Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recognition that chronologic age is not per se a cause of dementia opens the way for a more active approach to Alzheimer-type dementias as a specific disease syndrome. "Alzheimerism" in many respects is to the cholinergic brain system what Parkinsonism is to the dopamineragic. Whether cell loss or choline acetyltransferase deficiency comes first is still unclear, as is the role of vasopressin. There is a real possibility that research might produce a palliative for ACh-based defects similar to the action of L-dopa in dopaminergic defects.
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PMID:Alzheimer's disease or "Alzheimerism"? 4 21

Neurotransmitters including acetylcholine, dopamine, norepinephrine, serotonin, GABA and vasopressin were examined in control subjects and patients with Alzheimer-type dementia, involving presenile and senile dementia. Neurotransmitters exhibited various mode of changes with aging. Abnormalities found in senile or presenile dementia were not always parallel to the age-related changes. These results suggest that Alzheimer-type dementia cannot be understood as an accelerated senescence, but other etiological factors might be introduced for the manifestation of the dementia. Moreover, the disturbance in neurotransmitters revealed a difference between presenile Alzheimer's disease and senile dementia, indicating that further studies should be carried out taking the age of onset into consideration.
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PMID:Senile dementia and presenile dementia. 170 90

In individuals above 60 years of age, an age-related decrease in the concentrations of dopamine, noradrenaline, and 5-hydroxytryptamine has been found. This may indicate a neuron loss. As the metabolites are not simultaneously reduced, a compensatory mechanism would seem to exist. In the hypothalamus there are significant positive correlations between the neuropeptides galanin and corticotropin-releasing factor on the one hand, and age over 60 on the other. In brains from patients with dementia of Alzheimer type there are reduced concentrations of cholineacetyl transferase. However, in some brain areas reduced concentrations of 5-hydroxytryptamine, dopamine, and noradrenaline have also been found. The metabolites homovanillic acid and 5-hydroxyindolacetic acid are also reduced. These findings indicate that there is not only a neuron loss in these brains but also a dysfunction of the remaining neurons, reducing the compensatory capacity of the brain. Postmortem investigations of hypothalamus from Alzheimer brains have shown reduced concentrations of 5-hydroxytryptamine. However, the concentrations of galanin, arginin, vasopressin, and somatostatin were significantly increased. The latter may be the result of a disturbed higher control over the hypothalamus. Hypothalamic dysfunction is of interest with regard to the neuroendocrine disturbances seen in Alzheimer-demented patients. Investigations of patients with vascular dementia have suggested the same type of neurotransmitter disturbances as in Alzheimer's disease.
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PMID:Biochemical substrates in normal aging and Alzheimer's disease. 197 Aug 89

We carried out a double-blind study of a vasopressin-related peptide, DGAVP citrate (Org 5667), in 115 patients with mild dementia, probable Alzheimer's type (DAT). Neither clinical rating scales nor psychometric tests revealed any improvement over 84 days with once-daily intranasal treatment with 2 different doses of DGAVP. We conclude that vasopressin-like peptides are not satisfactory therapeutic agents in DAT.
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PMID:DGAVP (Org 5667) in early Alzheimer's disease patients: an international double-blind, placebo-controlled, multicenter trial. 219 1

Concentrations of vasopressin (AVP) and monoamine metabolites (HVA, 5-HIAA, MHPG) in cerebrospinal fluid (CSF) were measured and compared with memory functions in patients with dementia of Alzheimer type (DAT) and control subjects. CSF concentrations did not differ between the DAT patients and the controls, or between patients with different degrees of dementia. There were no correlations between concentrations of vasopressin and monoamine metabolites in CSF or between the CSF measures and psychological test scores, except for a correlation between CSF HVA and immediate and delayed story recall. These data suggest that probable damage to the vasopressinergic and monoaminergic systems in DAT is not reflected in the CSF of patients in early stages of the disease, nor is a deficit in these systems or their interaction the primary cause of cognitive impairment in DAT.
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PMID:Vasopressin levels in CSF of Alzheimer patients: correlations with monoamine metabolites and neuropsychological test performance. 247 86

When compared with those of age-matched control patients the number of nerve cells in the locus caeruleus in 30 patients with Alzheimer's disease is reduced by 65% while nucleolar volume in surviving cells of the locus caeruleus and in those of the paraventricular and supraoptic nuclei of the hypothalamus is reduced by 25%, 48% and 26% respectively. Furthermore the reduction in cell number and nucleolar volume in these 3 cell types are all interrelated, emphasizing the close functional linkage of these cell groups. Similar changes (for age) were seen in a group of 10 patients with a mixed Alzheimer/vascular type dementia and in 6 patients over 50 years of age with Down's syndrome whose brains also showed extensive senile plaque and neurofibrillary tangle formation. This damage to the locus caeruleus and hypothalamic systems is probably responsible for losses of noradrenaline and vasopressin reported in cerebral cortex and hypothalamus; the importance of these changes to the pathogenesis of Alzheimer's disease is emphasized.
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PMID:Changes in Alzheimer's disease in the magnocellular neurones of the supraoptic and paraventricular nuclei of the hypothalamus and their relationship to the noradrenergic deficit. 316 May 17

Nine elderly patients, some with preceding dementia, presented with adipsia, progressive dehydration, impaired consciousness, and hypernatremia following common acute infections without gastrointestinal disturbance. Studies before rehydration revealed inappropriately low plasma arginine-vasopressin (AVP) levels for plasma osmolality, insufficiently concentrated urine, absolutely or relatively low plasma angiotensin II (A-II) concentrations (compared with plasma renin activity and plasma angiotensin I concentrations), and low serum angiotensin I-converting enzyme activities. The plasma AVP concentrations were positively correlated with the plasma A-II concentrations (r = .677) but not with plasma osmolality. The plasma AVP level was raised by an intravenous infusion of A-II in one patient. These findings suggest the following sequence of events: impaired A-II production caused impairment of thirst perception, renal-concentrating capacity, and AVP secretion and contributed to development of hypernatremic dehydration in these elderly patients.
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PMID:Impaired arginine-vasopressin secretion associated with hypoangiotensinemia in hypernatremic dehydrated elderly patients. 327 39

The effects of peptides on brain function suggest therapeutic and pathologic roles for these substances. Many peptides cross the blood-brain barrier (BBB) by transmembrane diffusion as a function of their lipid solubilities. Other peptides, such as the enkephalins, Tyr-MIF-1, vasopressin-related peptides, and peptide T-like peptides, are transported by carrier-mediated systems. Passage is influenced by aging, stress, lighting, drugs, amino acids, and neurotoxins. Disruption of the BBB results in complex changes in the blood and CSF levels of peptides. Peptides influence the passage of glucose, amino acids, and inorganic acids and may affect the integrity of the BBB. Peptide-BBB interactions have been suggested to play direct roles in dialysis dementia and maple syrup urine disease; they may be expected to be involved in other disorders of the CNS.
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PMID:Interactions between the blood-brain barrier and endogenous peptides: emerging clinical implications. 328 19

Although nursing homes are potentially important sites for geriatric research, previous reports have identified impediments to subject recruitment in this setting. We are conducting five simultaneous clinical studies in a 725-bed nursing home. Utilizing a systematic subject recruitment methodology designed to minimize patient and staff burden, we have recruited over 100 subjects. The average recruitment rate over two years from nursing home residents meeting study entry criteria was 43%. The rate was highest (81%) for a study of urinary incontinence offering direct benefit to participants, and lowest (28% and 14% respectively) for physiologic studies of vasopressin regulation and dermal vitamin D production, offering no direct benefit. Studies of syncope and dementia which benefitted groups affected by these problems but not controls, had intermediate recruitment rates (46 and 44%, respectively, P less than .002 compared to incontinence). Thus, clinically relevant projects, sensitive to the needs of the patient and institution, can recruit subjects from the nursing home.
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PMID:Biomedical research in the nursing home: methodological issues and subject recruitment results. 358 66

Vasopressin peptides have been shown to facilitate learning and memory in both animals and humans; however, the effectiveness in humans is controversial. In a double blind parallel group study, 17 demented subjects (either Alzheimer's or alcoholic) were given either desglycinamide-9-arginine-8-vasopressin (DGAVP) 92 micrograms intranasally TID or an identical placebo for 1 week after having received 1 week of placebo. To our knowledge, this is the first report of DGAVP being used in subjects with dementia. The DGAVP group had a statistically significant improvement on the Buschke list learning of low imagery words. However, for various reasons discussed in the paper, we feel this finding needs to be replicated before any definite conclusions can be drawn. Since there were no other appreciable behavioral effects of this DGAVP regimen, our results should be considered negative. There was no evidence of any DGAVP-related adverse effects, except for possible weight gain.
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PMID:Desglycinamide-9-arginine-8-vasopressin (DGAVP, Organon 5667) in patients with dementia. 389 14


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