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)

The activity of total and heat-stable glutamate dehydrogenase (GDH) in lymphocytes increased with aging in 40 control subjects (p less than 0.001). The total GDH activity was lower in patients with olivopontocerebellar atrophy (OPCA), motor neuron disease, Parkinson's disease or Alzheimer's disease than in age-matched control subjects, but not in patients with nondegenerative neurological diseases. The decrease in heat-stable GDH activity was observed in patients with OPCA, Parkinson's disease or Alzheimer's disease, but heat-labile GDH was decreased only in patients with OPCA.
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PMID:Lymphocyte glutamate dehydrogenase activity in normal aging and neurological diseases. 258 34

Platelet MAO-B levels have been investigated in seventeen consecutively diagnosed and previously untreated patients with idiopathic Parkinson's disease using the non-hydroxylated catecholamine, beta-phenylethylamine, as substrate. Patients with Parkinson's disease had MAO-B activity levels that were considerably higher than sex and age matched normal controls or patients with Motor neurone disease or Myasthenia gravis.
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PMID:Platelet monoamine oxidase-B activity in Parkinson's disease. 259 11

Parkinsonism is due to an alteration of the dopaminergic nigro-striatal pathway the main morphological basis of which is a lesion of the substantia nigra (SN). Parkinson's disease, the etiology of which is unknown, is responsible for 90 p. cent of the cases of parkinsonism. It is characterized by a neuronal loss involving mainly the pigmented brainstem nuclei (substantia nigra, locus coeruleus and dorsal vagal nuclei) and a specific neuronal inclusion: the Lewy inclusion body. Involvement of other structures such as the nucleus basalis of Meynert, hypothalamus, reticular formations of the brainstem, spinal lateral horns, sympathetic ganglia, may be responsible for dementia and/or autonomic failure which are often associated with the extrapyramidal signs. Various other pathological processes, infectious, toxic, vascular, tumoral or traumatic, involving usually the SN, are occasionally responsible for parkinsonism. A number of degenerative diseases involving the SN may develop parkinsonism as major presenting sign. Most of them are diseases of the basal ganglia such as multiple system atrophy, primitive pallidal atrophies, Steele-Richardson-Olszewski disease, Hallervorden-Spatz disease. However, changes in the SN at the origin of parkinsonism are occasionally found in cortical degenerative diseases such as senile dementia of Alzheimer's type, Pick disease or the complex of Guam, in cerebellar atrophies or in motor neuron disease.
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PMID:[The neuropathology of Parkinson syndrome]. 284 79

Potential risk factors for various types of stroke were studied using a case-control study design. All 1978 US death certificates for which the registered underlying cause of death was subarachnoid hemorrhage (SAH), cerebral hemorrhage (CH), or cerebral infarction (CI) were identified. The frequency with which other conditions appeared on the death certificates of cases with and without hypertension was compared with controls. These data provide new information, such as the occurrence of peripheral vascular disease in association with SAH, the risk of CH in epileptic and cirrhotic patients, and the association of benign neoplasms of the nervous system, motor neuron disease, and 'paralysis agitans' with CI.
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PMID:Conditions associated at death with specific types of completed stroke in patients with and without hypertension: a case-control study. 291 91

Black patients with idiopathic Parkinson's disease (PD) present for neurological consultation much less frequently than white or Indian patients. That this is due to true rarity of PD among blacks is suggested by the observation that blacks with motor neuron disease and secondary parkinsonism are treated in numbers comparable with whites and Indians. These conclusions are derived from a series of 2,638 inpatient neurological consultations and from data on levodopa usage in three major hospitals in Durban. Lower life expectancy and failure of old people to attend hospital may be factors in the apparent low prevalence of PD among blacks, but other undetermined factors must play a part.
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PMID:Parkinson's disease in blacks. Observations on epidemiology in Natal. 334 81

The human neurological disorders--amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD)--share certain features: they occur in later stages of adult life; are slowly progressive; and involve specific groups of nerve cells. Different clinical syndromes result from dysfunction and death of these specific groups of neurons. In ALS, patients are weak due to disease of motor neurons in the spinal cord. The clinical features of PD, e.g. slow movements, tremor and rigidity, are attributed, in part, to degeneration of dopaminergic neurons of the substantia nigra. Impairments of cognition and memory in AD result from disease of neurons in a number of regions, including brainstem, basal forebrain, amygdala, hippocampus, and neocortex. In each of these diseases, affected neurons exhibit abnormalities of the neuronal cytoskeleton: in ALS, neurofilaments accumulate and distend proximal motor axons; in PD, nigral perikarya show Lewy bodies-intracytoplasmic inclusions containing neurofilament antigens; in AD, neurons develop neurofibrillary tangles, Hirano bodies, granulovacuolar degeneration and filament-filled neurites in plaques. Certain features of ALS, PD and AD are recapitulated in animal models, three of which are described in this review. Hereditary canine spinal muscular atrophy (HCSMA), a dominantly inherited motor neuron disease, shows many clinical and pathological features in common with ALS, including weakness, muscle atrophy, neurofilamentous swellings of proximal axons, impaired transport of neurofilament proteins, and degeneration of motor neurons. In primates, intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a parkinsonian syndrome due to injury of nigral dopaminergic neurons and associated denervation of the striatum. Finally, aged macaques exhibit memory deficits, and their cerebral cortices show senile plaques and filament-filled neurites derived from a variety of transmitter-specific populations of nerve cells. In human diseases, the causes and mechanisms leading to dysfunction and death of nerve cells are unknown. Investigators have begun using a variety of techniques derived from neurobiology to study animal models in an effort to clarify the mechanisms, evolutions, and consequences of structural-chemical abnormalities occurring in different neuronal systems implicated in human disease. Understanding such processes in these models should provide important new insights into the pathogeneses of similar processes occurring in ALS, PD and AD.
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PMID:Dysfunction and death of neurons in human degenerative neurological diseases and in animal models. 355 88

Amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD) are human neurological disorders which occur in middle and late life. These three diseases share certain features: they are slowly progressive; transmitter-specific groups of neurons are selectively affected by disease processes; and affected nerve cells exhibit cytoskeletal pathology. The causes and mechanisms of cell injury are unknown, and there are no treatments which directly affect the disease process. Dysfunction and death of these specific cell groups account for different clinical syndromes. In ALS, patients become paralyzed, at-risk cholinergic motor neurons in the spinal cord develop neurofilamentous swellings of proximal axons, and distal axons atrophy. In PD, affected individuals show slowed movements, tremor, and rigidity. These clinical findings are attributed to regeneration of dopaminergic neurons of the substantia nigra, a cell group showing abnormal accumulations of neurofilament antigens in the form of Lewy bodies. In AD, patients develop dementia (a syndrome of cognitive and memory impairment), and cholinergic neurons of the basal forebrain and certain other populations of nerve cells develop abnormalities of the cytoskeleton. These include perikaryal neurofibrillary tangles and enlarged distal axons which appear as neurites in senile plaques. Certain features of ALS, PD, and AD are recapitulated in three animal models described in this review. Hereditary Canine Spinal Muscular Atrophy (HCSMA), a dominantly inherited motor neuron disease, shows many clinical and pathological features in common with ALS. Affected dogs are clinically weak, have denervation atrophy of muscles, and develop neurofilamentous swellings of proximal axons, atrophy of distal axons, and degeneration of motor neurons. These abnormalities of axonal caliber are associated with impaired transport of the neurofilament triplet proteins and a maldistribution of phosphorylated neurofilaments. Intoxication of macaques with 1-methyl-4-]henyl-1,2,3,6,tetrahydropyridine (MPTP) produces a Parkinsonian syndrome due to selective injury of dopaminergic neurons in the substantia nigra and associated denervation of the striatum. Finally, aged rhesus monkeys (older than 23 years of age) show cognitive and memory deficits and exhibit senile plaques whose neurites are derived from cholinergic and other transmitter systems. Although these macaques do not have AD, they do provide a model for examining the relationships between age-associated cognitive deficits and pathological changes occurring in certain transmitter systems of primates.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Animal models of degenerative neurological disease. 360 87

Mortality rates for deaths "due to" and "with" motor neuron disease are presented for the first time. Age-specific mortality rates increase with age until 70 to 74 years and then decline. There appear to be no major differences by race in the age-adjusted mortality rates, but these rates are higher for males both white and nonwhite. A case-control study of all deaths with amyotrophic lateral sclerosis (ALS) was conducted for deaths due to ALS in the year 1971. Conditions associated with ALS at the time of death include pneumonia and bronchopneumonia, symptoms referable to respiratory system, superficial injury to shoulder and upper arm, essential benign hypertension, chronic skin ulcer, and malnutrition. No association was found between ALS and malignancies, Parkinson's disease, or dementia.
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PMID:Motor neuron disease in the United States, 1971 and 1973-1978: patterns of mortality and associated conditions at the time of death. 361 53

The cause of motor neuron disease (MND) remains unknown although recent reports have suggested a possible rise in mortality rate. The present account describes age-specific patterns in morbidity rate and cross-sectional and cohort analyses of mortality rate, and compares these with those in multiple sclerosis and Parkinson's disease. First hospital admission rate for motor neuron disease (a proxy for incidence rates) rose steadily with age in males and females until the age of 75 years or more, but then fell, but only in females. This irregular pattern suggested the possibility of an environmental effect on certain older birth cohorts. The validity of the results was supported by a similar pattern in the two hospital regional authorities studied and the difference between this pattern and that found in multiple sclerosis and Parkinson's disease. Age-specific mortality rates of motor neuron disease between 15 and 64 years for males and females in England and Wales from 1940 to 1982 rose steadily with age. Mortality rates after the age of 65 fell in all female cohorts studied, but only in the earlier male cohorts. Unlike Parkinson's disease there was no strong birth cohort effect. However an analysis of Office of Population Censuses and Surveys (Registrar General) reports has revealed a slight increase in the age-specific mortality rate in both males and females aged 65 and over for successive birth cohorts born since 1900. Neither changes in ICD coding or in diagnostic habits could account for this pattern, which differed from that seen in Parkinson's disease. No such effect was seen in multiple sclerosis.
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PMID:Morbidity and mortality in motor neuron disease: comparison with multiple sclerosis and Parkinson's disease: age and sex specific rates and cohort analyses. 387 17

The number of nerve cells of locus ceruleus and their nucleolar volume were determined in 63 normally aged individuals and in 41 cases with neurologic diseases. Pathologic alterations, such as a severe nerve cell loss and atrophy with or without extensive neurofibrillary degeneration or Lewy body formation, were generally seen in the nucleus locus ceruleus in Alzheimer's disease, Down's syndrome, dementia pugilistica, Parkinson's disease, and progressive supranuclear palsy, but such changes were only slight in normally aged individuals and minimal in motor neuron disease. Protein synthetic capacity was substantially reduced in the remaining nerve cells of the locus ceruleus, in Alzheimer's disease, Down's syndrome, and dementia pugilistica, but was unaltered in normally aged individuals (even in extreme old age), in motor neuron disease, and in the few remaining cells in Parkinson's disease and progressive supranuclear palsy. It is suggested that the pathologic alterations in the locus ceruleus found in these diseases, in conjunction with changes in the hypothalamus, lead to impairment of mental ability with eventual dementia through disturbance of the function of those pathways regulating homeostasis within the central nervous system.
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PMID:The pathology of the human locus ceruleus. 622 Aug 52


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