AD.
Cereb Cortex
PMID:The autonomic-related cortex: pathology in Alzheimer's disease. 902 36

The muscarinic receptor antagonist scopolamine produces a transient memory deficit in healthy humans. This deficit has been offered as a model of the cholinergic deficit of Alzheimer's disease (AD). However, we have previously shown that scopolamine produces a deficit of cortical perfusion maximal in the frontal lobe, dissimilar to the parietal cortex deficit characteristic of AD. The current experiment was aimed at replicating and extending this observation by critically testing the central cholinergic origin of both cognitive and perfusion deficits. Nine healthy subjects participated in regional cerebral blood flow (rCBF) measurements at baseline, after scopolamine (7.2 micrograms/kg i.v.), and after both physostigmine (22 micrograms/kg i.v.) and neostigmine (7 or 11 micrograms/kg i.v.). rCBF was quantified by the xenon 133 inhalation method. As expected, scopolamine reduced cortical perfusion, mainly in the frontal cortex, and produced a memory deficit. Physostigmine, but not neostigmine, reversed all three variables partially or completely. These results support the hypothesis that all three consequences of scopolamine, namely, reduction of mean flow, frontal deficit, and memory impairment, are cholinergically mediated. Furthermore, because neostigmine poorly crosses the blood-brain barrier, these findings confirm that the effect is centrally mediated and cannot be explained by peripheral effects. However, they also confirm the frontal cortex locus of action for both scopolamine and its reversal by physostigmine and therefore suggest a major dissimilarity to the characteristic rCBF appearance of AD. This study extends our previous preliminary findings with tacrine and strengthens the suggestion that only nicotinic receptors are associated with the characteristic parietal deficit of AD.
J Cereb Blood Flow Metab 1997 Feb
PMID:Physostigmine reversal of scopolamine-induced hypofrontality. 904 May 2

The entorhinal, perirhinal and parahippocampal cortices are anatomically positioned to mediate the bi-directional flow of information between the hippocampus and neocortex. Consistent with this organization, damage involving the parahippocampal region causes significant learning and memory impairment in young subjects. Although recent evidence indicates that neuron death in the hippocampus is not required to account for the effects of normal aging on learning and memory, other findings suggest that changes in parahippocampal interactions with the hippocampus may play a significant role. Prompted by this background, we tested the possibility that age-related deficits in hippocampal learning are coupled with neuron death in the parahippocampal region. The experiments took advantage of a well-characterized rat model of cognitive aging in combination with stereological methods for quantifying neuron number. The results demonstrate that total neuron number in the entorhinal, perirhinal and postrhinal cortices is largely preserved during normal aging. Furthermore, individual variability in hippocampal learning among the aged rats failed to correlate with neuron number in any region examined and there was no indication of selective or disproportionate loss among the aged animals with the most pronounced cognitive impairment. Taken together with earlier findings from the same study population, the results demonstrate that age-related cognitive decline can occur in the absence of significant neuron death in any major, cytoarchitectonically defined component of the hippocampal system. These findings provide an essential framework for identifying the basis of cognitive aging, suggesting that alterations in connectivity and other changes are more likely causative factors.
Cereb Cortex 2002 Nov
PMID:Neuron number in the parahippocampal region is preserved in aged rats with spatial learning deficits. 1237 5

We previously showed that dietary cytidine (5')-diphosphocholine (CDP-choline) supplementation could protect against the development of memory deficits in aging rats. In the present study, younger rats exposed to impoverished environmental conditions and manifesting hippocampal-dependent memory impairments similar to those observed in the aging rodents were given CDP-choline, and its effects on this cognitive deficit were assessed. Male Sprague-Dawley rats reared for 3 mo in impoverished (IC) or enriched environmental (EC) conditions concurrently received either a control diet or a diet supplemented with CDP-choline (approximately 500 mg/kg/d). After 3 mo, rats were trained to perform spatial and cued versions of the Morris water maze, and their rates of acquisition and retention were compared. Impoverished rats exhibited a selective deficit in hippocampal-dependent spatial memory which could be ameliorated by feeding them CDP-choline. The CDP-choline had no memory-enhancing effect in enriched rats, nor did it prevent the memory impairment of impoverished rats if the animals consumed it for the initial or final months instead of for the entire 3-mo period. These findings indicate that long-term dietary CDP-choline supplementation can ameliorate the hippocampal-dependent memory impairment caused by impoverished environmental conditions in rats, and suggest that its actions result, in part, from a long-term effect such as enhanced membrane phosphatide synthesis, an effect shown to require long-term dietary supplementation with CDP-choline.
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PMID:Dietary CDP-choline supplementation prevents memory impairment caused by impoverished environmental conditions in rats. 1564 94

An aging rat model of chronic brain hypoperfusion (CBH) that mimics human mild cognitive impairment (MCI) was used to examine the role of nitric oxide synthase (NOS) isoforms on spatial memory function. Rats with CBH underwent bilateral common carotid artery occlusion (2-vessel occlusion (2-VO)) for either 26 or 8 weeks and were compared with nonoccluded sham controls (S-VO). The neuronal and endothelial (nNOS/eNOS) constitutive inhibitor nitro-L-arginine methyl ester (L-NAME) 20 mg/kg was administered after 26 weeks for 3 days to 2-VO and S-VO groups and spatial memory was assessed with a modified Morris watermaze test. Only 2-VO rats worsened their spatial memory ability after L-NAME. Electron microscopic immunocytochemical examination using an antibody against eNOS showed 2-VO rats had significant loss or absence of eNOS-containing positive gold particles in hippocampal endothelium and these changes were associated with endothelial cell compression, mitochondrial damage and heavy amyloid deposition in hippocampal capillaries and perivascular region. In the 8-week study, three groups of 2-VO rats were administered an acute dose of 7-NI, aminoguanidine or L-NIO, the relatively selective inhibitors of nNOS, inducible NOS and eNOS. Only rats administered the eNOS inhibitor L-NIO worsened markedly their watermaze performance (P = 0.009) when compared with S-VO nonoccluded controls. We conclude from these findings that vascular nitric oxide derived from eNOS may play a critical role in spatial memory function during CBH possibly by keeping cerebral perfusion optimal through its regulation of microvessel tone and cerebral blood flow and that disruption of this mechanism can result in spatial memory impairment. These findings may identify therapeutic targets for preventing MCI and treating Alzheimer's disease.
J Cereb Blood Flow Metab 2005 Jun
PMID:Inhibition of vascular nitric oxide after rat chronic brain hypoperfusion: spatial memory and immunocytochemical changes. 1570

Tuberous sclerosis complex (TSC) is a multisystem syndrome classically associated with the occurrence of focal brain dysplasias. We used structural magnetic resonance imaging to test for neuroradiological abnormalities in TSC (tubers, white matter lesions, and subependymal nodules) and to explore the relationships between these lesions and computational morphometric abnormalities of gray and white matter distribution. We tested memory function in TSC and investigated the relationship between memory function and both morphometric variation and lesion load. Patients demonstrated deficits bilaterally in volume of subcortical gray matter regions including thalamus, basal ganglia, insula, and cerebellum, as well as white matter deficits bilaterally in intrahemispheric tracts. Morphometric deficits could not be explained as local effects of lesions. Patients demonstrated deficits in executive working memory and recall memory, sparing recognition. Structure-function mapping showed long-term and working memory function was positively correlated with gray matter density (in thalamus, caudate nucleus, and frontal cortex) but not with lesion load. The neuroanatomical endophenotype of TSC is more extensive than previously recognized and comprises abnormalities in the distribution of gray and white matter in addition to classical lesions. Normal intelligence quotient patients with TSC show a profile of long-term and working memory impairment that is related to gray matter deficits in thalamus and basal ganglia components of fronto-striatal circuits.
Cereb Cortex 2007 Feb
PMID:Neuroanatomical correlates of memory deficits in tuberous sclerosis complex. 1660 14


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