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)

Dinucleotide deletions (e.g. DeltaGA, DeltaGU) are created by molecular misreading in or adjacent to GAGAG motifs of neuronal mRNAs. As a result, the reading frame shifts to the +1 frame, and so-called "+1 proteins" are subsequently synthesized. +1 Proteins have a wild-type N-terminus, but an aberrant C-terminus downstream from the site of the dinucleotide deletion. Molecular misreading was discovered in the rat vasopressin gene associated with diabetes insipidus and subsequently in human genes linked to Alzheimer's disease (AD), e.g. beta amyloid precursor protein (betaAPP) and ubiquitin-B (UBB). Furthermore, betaAPP(+1) and UBB(+1) proteins accumulate in the neuropathological hallmarks (i.e. in the tangles, neuritic plaques, and neuropil threads) of AD. As these +1 proteins were also found in elderly nondemented controls, but not in younger ones (<51 years), molecular misreading in nondividing cells might act as a factor that only becomes manifest at an advanced age. Frameshift mutations (UBB(+1)) and pretangle staining (Alz-50 and MC1) seem to occur independently of each other during early stages of AD. We recently detected +1 proteins, not only in proliferating cells present in non-neuronal tissues such as the liver and epididymis, but also in neuroblastoma cell lines. These observations suggest that molecular misreading is a general source of transcript errors that are involved in cellular derangements in various age-related pathologies.
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PMID:Molecular misreading: a new type of transcript mutation expressed during aging. 1112 39

Requirements for an effective animal model of cognition are discussed with special reference to the cholinergic hypothesis of Alzheimer's disease. It is argued, with reference to research on vasopressin and ACE inhibitors, that many putative animal models of cognition lack predictive clinical validity because they either confound the effects of cognitive and arousal processes, or fail to model a specific component of cognitive functioning. A survey of recent research on the cholinergic hypothesis illustrates how these weaknesses can be overcome. Studies involving scopolamine and basal forebrain excitatory amino acid lesion models of the cholinergic deficit in Alzheimer's disease have employed a delayed-matching-to-position test in rodents which, unlike passive avoidance, allows the effects of memory and attentional variables to be distinguished. In combination with recent human studies, these experiments suggest that the cholinergic system has a major role in executive control of attentional resources, and lead to the recommendation of a 'top down' strategy in the investigation of neurochemical processes and pharmacological mechanisms underlying cognition.
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PMID:Pharmacological mechanisms and animal models of cognition. 1122 29

Many common problems encountered in the ageing patient can be related to neuroendocrine phenomena. These include Alzheimer's disease, dementia and cognitive dysfunction, depression, Parkinson's disease, hyponatraemia and the postmenopausal increase in both vascular risk and osteoporosis. This review concentrates on the hypothalamic neuroendocrine system, including the dopaminergic, noradrenergic, serotoninergic, cholinergic and neurohypophyseal systems and the roles of the anterior pituitary and monoamine oxidases, luteinizing hormone-releasing hormone, corticotrophin-releasing factor, the pro-opiomelanocortin-derived and opioid peptides, peptides involved in growth hormone and thyrotropin regulation, and amino acid transmitters.
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PMID:Neuroendocrinology of ageing. 1150 4

The neurohypophyseal hormones arginine-vasopressin (AVP) and oxytocin (OT) are produced in the neurons of the hypothalamic supraoptic (SON) and paraventricular (PVN) nucleus and in the much smaller cells of the suprachiasmatic (SCN) nucleus. The SON is the main source of plasma AVP. Part of the AVP and OT neurons of the PVN join the hypothalamo-neurohypophyseal tract, whereas others send projections to the median eminence or various brain areas, where AVP and OT are involved in a number of central functions as neurotransmitters/neuromodulators. AVP and OT from the PVN can also regulate via the autonomous innervation endocrine glands and fat tissue. OT is produced for a major part in the PVN but some OT neurons are present in the SON. Moreover, both AVP and OT containing neurons are observed in the "accessory nuclei", i.e. islands situated between the SON and PVN. The SCN is the biological clock, and the number of AVP expressing neurons in the SCN shows both diurnal and seasonal rhythms. In addition to these hypothalamic areas, AVP and OT may be found to a lesser extent in some other brain areas, such as the bed nucleus of the stria terminalis, diagonal band of Broca, nucleus basalis of Meynert, lateral septal nucleus, globus pallidus and the anterior amygdaloid nucleus, as well as in the peripheral tissues. The AVP and OT containing neurons should not be considered as one system. Prominent functional differences exist between the different nuclei. The heterogeneity also becomes clear from the marked differences in the neurohypophyseal peptides containing neurons of the SON, PVN and SCN during aging, and in the most prevalent age-related neurodegenerative diseases, i.e. Alzheimer's disease (AD). For those reasons, we will discuss the SON, PVN and SCN separately.
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PMID:Neurohypophyseal peptides in aging and Alzheimer's disease. 1206

In various hypothalamic and adjacent brain regions we have previously found a remarkable increase in nuclear estrogen receptor staining in Alzheimer's disease (AD). In order to see whether this was a general phenomenon or rather specific for those areas that are affected by the AD process we investigated ERalpha and ERbeta expression in the arginine-vasopressin (AVP) neurons of the human dorsolateral suparoptic nucleus (dl-SON), that is the major source of plasma AVP. These neurons remain exceptionally intact in AD. Changes in ER expression were studied in relation to early Alzheimer changes (i.e. hyperphosphorylated tau) and neuronal metabolism in AD as determined by the size of the Golgi apparatus (GA) or cell size. No difference in neuronal metabolism (i.e. GA size or cell size) of AVP neurons was observed between AD and control patients and no early cytoskeletal AD alterations were found confirming the resistance of the dl-SON to AD. While no differences between AD and control patients were present for ERalpha and ERbeta staining except for a lower proportion of nuclear ERbeta AVP-positive neurons in AD subjects, complex sex differences not directly related to AD were observed within each group. The main finding of the present study is that in the dl-SON, that remains active and spared of AD changes, the increase in nuclear ERs seen in adjacent affected areas in AD patients does not occur. This indicates that a rise of nuclear ERs is not a generally occurring phenomenon but rather related to the pathogenetic alterations of the AD process.
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PMID:Sex differences in estrogen receptor alpha and beta expression in vasopressin neurons of the supraoptic nucleus in elderly and Alzheimer's disease patients: no relationship with cytoskeletal alterations. 1227 May 12

We measured serum content of autoantibodies to beta-amyloid protein Abeta(1-42), its neurotoxic fragment Abeta(25-35), vasopressin, bradykinin, thrombin, antithrombin III, alpha(2)-macroglobulin, and angiotensin II in patients with various forms of Alzheimer's dementias, including presenile and senile dementias of the Alzheimer type. The ratio of antibradykinin and anti-Abeta(1-42) autoantibody contents differed by 39% in these patients. Our results can be used for the development of a new biochemical method for differential diagnostics of dementias of the Alzheimer type.
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PMID:Content of autoantibodies to bradykinin and beta-amyloid(1-42) as a criterion for biochemical differences between Alzheimer's dementias. 1453 9

In this article we show some recent findings that constitute a great progress in the molecular knowledge of synaptic dynamics. To communicate, neurons use a code that includes electrical (action potentials) and chemical signals (neurotransmitters, neuromodulators). At the moment a great variety of molecules are known, whose neurotransmitter function in brain and the peripheral nervous system are out of question. Monoamines like acetylcholine, dopamine, noradrenaline, adrenaline, histamine, serotonin, glutamate, aspartate, glycine, ATP and GABA are good examples. Opioid neuropeptides, vasoactive intestinal peptide (VIP), neurokinines (substance P), somatostatin, neurotensin, neuropeptide Y, cholecystokinine, vasopressin or oxitocin have been related to the control of the stress response, sexual behaviour, food intake, pain, learning and memory, qualities that are also related to nitric oxide (NO). A great part of the molecular structure of the secretory machinery is known to be responsible for fast neurotransmitter release at the synapse, in response to action potentials. Proteins like sinaptobrevin (located in the membrane of the synaptic vesicle), sintaxin and SNAP-25 (both located at the presynaptic plasma membrane) constitute a trimeric complex which is responsible of the vesicular docking at the active sites for exocytosis. From this strategic location, vesicles release their neurotransmitter within few milliseconds, when the action potential invades the nerve terminal and activates the opening of the different subtypes of voltage-dependent Ca2+ channels. The asymmetric geographical distribution of each type of channel, in different neurons, rose the hypothesis that Ca2+ that enters through each subtype of channel is compartmentalised, thus favouring the generation of Ca2+ microdomains, in the cytosol and the nucleus, involved in different cellular functions. This great biochemical synaptic heterogeneity is facilitating the selection of many biological targets to develop drugs with potential therapeutic applications in neuropsychiatric diseases i.e. Alzheimer's, Parkinson, epilepsies, stroke, vascular dementia, depression, schizophrenia, anxiety and so on.
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PMID:[Neurotransmitters, calcium signalling and neuronal communication]. 1515 88

Recent studies have shown that there is a relationship between an alteration of central neurotransmitters and the modification of some biohumoral parameters in Alzheimer's Disease (AD). In this study the authors evaluated, after metoclopramide (MTC) stimulation, the concentration curve of vasopressin (AVP), prolactin (PRL) and growth hormone (HGH) in the plasma of 34 subjects (20 males and 14 females, mean age 70.5+/-6.9 years; 17 were AD patients, the others constituted the control group). MTC increased AVP serum concentration in healthy (P <0.001), but not in AD patients. This result seemed to be due to the lack of 'procholinergic' action of the drug in the AD patients probably due to an alteration in their cholinergic pathways. The PRL response to MTC was reduced only in the AD female group (P <0.005), suggesting an alteration in dopaminergic control. Lastly, the HGH response in AD did not differ in the two groups, neither in basal conditions, nor after MTC stimulation. The absence of HGH response both in AD and in healthy subjects, demonstrated the ineffectiveness of MTC stimulation. We can conclude that AVP and PRL responses to MTC stimulation efficiently separated the two groups (AD and controls); the former test showing a higher discriminant power than the latter.
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PMID:Vasopressin, prolactin and growth hormone in Alzheimer's disease: their evaluation after metoclopramide stimulation. 1537 2

Previously, alterations in neuronal metabolism were found in a number of brain areas of Alzheimer disease (AD) patients. In the present study we aimed at determining for the first time whether metabolic changes would also occur in vascular dementia (VD) patients in the supraoptic (SON), infundibular (INF), tuberomamillary (TMN), medial mamillary nuclei, vertical limb of the diagonal band of Broca (VDB), and nucleus basalis of Meynert. The Golgi complex (GC) size, cell size, and vasopressin mRNA levels (in the SON) were used as measures of neuronal metabolic activity in postmortem material. The GC immunoreactivity was clearly diminished in the SON, INF and TMN and was increased in the VDB of VD cases. Interestingly, in the SON and TMN, a decrease in the GC size was more pronounced in male than in female VD patients in accordance with the higher prevalence of VD in men. In 7 of 11 VD cases, vasopressin mRNA levels were significantly reduced which may contribute to urinary incontinence, one of the most common clinical symptoms in VD, and to the lower blood pressure values that are often registered at the later stages of the VD. Since the human TMN is the sole source of cerebral histamine, our data suggest deficient histaminergic transmission in the brain in VD. Diminished neuronal metabolism in the SON and INF was not observed in AD in this and previous studies, whereas the changes in the VDB and TMN are similar in VD and AD. In the present study we thus found decreased metabolic activity in several hypothalamic nuclei in VD indicating diminished production of certain hormones and neurotransmitters.
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PMID:Metabolic alterations in the hypothalamus and basal forebrain in vascular dementia. 1562 61

Mutations in the human gene encoding the antidiuretic hormone vasopressin (VP) cause autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI), a rare inherited disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of VP from posterior pituitary nerve terminals. Work from our laboratories has shown that adFNDI, like other neurodegenerative diseases such as Alzheimer's, Parkinson's and Huntington's, is associated with autophagy. We have recently shown that the activation of autophagy in mouse neuroblastoma Neuro2a cells after adenoviral vector-mediated delivery of an adFNDI mutant VP transgene (Cys67stop) is a cell survival mechanism; its inhibition induces apoptosis. We now show that expression of Cys67stop sensitizes Neuro2a cells to the lethal effects of dopamine. This mode of cell death exhibits features typically associated with classical apoptosis. Yet inhibition of autophagy reversed these effects and rescued cell viability. We propose that autophagy-mediated cell death is a "two-hit" process: Following the cellular stress of the accumulation of a misfolded mutant protein, autophagy is prosurvival. However, a second insult triggers an autophagy-dependent apoptosis.
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PMID:Autophagy-dependent cell survival and cell death in an autosomal dominant familial neurohypophyseal diabetes insipidus in vitro model. 1578 8


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