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)

Conflicting reports about the effects of depression on cognition in Parkinson's disease (PD) are difficult to interpret because they are based on small sample sizes and confound depression with other variables. We found that a sample of 45 PD patients with current depression was cognitively more impaired than a sample of 45 PD patients without current depression matched for age, education, gender, age at disease onset, disease duration, and disease severity. The domains of cognition impaired in the two PD groups (compared with 45 age-, education-, and gender-matched controls) overlapped considerably, but only the depressed PD group had impaired memory relative to the control group. Our comparison of 22 depressed PD patients and 22 Alzheimer's disease (AD) patients matched for over-all severity of cognitive impairment, age, education, and gender indicated that the depressed PD group performed significantly worse on visuoconstructive tasks and marginally worse on conceptualization tasks. In contrast, the AD group performed significantly worse than the depressed PD group on memory tasks. Together, our results suggest that depression has a negative impact on cognition (and, in particular, memory) in PD, and that the pattern of this cognitive impairment is distinguishable from that associated with AD.
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PMID:The influence of depression on cognition in Parkinson's disease: a pattern of impairment distinguishable from Alzheimer's disease. 772 54

Regional cerebral blood flow (rCBF) was measured using the stable xenon enhanced CT method in previously untreated 13 patients with Parkinson's disease to evaluate CBF abnormality related to dysfunction of the nigrostriatal dopaminergic neurons. The patients comprised 5 men, 8 women with Hoehn-Yahr stage II-III. Age at onset ranged from 51 to 73 years (mean +/- SD, 61.8 +/- 8.9) and the duration of illness ranged from 1 to 96 months (15.1 +/- 24.1 months). In this series, there was no clinical evidence of hypertension, diabetes mellitus and cognitive impairment. rCBF was measured during 4-5-minutes inhalation of 33% stable xenon gas-67% oxygen. The first measurement of rCBF was performed in all of the patients before L-dopa treatment. After initiation of L-dopa treatment (333.3 +/- 47.1 mg/day), the second measurement was carried out in 6 patients (1 man and 5 women) who had shown symptomatic improvement. The interval between both measurements was 57.7 +/- 16.9 days. The following results were obtained. 1) No significant CBF asymmetry was noted in any of the striatum, pallidum, thalamus, cerebrum, cerebellum and frontal lobe in untreated patients with Parkinson's disease. 2) After L-dopa treatment, rCBF was significantly increased only in the striatum as compared with the pretreatment level (51.9 +/- 9.3-->63.1 +/- 9.9 ml/100 g/min, p < 0.01). 3) This increase was significantly greater on the more severely affected side (contralateral to the predominantly symptomatic limb) (p < 0.05). These results suggest that the increase of rCBF in the striatum is closely related to functional improvement of the nigrostriatal dopaminergic neurons.
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PMID:[The effects of dopamine on regional cerebral blood flow in patients with Parkinson's disease before and after L-dopa--measurement by Xe-enhanced CT]. 772 88

Stereotactic thalamotomy was performed in ten patients with Parkinson's disease for the suppression of their tremor. After VL-thalamotomy, contralateral tremor and rigidity disappeared or was significantly reduced. Activities of daily living (ADL) measured by functional independence measure and Parkinson's disability score were improved postoperatively in all patients. There was significant improvement in anxiety index. However, other neuropsychological tests showed no significant change postoperatively. ADL improved after thalamotomy. It is concluded that stereotactic VL-thalamotomy is a useful treatment which improves ADL without cognitive dysfunction.
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PMID:[Effects on cognitive function and activities of daily living after stereotactic thalamotomy for Parkinson's disease]. 775 21

The study assessed cognitive decline in non-demented, non-depressed patients with well defined Parkinson's disease and determined the predictive value for cognitive decline of different motor symptoms. Motor disability was measured with the Unified Parkinson's disease rating scale, impairment in activities of daily living, levodopa test, and long term clinical follow up. Neuropsychological evaluations included modified mini mental state, fluency, Wechsler logical memory, Wisconsin card sorting test, and the Montgomery and Asberg depression rating scale. Fifty three patients fulfilling clinical criteria for idiopathic Parkinson's disease were studied. Cognitive performance on initial testing was significantly correlated with education and disease duration but not with age at disease onset. Cognitive performance on retesting after three years of follow up was significantly reduced. This reduction was significantly greater in the late onset group, in patients with isolated dystonic dyskinesiae, and in patients with a lower percentage of motor improvement on levodopa. Cognitive decline in idiopathic Parkinson's disease may depend on both the prevalence of non-dopaminergic lesions and the topography of dopaminergic denervation. Predictive factors for cognitive decline, especially in executive tasks, relate more to non-dopaminergic than to dopaminergic lesions.
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PMID:Which factors predict cognitive decline in Parkinson's disease? 782 67

The in vivo generation of .OH free radicals in specific brain regions can be measured by intracerebral microdialysis perfusion of salicylate, avoiding many of the pitfalls inherent in systemic administration of salicylate. Direct infusion of salicylate into the brain can minimize the hepatic hydroxylation of salicylate and its contribution to brain levels of 2,5-DHBA. Levels of 2,5-DHBA detected in the brain dialysate may reflect the .OH adduct plus some enzymatic hydroxylation of salicylate in the brain. After minimizing the contribution of enzyme and/or blood-borne 2,5-DHBA, the present data demonstrate the validity of the use of 2,3-DHBA and apparently 2,5-DHBA as indices of .OH formation in the brain. Therefore, intracranial microdialysis of salicylic acid and measurement of 2,3-DHBA appears to be a useful .OH trapping procedure for monitoring the time course of .OH generation in the extracellular fluid of the brain. These results indicate that nonenzymatic and/or enzymatic oxidation of the dopamine released by MPTP analogues in the extracellular fluid may play a key role in the generation of .OH free radicals in the iron-rich basal ganglia. Moreover, a site-specific generation of cytotoxic .OH free radicals and quinone/semiquinone radicals in the striatum may cause the observed lipid peroxidation, calcium overload, and retrograde degeneration of nigrostriatal neurons. This free-radical-induced nigral injury can be suppressed by antioxidants (i.e., U-78517F, DMSO, and deprenyl) and possibly hypothermia as well. In the future, this in vivo detection of .OH generation may be useful in answering some of the fundamental questions concerning the relevance of oxidants and antioxidants in neurodegenerative disorders during aging. It could also pave the way for the research and development of novel neuroprotective antioxidants and strategies for the early or preventive treatment of neurodegenerative disorders, such as Parkinson's disease (Wu et al., this issue), amyotrophic lateral sclerosis, head trauma, and possibly Alzheimer's cognitive dysfunction as well. In conclusion, this in vivo free-radical trapping procedure provides evidence to support a current working hypothesis that a site-specific formation of cytotoxic .OH free radicals in the basal ganglia may be one of the neurotoxic mechanisms underlying nigrostriatal degeneration and Parkinsonism caused by the dopaminergic neurotoxin MPTP. Addendum added in proof: The controversy concerning possible neurotoxic and/or neuroprotective roles of NO. in cell cultures was discussed and debated at the symposium (Wink et al., this issue; Dawson et al., this issue; Lipton et al., this issue).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:In vivo generation of hydroxyl radicals and MPTP-induced dopaminergic toxicity in the basal ganglia. 783 34

The performances of 12 patients with Parkinson's disease (PD), 16 with Huntington's disease (HD), and young and old healthy controls were assessed on a number of tests of verbal and nonverbal declarative memory, on a test of nonmotor conditional associative learning (words and colors), and on a number of reaction time (RT) tasks. The RT tasks consisted of cued simple and choice reactions. The relationship between the precue and the imperative stimulus in the S1-S2 paradigm was nonarbitrary in the first series and arbitrary in the second series. The series with arbitrary S1-S2 associations was repeated across two successive blocks of trials. The rationale of the study was to investigate the function of the basal ganglia "complex loop," and it was postulated that HD patients would show greater deficits because of greater involvement of the caudate nucleus. The patients with HD had the slowest RTs. Across the two blocks with arbitrary S1-S2 associations, the patients with HD but not PD nevertheless showed evidence of learning in their precued RTs. In contrast, the patients with PD were better able to remember the associations in free recall than were the HD patients. It is concluded that patients with PD have relatively greater deficits in procedural learning, whereas those with HD have relatively more impairments in declarative memory, and the greater level of cognitive impairment in HD overall is interpreted as being due to more serious damage to the caudate loop.
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PMID:Associative learning in degenerative neostriatal disorders: contrasts in explicit and implicit remembering between Parkinson's and Huntington's diseases. 788 56

Neuropsychological data collected from two groups of patients with idiopathic Parkinson's disease (n = 50, 159) were analysed to investigate the association between presenting motor symptoms determined from retrospective chart review and the risk of cognitive impairment. Presenting motor symptoms were abstracted from the medical records and coded by type, location, and laterality. Longitudinal data on changes in the maximum speed of voluntary arm movements were available for a subsample of patients. Bilateral (v unilateral) presentation was associated with an increased risk of cognitive impairment an average of nine years after onset of disease as measured by memory tests and the mini-mental state examination. A higher rate of decline of arm movement speed was also predictive of greater memory dysfunction. The type, side (left v right), and location (lower v upper extremity) of the presenting symptoms were not, however, consistently associated with the risk of cognitive impairment later in the course of the disease.
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PMID:Association between presenting motor symptoms and the risk of cognitive impairment in Parkinson's disease. 793 81

Studies of the neurochemical pathology of Alzheimer's disease and Parkinson's disease reveal a severe and specific loss of central nicotinic cholinergic receptors. We have investigated the functional significance of this finding for cognitive functioning by studying the effects of the centrally active nicotinic antagonist mecamylamine. Single oral doses of mecamylamine were administered to 12 healthy young males and 15 healthy elderly subjects in doses of 5, 10, and 20 mg in a placebo-controlled, double-blind study. In both groups, the 20-mg dose caused a significant increase in errors in the learning condition of the Repeated Acquisition Task, producing a slower acquisition curve. There was no effect of drug on the performance component (retrieval of previously learned information). However, elderly subjects showed enhanced sensitivity to mecamylamine, with 10-mg dose producing significant impairment of learning not seen in the young normals. On a recognition memory task, there was an age-associated shift in response bias, with the elderly subjects becoming more liberal with increasing dose. Reaction-time measures suggested a dose-related slowing of reaction time on several tasks. Behavioral effects were minimal and physiologic effects were consistent with dose-related ganglionic blockade. These results indicate that acute blockade of nicotinic receptor function can produce measurable and significant cognitive impairment similar to some deficits seen in dementing illnesses, and that there is an age-related increase in sensitivity to nicotinic blockade.
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PMID:Age-related effects of the nicotinic antagonist mecamylamine on cognition and behavior. 802 77

We compared demographic, medical, and other epidemiologic factors among 113 African-American Alzheimer's disease (AD) patients and 79 African-American vascular dementia (VaD) patients. The typical background profile of our AD and VaD patients who entered into the study was that of women who were born and raised on farms in the southeastern United States, currently lived in an apartment or home in Chicago with other family members, and were retired, widowed, and had some form of medical insurance. The following distinct patient profiles emerged: (1) African-American AD patients were generally older than their VaD counterparts, more likely to have a family history of AD, Parkinson's disease and dementia, a history of head injury with loss of consciousness and hip fracture, and more severe cognitive impairment and difficulty with instrumental activities of daily living. (2) African-American VaD patients had a higher frequency of cardiovascular disease risk factors and focal neurologic findings, more difficulty with activities of daily living, and a higher frequency of medication use. Differences in risk-factor profile may help explain differential susceptibility by dementia subtype. Since ethnic minorities will constitute a higher proportion of the United States population in the future, targeted epidemiologic research to better understand etiology and risk factors for the dementias of middle and later life among minorities is needed.
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PMID:Epidemiology of vascular and Alzheimer's dementia among African Americans in Chicago, IL: baseline frequency and comparison of risk factors. 805 35

Epidemiological studies suggest an apparent protective effect of cigarette smoking on the risk of Parkinson's disease. There is also a report suggesting that patients with Parkinson's disease who smoke are less likely to develop dementia. I investigated the relationship of smoking to the severity of cognitive functions and presence of drug-induced parkinsonism in a group of 111 neuroleptic-treated chronic institutionalized schizophrenic patients. Patients who smoked had significantly less cognitive impairment (p < .02) and a lower prevalence of drug-induced Parkinsonism (p < .02) compared to nonsmokers. These findings suggest that cigarette smoking may protect against the development of dementia and drug-induced Parkinsonism in schizophrenia.
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PMID:Cigarette smoking: effects on cognitive functions and drug-induced parkinsonism in chronic schizophrenia. 806 38


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