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)

Amyloid deposits in Alzheimer's disease brains consist of aggregated amyloid beta-peptides (A beta) which are derived by proteolytic processing of the amyloid beta-protein precursor (APP). Proteolytic APP processing can be regulated by the activity of neuronal cell surface receptors including the muscarinic m1 and m3, the serotoninergic 5-HT2 and 5-HT1C, vasopressin and bradykinin receptor subtypes. Receptor stimulation with appropriate agonists rapidly increases the rates of release of the alpha-secretase processing product APPs which is cleaved within the A beta domain and thus is a non-amyloidogenic derivative. Moreover, stimulation of m1 receptors also decreases the formation of A beta, a secreted potentially amyloidogenic and possibly neurotoxic APP fragment. Similar biochemical events occur in stimulation experiments of fresh rat brain slices suggesting that neuronal activity may be involved in regulating APP processing in mammalian brain. Activation of non-amyloidogenic APP processing and inhibition of amyloidogenic processing pathways by subtype-specific agonists of muscarinic, serotoninergic or peptidergic receptors provides a novel approach for the pharmacological modulation of APP processing in Alzheimer's disease.
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PMID:Regulation of proteolytic processing of the amyloid beta-protein precursor by first messengers. A novel potential approach for the treatment of Alzheimer's disease. 776 40

The supraoptic (SON) and paraventricular nuclei (PVN) of the human hypothalamus are production sites of vasopressin (AVP) and oxytocin (OXT). Although the hypothalamus is affected in Alzheimer's disease (AD), previous work has not only shown that in these two nuclei no neurons are lost, neither during aging nor in AD, but that the number of AVP-expressing neurons and their nucleolar size had even increased with age. These observations indicated that the peptide synthesis of the AVP neurons was activated in the oldest age-groups. Recently published, qualitative observations, using the area of the Golgi Apparatus (GA) as a sensitive parameter for neurosecretory activity, confirmed the activation of SON and PVN neurons with age in human; however, in this report the neurons were not identified according to their neuropeptide content. In the present quantitative study we determined whether the AVP neurons were indeed activated as a result of the aging process in controls and AD patients. We applied a polyclonal antiserum directed against the medial cisternae of the GA on formalin-fixed, paraffin-embedded tissue sections taken from the dorsolateral SON (dl-SON) of 10 controls and 10 AD patients, and performed our measurements in this area that is known to be predominantly occupied (90-95%) by AVP neurons. In addition, the sparse OXT cells present in the area of study, were excluded from the measurements on the basis of alternative sections stained for OXT. In the dl-SON, the area occupied by the GA and the cellular profile area per patient were quaNtified by means of image analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of vasopressin neurons in aging and Alzheimer's disease. 789 70

beta A4 is the principal component of Alzheimer's disease brain amyloid. It is derived from proteolytic processing of amyloid beta-protein precursors (APP), a family of transmembrane glycoproteins. Secretion of APPs, a secreted proteolytic derivative that is cleaved within the beta A4 domain of APP, is increased many-fold by the activation of cell-surface receptors, like the muscarinic m1 and m3 receptor subtypes, which are coupled to protein kinase C. Concomitantly, their activation decreases the formation of both secreted soluble beta A4 and of endosomal-lysosomal C-terminal APP derivatives. These data suggest that muscarinic m1 and m3 receptors accelerate non-amyloidogenic APP processing and depress the formation of potentially amyloidogenic derivatives. Other receptors that stimulate APPs secretion include those for bradykinin, vasopressin, and interleukin-1 receptors. A similar control mechanism is present in rat brain tissue slices, in which the release of both APPs and endogenous neurotransmitters is increased by electrical depolarization. This increase is tetrodotoxin-sensitive and frequency-dependent, suggesting that APPs release may normally depend on neuronal activity. Taken together, our findings suggest that specific receptor agonists might be effective in reducing the formation of potentially amyloidogenic APP derivatives in vivo.
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PMID:Regulation of proteolytic processing of the amyloid beta-protein precursor of Alzheimer's disease in transfected cell lines and in brain slices. 789 93

Scrapie is a transmissible neurodegenerative disease which shares some characteristics with Alzheimer disease (AD). Recent studies show abnormal enlargement of the adrenal glands and kidneys in 139H-affected hamsters. Using immunocytochemical techniques with antibodies to corticotropin-releasing factor (CRF) and vasopressin (VP), we observed the following: (1) a significantly higher number of CRF-immunostained neurons in the preoptic nucleus of hypothalamus of 139H-affected hamsters than controls; (2) the area of VP-immunostained (ir-VP) neurons in the lateral hypothalamus, which includes the internuclear group of magnocellular neurons and the nucleus circularis, was significantly lower for 139H-affected hamsters than for controls; and (3) no significant difference between 139H-affected and control hamsters with regard to the number of ir-VP neurons in the dorsal-medial hypothalamus (DMH), including the paraventricular hypothalamus, or the supraoptic nuclei. However, the population of ir-VP neurons in the DMH shifted to the anterior part of the hypothalamus in 139H-affected hamsters. Three-dimensional models of the immunostaining were prepared and these provide clear depictions of the changes noted. The changes in the CRF and VP systems in 139H-affected hamsters suggest that the neuroendocrine system can be affected by unconventional slow infections.
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PMID:Effect of infection with the 139H scrapie strain on the number, area and/or location of hypothalamic CRF- and VP-immunostained neurons. 794 71

The vasopressin (VP) innervation of the human locus coeruleus (LC) was immunocytochemically investigated in Alzheimer's disease (AD) patients and non-demented controls. A dense innervation of VP fibers was present throughout the entire rostro-caudal length of the LC in both, controls and AD-patients. The VP immunoreactivity was confined to fibers; no signs of cell body staining could be found. Comparison of five non-demented control subjects and five AD patients on fifteen different levels throughout the LC revealed that the VP innervation of this nucleus remained intact in AD, even in the rostral part of the LC, which is the most affected region with respect to neuronal loss.
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PMID:Stable vasopressin innervation in the degenerating human locus coeruleus in Alzheimer's disease. 795 48

Recent studies on experimental animals showed that long term activation of the hypothalamo-pituitary-adrenal axis is associated with increased vasopressin (AVP) colocalization in paraventricular corticotropin-releasing hormone (CRH) neurons. In the present study we estimated the fraction of CRH neurons in which AVP is colocalized by double label immunocytochemistry in hypothalami of 10 control subjects of 21-91 years of age and 10 age-matched Alzheimer patients. CRH neurons in the paraventricular nucleus (PVN) of Alzheimer patients and control subjects showed similar age dependent increases in AVP colocalization. Based on this parameter, it seems that CRH neurons of Alzheimer patients are not overactivated as compared to age-matched controls, but e.g. changes in m-RNA for CRH should still be established.
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PMID:Similar age related increase of vasopressin colocalization in paraventricular corticotropin-releasing hormone neurons in controls and Alzheimer patients. 804 11

Individuals with Alzheimer's disease (AD) have been shown to have abnormalities in response to fluid restriction. Twelve subjects with AD and ten elderly controls underwent overnight fluid restriction followed by measurement of plasma and urine vasopressin and serum osmolality. Estimates of "thirst" were determined after one hour of ad libitum water intake. All subjects were tested with a Mini-Mental State Examination (MMSE) and Global Deterioration Scale (GDS). Individuals with AD had a greater degree of overnight dehydration than the elderly control group (serum osmolality 310 +/- 1 vs. 305 +/- 1 mosmol/kg, p = 0.02). There was no difference between the groups in the plasma or urinary levels of vasopressin. There was a direct correlation (r = 0.45, p = 0.03) of the amount of water intake as a measure of "thirst" with the MMSE score as a measure of cognitive functioning. Individuals with advanced cognitive impairment may be at risk of dehydration due to loss of protective "thirst" responses with secondary complications of dehydration.
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PMID:Drinking behavior and vasopressin responses to hyperosmolality in Alzheimer's disease. 805 97

The supraoptic (SON) and paraventricular nucleus (PVN) of the human hypothalamus produce vasopressin (AVP) and oxytocin (OXT). Since in these nuclei no cells are lost during aging or Alzheimer's Disease (AD), factors are searched for which may be responsible for this remarkable stability. Earlier work in both rat and human indicated that the peptide synthesis of these neurons was activated in the oldest age groups as judged from increased neuronal and nuclear size and AVP plasma levels. The size of the Golgi Apparatus (GA) has proved to be a very sensitive parameter for the synthetic activity of these neurosecretory cells in animal experiments. In order to determine changes in the GA during aging and in Alzheimer's Disease, we applied a polyclonal antiserum against immunoaffinity purified MG-160, a sialoglycoprotein of the medial cisternae of the GA, on formalin-fixed and paraffin-embedded sections of the SON and PVN of patients ranging in age from 29 to 97 years. However, our standard fixation procedure masked antigenic sites resulting in a minimal immunocytochemical staining in most of the tissues examined. It appeared to be possible, however, to retrieve the antigen and to obtain an excellent staining of the GA by heating sections in a microwave oven before immunostaining. Following this procedure, an increase in size and intensity of the GA became apparent in individuals from about 70 years and older. In AD patients a similar increase in size and intensity of the immunostained GA was observed. Taken together, these results indicate that SON and PVN neurons are activated during the course of aging and also in AD and that this activation takes place at an earlier age than observed previously by other cellular parameters.
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PMID:Activation of the human supraoptic and paraventricular nucleus neurons with aging and in Alzheimer's disease as judged from increasing size of the Golgi apparatus. 814 18

The two major primary degenerative dementias, dementia of Alzheimer type (DAT) and frontal lobe degeneration of non-Alzheimer type (FLD) have several clinical features in common but also many symptoms that differ. In a clinical material of 80 patients with either of the two forms of dementia (DAT = 39, FLD = 41) we have studied the levels of neuropeptides in the cerebrospinal fluid (CSF) in order to find biochemical markers for CNS affection. The dementia forms were evaluated by careful clinical analysis, psychometric testing and measurement of regional cerebral blood flow. Approximately one third of the subjects died during the completion of the study and neuropathology was performed, confirming the diagnoses. We observed reductions in the CSF levels of antidiuretic hormone and somatostatin in both DAT and FLD. A strong tendency to reduction was noted for neuropeptide Y (NPY). There was a correlation with the duration of disease demonstrating a significant reduction in NPY levels in subjects with DAT. Most notably there was a strong reduction in the levels of delta sleep inducing peptide (DSIP) in DAT cases only. The levels of DSIP in FLD were the same as in controls. The reverse was found for corticotropin releasing factor (CRF) which had a significant reduction in FLD patients but not in those with DAT. The present study indicates a difference in the CSF levels of neuropeptides, observations that these may serve as biochemical markers which differentiate DAT and FLD.
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PMID:Neuropeptides in cerebrospinal fluid of patients with Alzheimer's disease and dementia with frontotemporal lobe degeneration. 840 87

Previous studies have shown an activation of the hypothalamo-neurohypophyseal system (HNS) in normal aging and in senile dementia. Among other explanations, this activation might be secondary to cell loss in the supraoptic (SO) and paraventricular (PV) nuclei. This study reports a 63% loss in the SO and a 56% loss in the PV in a group of Alzheimer disease (AD) patients. The remaining neurons undergo a compensatory hypertrophy that is more pronounced in the SO, affecting cell and nuclear size as well as nucleolar volume. The group of patients with a diagnosis of moderate dementia showed the greatest hypertrophy, as compared to the severely demented patients. Our results suggest that there is a compensatory capacity in the earlier stages of the dementia, that is lost in the final stages of Alzheimer's disease.
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PMID:Cell loss in supraoptic and paraventricular nucleus in Alzheimer's disease. 850 99


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