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)

Dementia is common in patients with Parkinson's disease (PDD). The etiology of PDD is still unclear, but exciting advances have been made in discovering pathogenetic components in Parkinson's disease (PD), implicating the role of genetic factors. It is, however, still controversial whether genetic factors also contribute to the development of dementia in PD. Thus, we investigated the association between development of dementia and a positive family history of PD or dementia in a community-based study of PD in Rogaland County, Norway (n = 219). The patients were followed prospectively with neurological and neuropsychological assessments. Dementia was more common in patients with a strong family association of PD (first-degree relatives > second-degree relatives > no family history; P < 0.05). However, time to dementia did not differ between the two groups. No associations between dementia in PD and familial occurrence of dementia could be shown. Further studies with larger samples are needed to explore a possible relationship between a family history of PD and development of dementia in PD and its potential pathogenetic mechanisms.
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PMID:Associations between family history of Parkinson's disease and dementia and risk of dementia in Parkinson's disease: A community-based, longitudinal study. 1702 73

Arrestins and G proteins-coupled receptor kinases (GRKs) regulate signaling and trafficking of G protein-coupled receptors. We investigated changes in the expression of arrestins and GRKs in the striatum of patients with Parkinson's disease without (PD) or with dementia (PDD) at postmortem using Western blotting and ribonuclease protection assay. Both PD and PDD groups had similar degree of dopamine depletion in all striatal regions. Arrestin proteins and mRNAs were increased in the PDD group throughout striatum. Protein and mRNA of GRK5, the major subtype in the human striatum, and GRK3 were also upregulated, whereas GRK2 and 6 were mostly unchanged. The PD group had lower concentration of arrestins and GRKs than the PDD group. There was no statistical link between the load of Alzheimer's pathology and the expression of these signaling proteins. Upregulation of arrestins and GRK in PDD may confer resistance to the therapeutic effects of levodopa often observed in these patients. In addition, increased arrestin and GRK concentrations may lead to dementia via perturbation of multiple signaling mechanisms.
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PMID:Arrestins and two receptor kinases are upregulated in Parkinson's disease with dementia. 1712 86

Parkinson disease (PD) is the most common neurodegenerative movement disorder, affecting 1 in 100 individuals over the age of 60. Dementia in the setting of PD (PDD) may be among the most debilitating symptoms associated with disease progression. Estimates of cognitive decline and dementia in PD suggest that up to 14% per year of patients over age 65 with PD will develop some cognitive impairment. Unfortunately, PDD is not well characterized and the relationship of PDD to Alzheimer disease remains unclear. PDD has been proposed as part of a spectrum with dementia with Lewy bodies, and PDD and dementia with Lewy bodies frequently coexist with Alzheimer disease. It is uncertain, however, whether there is a meaningful distinction between the different disorders. It has also been difficult to gain understanding of the interaction of motor and non-motor symptoms that affect quality of life in PD and confound cognitive and psychomotor performance. This review will examine the clinical, cognitive, neuropsychiatric features of cognitive deficits associated with PD, discuss their pathologic basis and propose avenues for future research.
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PMID:Cognitive change in Parkinson disease. 1713 78

Overlaps in clinical, pathological and molecular features of Parkinson's disease (PD), dementing and motor tauopathies have prompted association studies in search of common genetic risk factors that may predispose or modify this spectrum of disorders. To explore possible phenotypic implications, we studied common tau and ApoE gene polymorphisms, associated with Alzheimer's disease (AD), progressive supranuclear palsy (PSP) and PD, in a clinically and pathologically characterized cohort of PD patients and aged control subjects. Our results reveal a novel association between PD-related hallucinations and H1H1 genotype. We also report an association between PDD and the presence of the ApoE epsilon4 allele. Better determination of subsets of PD patients based upon the presence of specific phenotypic features may improve the accuracy of association studies.
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PMID:Phenotypic associations of tau and ApoE in Parkinson's disease. 1720 69

The hippocampus (HC) and amygdala (AG) decrease in volume with age and in Parkinson's disease (PD) with (PDD) and without dementia. We compared 44 PD to 44 age, sex and education-matched subjects without PD (non-PD) and 13 PDD subjects. T1-weighted MR images were used to manually segment the head, body and tail of the HC and the AG. HC volumes, corrected to intracranial volume, were smaller in PDD than non-PD (p=0.04), reflected predominantly by head atrophy. Right AG volumes were smaller in PD compared to non-PD (p=0.03). HC volumes in older (>70), but not younger, non-demented PD differed from non-PD (HC, p=0.02; head, p=0.03). Age correlated negatively with overall HC (r=-0.43, p=0.004) and head (r=-0.48, p=0.001) in PD, but not in non-PD. In PD, left HC head volumes correlated with recall, but not recognition scores on the CVLT-II (r=0.35, p=0.02) and BVMT-R (r=0.35, p=0.02); AG volumes correlated with CVLT-II recall (r=0.35, p=0.02). No correlations were found in non-PD (p>0.4). In conclusion, functionally meaningful age-associated hippocampal and amygdala atrophy occurs in PD.
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PMID:Age and dementia-associated atrophy predominates in the hippocampal head and amygdala in Parkinson's disease. 1736 53

An effect of subthalamic nucleus deep brain stimulation (STN-DBS) on cognition has been suspected but long-term observations are lacking. The aim of this study was to evaluate the long-term cognitive profile and the incidence of dementia in a cohort of Parkinson's disease (PD) patients treated by STN-DBS. 57 consecutive patients were prospectively assessed by the mean of a neuropsychological battery over 3 years after surgery. Dementia (DSM-IV) and UPDRS I to IV were recorded. 24.5% of patients converted to dementia over 3 years (incidence of 89 of 1,000 per year). This group of patients cognitively continuously worsened over 3 years up to fulfilling dementia criteria (PDD). The rest of the cohort remained cognitively stable (PD) over the whole follow-up. Preoperative differences between PDD and PD included older age (69.2 +/- 5.8 years; 62.6 +/- 8 years), presence of hallucinations and poorer executive score (10.1 +/- 5.9; 5.5 +/- 4.4). The incidence of dementia over 3 years after STN-DBS is similar to the one reported in medically treated patients. The PDD presented preoperative risk factors of developing dementia similar to those described in medically treated patients. These observations suggest dementia being secondary to the natural evolution of PD rather than a direct effect of STN-DBS.
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PMID:Long-term cognitive profile and incidence of dementia after STN-DBS in Parkinson's disease. 1744 91

Here, we investigated if TAR-DNA-binding protein-43 (TDP-43), the disease protein in frontotemporal lobar degeneration and ubiquitin inclusions with or without motor neuron disease as well as amyotrophic lateral sclerosis, also formed inclusions in Lewy body (LB) disorders including Parkinson's disease (PD) without or with dementia (PDD), and dementia with LBs (DLB) alone or in association with Alzheimer's disease (AD). Immunohistochemical analyses of TDP-43 in clinically well characterized and pathologically confirmed cases of DLB + AD, PD and PDD demonstrated TDP-43 pathology in the following percentage of cases: DLB + AD = 25/80 (31.3%); PD = 5/69 (7.2%); PDD = 4/21 (19%), while DLB and normal controls exhibited no (0/10, 0%) and one cases (1/33, 3%) presenting TDP-43 pathology, respectively. Significant differences in the prevalence of TDP-43 lesions were noted between disease versus normal brains (P < 0.001) as well as demented versus non-demented brains (P < 0.001). Statistical analyses revealed a positive relationship between TDP-43 lesions and several clinical and pathological parameters in these disorders suggesting the TDP-43 pathology may have co-morbid effects in LB diseases. This study expands the concept of TDP-43 proteinopathies by implicating TDP-43 lesions in mechanisms of neurodegeneration in LB disorders.
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PMID:Co-morbidity of TDP-43 proteinopathy in Lewy body related diseases. 1765 32

Blood-based tests for the differential diagnosis of Alzheimer's disease (AD) are under intensive investigation and have shown promising results with regard to Abeta40 and Abeta42 peptide species in incipient AD. Moreover, plasma Abeta40 was suggested as an independent cerebrovascular risk factor candidate. These considerations prompted us to analyse a total of 72 plasma samples in vascular dementias (VAD, n = 15), AD with cerebrovascular disease (AD with CVD, n = 7), AD (n = 15), Parkinson's disease and Parkinson's disease dementia (PD/PDD, n = 20) and 15 patients with depression that served as controls (DC) for distinct plasma amyloid-beta (Abeta) peptide patterns. For the analysis of plasma we used immunoprecipitation followed by the quantitative Abeta-SDS-PAGE/immunoblot. For comparison, CSF tau and Abeta1-42 analyses were performed. The major outcome was an increase in Abeta1-40 in plasma of VAD paralleled by a decrease in the ratio of Abeta1-38/Abeta1-40. The ratio Abeta1-38/Abeta1-40 in plasma enabled contrasts of beyond 85% and 80% for discriminating VAD from DC and all other patients, respectively. In CSF, we confirmed the typical CSF biomarker constellation of increased tau and diminished Abeta1-42 levels for AD. The diagnostic accuracy of plasma Abeta1-38/Abeta1-40 for VAD resembled the accuracy of CSF biomarkers for AD. From the presented results, we consider the ratio of plasma Abeta1-38/Abeta1-40 peptides to be a blood-based biomarker candidate for VAD.
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PMID:Blood-based neurochemical diagnosis of vascular dementia: a pilot study. 1766 50

In parkinsonian syndromes dementia frequently occurs in the disease progress. The cholinergic system has been proposed as playing a key role in cognitive disturbances. Therefore the application of cholinesterase inhibitors (ChEI) is also hotly argued for dementia associated with parkinsonian syndromes. This review focuses on the specific symptoms of dementia in Parkinson's disease (PDD), dementia with Lewy bodies (DLB), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). The effect of cholinergic treatment on cognition and behaviour is reported and critically discussed. There is evidence that medication with some ChEIs reduces cognitive disturbances and to a lesser extent improves activities of daily living in PDD. Behavioural symptoms also seem to be positively influenced by treatment with ChEIs in both PDD and DLB. The effect of treatment with cholinesterase inhibitors in PSP and CBD warrants more carefully designed studies including sufficient numbers of patients.
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PMID:[Treatment for dementia in parkinsonian syndromes. Efficacy of cholinesterase inhibitors]. 1768 35

Cognitive and affective dysfunctions are frequent but often neglected symptoms in Parkinson's disease (PD). We developed the screening tool Parkinson neuropsychometric dementia assessment (PANDA) with five cognitive tasks and a short depression questionnaire. Healthy subjects and patients without cognitive impairment (PD), mild cognitive disorder (PD-MCD), or dementia (PDD) were examined. The cognition part had a specificity of 91% and a sensitivity of 90% for PDD and 77% for PDD plus PD-MCD patients. The mood questionnaire also had high sensitivity and specificity. We conclude that the PANDA is an economical, easy-to-use and sensitive tool to detect neuropsychological dysfunctions in PD patients in clinical practice.
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PMID:Screening for cognitive deficits in Parkinson's disease with the Parkinson neuropsychometric dementia assessment (PANDA) instrument. 1770 78


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