Whilst the association between dementia and poorer health-related quality of life (Hr-QoL) in Parkinson's disease (PD) has been well established, we aimed to explore the relationship between cognitive performance and Hr-QoL in PD without dementia. Consecutive PD patients (n = 124, 54% men, age 60.4 +/- 10.3 years) judged as non-demented based on DSM-IV criteria and Mini Mental State Examination, free of other neurodegenerative diseases or psychotic difficulties and antipsychotic/antidepressive/anxyolitic treatment were assessed in a battery of neuropsychological tests. We used Parkinson's disease questionnaire (PDQ-39) to asses Hr-QoL and Beck's Depression Inventory (BDI) to quantify depression. In the univariate analysis, better performance in each of the tests evaluating visual attention/memory or visuospatial and executive functions was associated with better Hr-QoL. In multivariate analysis [adjustment for BDI score, PD severity and duration, l-dopa dose, age, sex, education, employment status and early PD onset (<50 years of age)] in which these tests were either represented by a common variable identified in a principal components analysis or were considered individually, better cognitive performance was independently associated with better Hr-QoL. The association was conditional on the level of depression, i.e., apparent only in patients with low(er) BDI scores. Cognitive performance appears associated with Hr-QoL even in non-demented PD patients.

Oxidative stress parameters in plasma of Huntington's disease patients, asymptomatic Huntington's disease gene carriers and healthy subjects : A crosssectional study. Journal of Neurology, 254 (12). pp. 1676-1683.

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Assessment of quality of life (QoL) has become an important measure in Parkinson's disease (PD) healthcare as a part of the efforts to evaluate the 'total burden' of the illness, and not only the motor disabilities. By analogy with some other diseases, we aimed to investigate potential urban-rural disparities in QoL in PD patients. A total of 111 consecutive PD patients were assessed for QoL using a specific 39-item version of PD quality of life questionnaire (PDQ-39) in a cross-sectional study involving two centers in Croatia. Rural life setting (adjustment for center, age, sex, levodopa dose, disease duration and severity, education, employment status and number of household co-members) was an independent negative predictor of QoL: rural patients had significantly (P < 0.05) worse PDQ-39 Summary Index Score and most of the PDQ-39 subscale scores (cognition, social support, stigma, emotional wellbeing and mobility score, and communication and activity of daily living scores with borderline significance) than their urban counterparts. Socioeconomic background should be considered in attempts to achieve the best management of PD patients' needs.

These results indicate that FS (p-tau231 and MMSE) has a strong potential to provide an early distinction between AD and VaD.

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The noradrenergic and dopaminergic systems are affected in Alzheimer's disease (AD). Polymorphisms in genes encoding enzymes and proteins that are components of these systems can affect products of transcription and translation and lead to altered enzymatic activity and alterations in overall dopamine and noradrenaline levels. Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine ␤hydroxylase (DBH) is involved in synthesis of noradrenaline. COMT Val158Met (rs4680), DBH rs1611115 (also called -1021C/T or -970C/T), and MAOB rs1799836 (also called A644G) polymorphisms have been previously associated with AD. We assessed whether these polymorphisms are associated with cerebrospinal fluid (CSF) AD biomarkers including total tau (t-tau), phosphorylated tau proteins (p-tau 181 , p-tau 199 , and p-tau 231 ), amyloid-␤ 42 (A␤ 42 ), and visinin-like protein 1 (VILIP-1) to test possible relationships of specific genotypes and pathological levels of CSF AD biomarkers. The study included 233 subjects: 115 AD, 53 mild cognitive impairment, 54 subjects with other primary causes of dementia, and 11 healthy controls. Significant decrease in A␤ 42 levels was found in patients with GG compared to AG COMT Val158Met genotype, while t-tau and p-tau 181 levels were increased in patients with AA compared to AG COMT Val158Met genotype. A␤ 42 levels were also decreased in carriers of A allele in MAO-B rs1799836 polymorphism, while p-tau 181 levels were increased in carriers of T allele in DBH rs1611115 polymorphism. These results indicate that COMT Val158Met, DBH rs1611115, and MAOB rs1799836 polymorphisms deserve further investigation as genetic markers of AD.