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)

Several neurotransmitter markers were investigated in the cerebrospinal fluid (CSF) from patients with Alzheimer's disease (AD) (n = 27), Parkinson's disease (PD) (n = 35) and ALS (n = 26) and from control subjects (n = 34) to compare the possible alterations in the biochemical profiles of these different neurodegenerative diseases. The main proportion of the patients represented an early phase of the illness at the time of the diagnosis. Correlations of the degree of dementia and the stage of the disease with CSF measures were evaluated. The CSF levels of somatostatin like-immunoreactivity (SLI) were significantly reduced in AD patients when compared with those of normals and ALS patients. The CSF concentrations of homovanillic acid (HVA) were significantly decreased for PD patients and the decrease focused on the non-demented patients. A trend of decreasing HVA values towards the most advanced stage of Parkinson's disease assessed by Webster's scale was also displayed. The content of 3-methoxy-4-hydroxyphenylglycol (MHPG) in the CSF was higher for ALS patients than for other groups. The lowest 5-hydroxy-indoleacetic acid (5HIAA) levels were observed in the PD group and the lowest acetylcholinesterase (AChE) activities were found in the PD patients with the most severe disease. Changes in CSF measures were too subtle to be beneficial for diagnostic purposes, but adequate for reflecting the different neurochemical profiles of these three degenerative neurological disorders.
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PMID:Neurochemical markers in the cerebrospinal fluid of patients with Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis and normal controls. 134 20

Somatostatin (somatotropin release-inhibiting factor, SRIF) was originally discovered (1) during the purification of growth hormone-releasing factor from rat hypothalamus and was subsequently isolated and characterized (2) in 1972 from ovine hypothalamus. Since its initial characterization, SRIF has been shown to fulfill criteria for a neurotransmitter and to directly modulate neuronal activity as well as acting as an inhibitory factor regulating endocrine and exocrine secretion. Alterations in cerebrospinal fluid (CSF) concentrations of SRIF have been reported in several diseases exhibiting prominent cognitive dysfunction, including Alzheimer's disease (AD), major depression, Huntington's chorea, multiple sclerosis, schizophrenia and Parkinson's disease, while evidence for regional brain tissue concentration deficits in SRIF are more specific for AD. This mini-review will focus on the studies reporting alterations in CSF and postmortem tissue concentrations of SRIF in AD and depression.
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PMID:Somatostatin in Alzheimer's disease and depression. 135 21

The lateral tuberal nucleus is a circumscribed cell mass in the lateral posterior part of the hypothalamus, containing about 60000 neurons. It can be recognized in man and higher primates, probably not in other mammals. Its neurotransmitter content and connections with other parts of the brain are as yet unknown. But receptors for corticotropin-releasing factor and somatostatin, as well as muscarinic cholinergic receptors, benzodiazepine receptors and N-methyl-D-aspartate receptors have been localized within the confines of the nucleus. The lateral tuberal nucleus is affected in a number of human neurodegenerative diseases. Changes in Parkinson's disease are the least obvious: Lewy bodies appear in small amounts, the majority of them apparently lying outside a neuronal perikaryon. Neuronal loss does not occur. In Alzheimer's disease the number of neurons seems to be normal as well. Rarely silver staining tangles occur, and the deposition of A4/beta-protein in amorphous plaques is moderate. Yet, NTL neurons stain heavily in Alz-50 immunocytochemistry, while Alz-50 staining in NTL neurites is very dense. These changes are interpreted as indicating early Alzheimer-related pathology. In Huntington's disease the NTL loses neurons. This loss is related to the severity of the disease: patients who first display motor disturbances at an early age will lose more neurons than those who start later. The relation between these clinical characteristics and the severity of neuronal loss is such, that it seems likely that NTL neurons possess a special vulnerability for the effect of the Huntington gene. This could be related to their NMDA-receptor content. It is hypothesized that the NTL is involved in a neuronal network that regulates feeding and metabolism. NTL pathology may explain the peculiar catabolic state of many patients with Alzheimer's or Huntington's diseases.
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PMID:The hypothalamic lateral tuberal nucleus: normal anatomy and changes in neurological diseases. 136 79

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 distribution and level of labeling for the messenger RNA encoding preprosomatostatin was studied in the striatum and entopeduncular nucleus of rats with and without a selective destruction of the dopaminergic nigrostriatal pathway. 6-Hydroxydopamine was injected unilaterally in the substantia nigra and the animals were killed 2 or 3 weeks after the lesion. Preprosomatostatin messenger RNA was visualized with a 35S-labeled RNA or DNA probe in frontal cryostat-cut sections by in situ hybridization histochemistry. The number of labeled cells as well as the intensity of labeling overlying each cell were measured on radioautograms developed before saturation of the emulsion. In rats with a 6-hydroxydopamine lesion, the number of labeled cells and the intensity of labeling over each cell were decreased in the striatum ipsilateral to the lesion compared to the contralateral side and to both striata of control rats. In the same sections, the number of cells in the cerebral cortex was lower in the ipsilateral side of the lesion but the difference was only significant in the frontoparietal cortex. In contrast, a massive increase (+300%) in the number of labeled cells and in the intensity of labeling per cell was observed in the entopeduncular nucleus and the adjacent lateral hypothalamus on the side ipsilateral to the lesion when compared to the contralateral side and to control rats. The results suggest that dopamine exerts opposite effects on somatostatin gene expression in neurons of the striatum and the entopeduncular nucleus/lateral hypothalamus, effects which are likely to be of importance for the control of basal ganglia output activity. In addition, the dramatic changes observed in the somatostatinergic neurons of the lateral hypothalamus, an area involved in the control of food and water intake, may be related to some aspects of the symptomatology of Parkinson's disease.
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PMID:Lesions of the dopaminergic nigrostriatal pathway alter preprosomatostatin messenger RNA levels in the striatum, the entopeduncular nucleus and the lateral hypothalamus of the rat. 167 45

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

Cerebrospinal fluid (CSF) somatostatin concentrations were measured in 35 aged patients with Parkinson's disease (mean age, 79.5 years) and 11 control subjects (mean age, 82.3 years). In patients with Parkinson's disease the levels of somatostatin-like immunoreactivity were lower than in controls (P less than .02); these values were lowest in the untreated group. Somatostatin-like immunoreactivity levels in the CSF tended to increase with treatment but not significantly (P = .11). Somatostatin values were not correlated to age, sex, or duration of the disease. Somatostatin concentrations tended to be lower in more severely affected patients with higher scores on the Hoehn and Yahr (P = .13) and Webster staging scales (P = .13) and lower scores on Mini-Mental State (P = .10), but without statistical significance for these correlations.
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PMID:Somatostatin-like immunoreactivity in the cerebrospinal fluid of aged patients with Parkinson's disease. The effect of dopatherapy. 168 71

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

Somatostatin may play a role in several neurodegenerative diseases. Somatostatin concentrations are depleted in cerebral cortex in both Alzheimer's disease and in the dementia that accompanies Parkinson's disease. Somatostatin neurons in both illnesses are markedly dystrophic and may be reduced in number. In Huntington's disease, somatostatin concentrations are increased in the basal ganglia, as is the density of somatostatin neurons. The precise role of somatostatin changes in the pathophysiology of these illnesses requires further study.
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PMID:Somatostatin in neurodegenerative illnesses. 197 4

1. The tetradecapeptide somatostatin (SS) has a widespread, uneven distribution within several organs including the central nervous system (CNS), with particularly high concentration in the hypothalamus. 2. The SS-related peptides (SS28, SS28(1-12), SS28(15-28)) are originated from the precursor pre-prosomatostatin. 3. SS is suggested to be involved in a large number of CNS functions, locomotion, sedation, excitation, catatonia, body temperature, feeding, nociception, paradoxical sleep, self-stimulation, seizure, learning and memory. 4. SS influences central neurochemical processes. 5. It is possible that SS is related to various neurological and psychiatric illnesses, like Huntington's disease, multiple sclerosis, Parkinson's disease, epilepsy, eating disorders, Alzheimer's disease, schizophrenia and major depressive illness.
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PMID:Preclinical and clinical studies with somatostatin related to the central nervous system. 197 75


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