Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peptides have found a progressively more important role in the biochemistry and physiology of the brain in recent years. Many possess neurological and behavioral actions in addition to their function in endocrinology. This paper reviews the formation and distribution, as well as the neurological action, of peptides probably involved in Parkinson's disease: beta-LPH and its derivatives (MSH, ACTH4-10, beta-endorphin). It also recounts the experience of many authors with prolyl-leucyl-glycine-amide (PLG) in that disease. Finally we propose a new theory of the etiology of Parkinson's disease, based on a postulated deficiency in the important trophic function upon catecholaminergic neurons of A.P.U.D. cells.
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PMID:Peptides in Parkinson's disease. 75 85

A number of questions remain unsettled about the release of melanocyte-stimulating hormone (MSH) and about its function. Even though relatively few investigators are studying this area, some generalities have emerged during the last 10 years. It now seems that release of MSH from the pituitary is inhibited by a substance present in the hypothalamus. The structure of this physiologic inhibitor of MSH release may still not be considered an established entity but there is evidence for additional mechanisms capable of exerting a fine control on the release of MSH. Contrary to some opinions, the release of MSH does not always occur together with the release of ACTH, and the release of the two hormones can be dissociated in several laboratory and clinical situations. In addition, many studies have shown that the pituitary peptide, MSH, exerts behavioral and electroencephalographic effects in both the rat and man. The hypothalamic peptide Pro-Leu-Gly-NH2 (MIF-I) also has direct effects on the central nervous system that may include alleviation of the symptoms of Parkinson's disease.
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PMID:Some questions related to melanocyte-stimulating hormone. 96 14

The response of plasma beta-endorphin (beta-EP) to dexamethasone suppression was studied in 14 patients with Alzheimer's disease (AD), 14 patients with Parkinson's disease (PD), and 13 age-matched controls in order to evaluate whether an impairment of the opiate system is present in these neurodegenerative disorders. Basal circulating beta-EP was in normal range in all subjects, although the mean concentration was slightly reduced in the patients compared to controls. After 1 mg dexamethasone given at 11:00 p.m. the night before, plasma beta-EP concentration measured at 08:00 a.m. and 04:00 p.m. was not inhibited in AD and PD patients while it was significantly reduced in controls. Circulating ACTH and cortisol were similar in patients and controls and a normal inhibition of plasma cortisol after dexamethasone was observed in 13/14 AD and 12/14 PD patients. The resistance of beta-EP to dexamethasone inhibition is consistent with previous clinical and experimental data indicating a disorder of the opiate system in brain degenerative diseases.
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PMID:Resistance of beta-endorphin to dexamethasone inhibition in Parkinson's and Alzheimer's diseases. 165 8

Corticotropin releasing hormone (CRH), somatostatin (SRIF), and arginine vasopressin (AVP) concentrations were estimated using radioimmunoassay in the temporal and occipital cortices in postmortem brain from patients clinically and neuropathologically diagnosed as senile dementia of the Lewy body type (SDLT), senile dementia of the Alzheimer type (SDAT), and Parkinson's disease (PD) and from neurologically normal controls. The concentration of temporal and occipital neocortical CRH was diminished in both SDAT and SDLT compared to control values, whereas SRIF was reduced only in temporal cortex in both these conditions. In contrast, the concentrations of both CRH and SRIF were unaltered in PD. The concentrations of AVP in SDLT, SDAT, and PD were similar to those found in the control groups. The decrement in SRIF, but not CRH, was found to be correlated with some indices of severity of illness in SDAT; a similar but nonsignificant trend for SRIF was observed in SDLT.
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PMID:Neocortical concentrations of neuropeptides in senile dementia of the Alzheimer and Lewy body type: comparison with Parkinson's disease and severity correlations. 167 64

The concentrations of somatostatin (SRIF), vasoactive intestinal polypeptide (VIP), beta-endorphin (beta-EP), adrenocorticotropin (ACTH) and corticotropin-releasing factor (CRF) immunoreactivity were measured in cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), patients with Parkinson's disease (PD) and controls. In order to study the mechanisms that regulate peptide levels in CSF and peptide interactions, correlations between CSF peptides were determined. Within all patient groups a number of significant correlations were shown to exist between CSF peptides. The correlations were apparently not coincidental, since there was no such relation between the concentrations of CSF peptides and CSF protein content. Neither age, sex, severity of dementia nor the presence of extrapyramidal signs could explain the number of significant correlations. These results indicate, that the correlations found between CSF peptides may be due to common regulatory mechanisms or general physiological behaviour of peptides in the CSF.
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PMID:A correlation study of CSF neuropeptides in Alzheimer's and Parkinson's disease. 168 48

Complementary oligonucleotide probes specific for the human pro-opiomelanocortin (POMC) mRNA were used to analyze the expression of POMC gene in 56 human postmortem pituitaries by in situ hybridization histochemistry. POMC transcripts were visualized by autoradiography in anterior lobe of the pituitary where their distribution was in a 'patchy-like' pattern. No hybridization could be observed in the posterior lobe of the pituitary. We examined pituitaries from several controls and from patients dying with schizophrenia, Parkinson's disease. Alzheimer's disease, Wernicke's encephalopathy and depressive illness. Computer-assisted microdensitometric semiquantification of POMC mRNA using a complementary oligonucleotide as hybridization standard, revealed no statistically significant effect of postmortem delay (between 2.5 and 66 h), of gender, age (between 22 and 103) or cause of death in 56 human pituitary glands. A large variation in POMC levels was already observed among all 30 control cases. The levels of POMC mRNA observed in pituitaries from different pathologies did not show a significant variation when compared with control cases.
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PMID:Study of pro-opiomelanocortin mRNA expression in human postmortem pituitaries. 171 87

Dopaminergic neuron controls CNS functions such as meso-limbic, striato-nigral and tubero-infundibular systems. The purpose of the present study is the evaluation of the hypothalamic dopaminergic neuron activity in neuro-degenerative disorders. alpha-melanocyte-stimulating hormone (alpha-MSH) is synthesized in the arcuate nucleus and lateral part of the hypothalamus, and its secretion is under the inhibitory control of the dopaminergic neuron both in the hypothalamus and pituitary. alpha-MSH-like-immunoreactivity (alpha-MSH-LI) in CSF is thought to be representative to the dopaminergic neuron activity in the hypothalamus. We therefore evaluated CSF levels of alpha-MSH-LI in spinocerebellar degenerations and extrapyramidal diseases. The subjects are 11 patients with Parkinson's disease, 16 with Shy-Drager syndrome (SDS), 16 with cerebellar cortical atrophy, 3 with Machado-Joseph disease, 3 with dentato-rubro-pallido-luysian atrophy and 2 with Huntington's disease as well as 24 controls. All patients with Parkinson's disease were administered levodopa and carbidopa. CSF was sampled through lumbar puncture in the morning. After the centrifugation, supernatant of CSF was stored at -40 degrees C until used. alpha-MSH in CSF was extracted by Rainero's method and measured by RIA. alpha-MSH-LI levels in control was 23.9 +/- 2.6 pg/ml (mean +/- SD). The significant elevation was observed in Parkinson's disease (40.3 +/- 7.5, p less than 0.001) and SDS (42.3 +/- 9.4, p less than 0.001). The levels showed not significant correlation with age, duration of illness or severity of autonomic disorder. Most of other diseases demonstrated the levels within normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abnormality of hypothalamic dopaminergic system in neuro-degenerative diseases--evaluation of alpha-melanocyte-stimulating hormone-like immunoreactivity in cerebrospinal fluid]. 176 56

Plasma profiles of prolactin, growth hormone, adrenocorticotropic hormone (ACTH) and cortisol were evaluated in a group of untreated patients with idiopathic Parkinson's disease and a group of healthy age-matched controls. Plasma integrated concentrations of all hormones except prolactin were significantly lower in the patients as compared with the controls; however, prolactin nocturnal peak concentration was significantly elevated in the patients; nocturnal growth hormone levels were significantly reduced in the Parkinson group; ACTH and cortisol plasma concentrations were also consistently lower during most of the day in the patients with Parkinson's disease. These data confirm the presence of a hypothalamic disturbance in patients with idiopathic Parkinson's disease, which can affect pituitary function.
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PMID:Plasma profiles of adrenocorticotropic hormone, cortisol, growth hormone and prolactin in patients with untreated Parkinson's disease. 185 13

We performed immunohistochemical analysis of specimens from three autopsied patients with Parkinson's disease, using antibodies to tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP), somatostatin, met-enkephalin, leu-enkephalin and substance P in an attempt to reveal the types of neurons that contain Lewy bodies (LBs) in the paravertebral and celiac sympathetic ganglia and in the enteric nervous system of the alimentary tract. In the sympathetic ganglia, almost all LB-containing neuronal cell bodies and processes were immunoreactive for TH. In the alimentary tract, however, most LBs were found in the VIP-immunoreactive (VIP-IR) neuronal cell bodies and processes. In spite of the significant presence of TH-IR neuronal cell bodies and processes in the alimentary tract, LB-containing TH-IR neuronal elements were rarely encountered. These findings indicate that in the alimentary tract, the VIP neuron system is mainly involved in the disease process of Parkinson's disease.
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PMID:Parkinson's disease: an immunohistochemical study of Lewy body-containing neurons in the enteric nervous system. 197 53

The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value greater than or equal to 5 micrograms/100 ml). PD patients without dementia (nonsuppressors) showed higher basal plasma values of cortisol (22.06 +/- 5.30 micrograms/100 ml) compared with the suppressors (13.38 +/- 3.30 micrograms/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). This suggests that although the depression is clinically undetectable, both disorders may share some pathophysiological features at the hypothalamic hypophyseal adrenal level.
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PMID:Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia. 215 5


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