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

1. In the human brain, DA was found in appreciable amounts in most of the examined basal telencephalic limbic regions, with the nucleus accumbens having the highest mean level (3.38 microgram/g). In the cortical areas of the limbic lobe of Broca, DA could be measured with certainty only in the parolfactory gyrus (0.35 microgram/g). 2. In patients with Parkinson's disease, the DA concentration in the parolfactory gyrus and nucleur accumbens was markedly reduced, whereas little change was seen in the olfactory areas. Quantitatively, the DA decrease in the nucleus accumbens was of the same magnitude as in the caudate nucleus, being, in both regions, distinctly less severe than in the putamen. 3. In three cases of paranoid schizophrenia, there were no statistically significant changes of the mean levels of DA or HVA in the nucleus accumbens. However, the DA/HVA ratio was shifted noticeably in favor of HVA, possibly indicating an increase in DA turnover. This change was less pronounced in the putamen of these cases and was absent in the caudate nucleus. 4. The possibility of the substantia nigra contributing to the dopaminergic innervation of the human nucleus accumbens, as well as the significance of the observations on DA metabolism in the schizophrenic cases, is discussed.
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PMID:Dopamine in thelimbic regions of the human brain: normal and abnormal. 88 59

Although olfactory complaints prompt an estimated 200,000 people each year to seek medical consultation in the U.S., there is a dearth of information available in the nursing literature. Recent research links olfaction to degenerative processes in Alzheimer's disease, Parkinson's disease and human immunodeficiency virus infection. This article reviews anatomy and physiology of the olfactory system, describes alterations in smell function and reviews assessment with the University of Pennsylvania Smell Identification Test and odor detection threshold testing. Nurses can advocate thorough assessment and prompt treatment of associated conditions, and educate the patient and family regarding ways to maximize current functioning when olfaction is impaired.
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PMID:Olfaction: the neglected sense. 140 52

Male retired breeder C57/Bl and CD-1 mice were treated with either MPTP or its vehicle. At 7-10 days post-treatment, catecholamine concentrations within the olfactory bulbs (OB) and hypothalamus were determined. Norepinephrine concentrations within the OB were significantly decreased in MPTP-treated mice. These effects were more pronounced in the CD-1 (50% reduction) compared to the C57/Bl (20% reduction) strain. No effects of MPTP were observed on norepinephrine concentrations within the hypothalamus. Dopamine concentrations in the OB and hypothalamus did not differ between MPTP- and vehicle-treated mice in either strain. Overall, catecholamine concentrations within the OB, but not the hypothalamus, were significantly greater in C57/Bl compared to CD-1 mice. The reduction in OB norepinephrine concentration in the MPTP-treated animals may be related to the olfactory deficits which accompany Parkinson's disease.
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PMID:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) reduces norepinephrine concentrations in the olfactory bulbs of male mice. 151 43

Decreased olfactory function is among the first signs of idiopathic Parkinson's disease (PD). Whether such dysfunction is present to the same degree on both sides of the nose, however, is unknown. Furthermore, whether the deficit results from or is influenced by anti-Parkinsonian medications has not been definitely established. Odour identification ability was evaluated on the left and right sides of the nose in 20 early-stage untreated PD patients, 20 early-stage treated PD patients, and 20 controls. In all cases, the PD related olfactory dysfunction was bilateral and no difference was observed between the test scores of patients taking or not taking drugs for PD. Although asymmetries of unsystematic direction were present in the test scores of some PD patients, similar asymmetries were observed in the controls and the asymmetries were not related to the side of the major motor dysfunction. As in earlier work, no relation was present between the olfactory test scores and the degree of tremor, rigidity, bradykinesia, or gait disturbance at the time of testing. These findings indicate that the olfactory dysfunction of early stage PD is robust, typically of the same general magnitude on both sides of the nose, and uninfluenced by anti-Parkinsonian medications.
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PMID:Bilateral olfactory dysfunction in early stage treated and untreated idiopathic Parkinson's disease. 153 21

The olfactory function of 6 patients whose parkinsonism was the result of intravenous administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was compared to that of 12 age-matched patients with idiopathic Parkinson's disease (PD) and 10 age-matched normal control subjects. Unlike their PD counterparts, the olfactory test scores of patients with MPTP-induced parkinsonism did not differ significantly from those of control subjects. These findings suggest that MPTP-induced parkinsonism, unlike idiopathic PD, is unaccompanied, on average, by major alterations in the ability to smell.
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PMID:Lack of major olfactory dysfunction in MPTP-induced parkinsonism. 164 78

The ability to identify smells was tested in nine males and six females with motor neuron disease (MND) of varying severity, using the University of Pennsylvania Smell Identification Test (UPSIT). The olfactory impairment found in MND patients compared with age and sex matched controls is statistically significant at the 0.005 level. The relationship with Parkinson's disease, with Alzheimer's dementia and the possible aetiological implications of this new aspect of the MND are discussed.
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PMID:Olfactory impairment in motor neuron disease: a pilot study. 174 50

Adenosine A2 receptors were labeled and visualized by autoradiography in tissue sections of the human brain using the A2-selective agonist ligand [3H](2-p-(2-carboxyethyl)phenylamino)-5'-N-carboxamidoadenosine (CGS 21680). The binding of this ligand was of high affinity, reversible, and was blocked by adenosine A2 agents. Autoradiographic mapping of adenosine A2 sites revealed them to be exclusively restricted to the caudate nucleus, putamen, nucleus accumbens, olfactory tubercle and the lateral segment of the globus pallidus. The densities of adenosine A2 receptors in other brain areas did not differ from background levels. This selective localization prompted us to study the consequences of neurodegenerative diseases such as Parkinson's disease and Huntington's chorea on the densities and localization of these sites in the basal ganglia. In Parkinson's disease the density of adenosine A2 binding sites was comparable to that seen in control cases. In contrast, density values of A2 sites were dramatically decreased, compared to control values, in the basal ganglia of patients with Huntington's chorea. Similar losses of A2 receptors were observed in the guinea-pig striatum after local application of quinolinic acid while lesioning of the dopaminergic neurons was without effect. All these results taken together suggest that adenosine A2 receptors are localized on striatal output neurons which degenerate in Huntington's chorea.
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PMID:Adenosine A2 receptors: selective localization in the human basal ganglia and alterations with disease. 183 21

An olfactory function test in 18 patients with Parkinson's disease (PD) and 10 age-matched control subjects was performed. Both detection and recognition thresholds were measured with five kinds of synthesized odorants (T & T olfactometry). Before each test, rhinoscopic inspections were performed to exclude subjects who could have respiratory hyposmia. Both detection and recognition thresholds in patients with PD were significantly elevated in comparison with those of control subjects. Auditory acuity of PD patients, however, was well preserved and there was no significant correlation between auditory and olfactory threshold. On the basis of the present study, the authors conclude that olfactory dysfunction is one of the characteristic symptoms of PD and it may be attributed to lesions in the olfactory neural pathway including olfactory neuroepithelium.
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PMID:Olfactory dysfunction in Parkinson's disease. 185 11

Olfactory dysfunction is among the first signs of Alzheimer's disease (AD), idiopathic Parkinson's disease (PD), and the parkinsonism-dementia complex (PDC) of Guam. We have recently demonstrated that the odor identification and detection deficits of patients with PD are equivalent to those of patients with mild AD when subtle differences in cognitive function are statistically controlled for by analysis of covariance. In contrast, patients with progressive supranuclear palsy (PSP) and patients with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism evidence olfactory function much more similar to that of normal controls. In the present study, we administered the University of Pennsylvania Smell Identification Test and the Picture Identification Test to 24 patients with early signs of the PDC of Guam and statistically compared their test scores to those of 24 early-stage AD and 24 early-stage PD patients of similar age and gender from the United States mainland. Although the PDC group evidenced slightly more difficulty in identifying pictures than did the other 2 groups, the odor identification deficit associated with this disorder was of the same magnitude as that observed in AD and PD, suggesting that olfactory testing cannot be used to distinguish among these 3 diseases and that the olfactory dysfunction of these disorders may reflect a common neurologic substrate.
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PMID:Olfactory dysfunction in three neurodegenerative diseases. 189 45

Recent immunohistochemical studies have shown the distribution of histaminergic neurons in the mammalian brain, which are concentrated in the tuberomammillary nucleus of the posterior hypothalamus and project efferent fibers to almost all parts of the brain from the olfactory bulb to the spinal cord. Histaminergic neurons co-express other neuroactive substances, such as gamma-aminobutyric acid, adenosine, substance P, galanin and Met-enkephalin-Arg-Phe. In addition, pharmacological studies have demonstrated the presence of presynaptic histamine H3-receptors (autoreceptor) in addition to H1- and H2-receptors. The specific agonist (alpha-methylhistamine) and antagonist (thioperamide) of H3-receptors were developed. Results from a number of studies indicate a variety of physiological roles of neuronal histamine such as thermoregulation, feeding behavior, sexual activity, sleep-wakefulness cycle, hormonal regulation and so on. Moreover, histaminergic drugs affect not only the emotional behavior, but also are effective to treat some patients of depression, Parkinson's disease, akathisia, motion sickness and so on. The central histaminergic neuron system is also affected by mental disorders and neuropsychopharmacological drugs. This review especially focused on these points and suggests that the central histaminergic neuron system may play an important role in the regulation of mental functions.
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PMID:[Recent advances in neuropsychopharmacology of the central histaminergic neuron system]. 192 57


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