Executive functioning and serum lipid fractions in Parkinson’s disease—a possible sex-effect: the PACOS study

The association between dyslipidemia and cognitive performance in Parkinson’s disease (PD) patients still needs to be clarified. Aim of the study was to evaluate the presence of possible associations between serum lipids fractions and executive dysfunction also exploring the sex-specific contribute of lipids level on cognition. Patients from the PACOS cohort, who underwent a complete serum lipid profile measures (total cholesterol-TC, low-density lipoprotein cholesterol-LDL, high-density lipoprotein cholesterol-HDL and triglycerides-TG) were selected. Adult Treatment Panel III guidelines of the National Cholesterol Education Program were used to classify normal/abnormal lipid fractions. Executive functioning was assessed with the Frontal Assessment Battery (FAB). Logistic regression was performed to assess associations between lipids fractions and FAB score. Correlations between lipids fractions and FAB score were explored. Sex-stratified analysis was performed. Three hundred and forty-eight PD patients (148 women; age 66.5 ± 9.5 years; disease duration 3.9 ± 4.9 years) were enrolled. Women presented significantly higher TC, LDL and HDL than men. In the whole sample, any association between lipid profile measures and FAB score was found. Among women, a positive association between hypertriglyceridemia and FAB score under cutoff was found (OR 3.4; 95%CI 1.29–9.03; p value 0.013). A statistically significant negative correlation was found between the FAB score and triglyceride serum levels (r = − 0.226; p value 0.005). Differently, among men, a statistically significant negative association between hypercholesterolemia and FAB score under cutoff (OR 0.4; 95%CI 0.17–0.84; p value 0.018) and between high LDL levels and FAB score under cutoff (OR 0.4; 95%CI 0.18–0.90; p value 0.027) were found. Our data suggest a sex-specific different role of lipids in executive functioning.

The neurochemical pathology of schizophrenia: post-mortem studies from dopamine to parvalbumin

Research in Peter Riederer’s lab in Vienna in the late 1970’s came from a strong tradition in post-mortem neurochemical studies, at that time a relatively niche approach in neuroscience research. He was also early to recognise the value of post-mortem brain tissue in elucidating pharmacological mechanisms of neuropsychiatric treatments. I was fortunate to have Peter Riederer as a mentor in my early post-doctoral career; his generous support and the opportunities to use post-mortem brain tissue provided an invaluable grounding on which much of my future research was based. In this paper, I shall provide a brief overview of one trajectory of my research into the neurobiology of schizophrenia that started in the Riederer lab in Vienna investigating dopamine and the D2 receptor. Subsequent research to understand findings of increased dopamine resulted in the identification of reduced GABAergic innervation, culminating in the finding of a deficit in the parvalbumin-containing subtype of GABAergic neurons. Most recent work has been studying how changes in DNA methylation of the parvalbumin gene may relate to these findings in psychotic illness and its animal models.