The effect of dopamine agonists on adaptive and aberrant salience in Parkinson's disease

Clinical evidence suggests that after initiation of dopaminergic medications some patients with Parkinson's disease (PD) develop psychotic symptoms, such as hallucinations and delusions. Here, we tested the hypothesis that the neurocognitive basis of this phenomenon can be defined as the formation of arbitrary and illusory associations between conditioned stimuli and reward signals, called aberrant salience. Young, never-medicated PD patients and matched controls were assessed on a speeded reaction time task in which the probe stimulus was preceded by conditioned stimuli that could signal monetary reward by color or shape. The patients and controls were re-evaluated after 12 weeks during which the patients received a dopamine agonist (pramipexole or ropinirole). Results indicated that dopamine agonists increased both adaptive and aberrant salience in PD patients, that is, formation of real and illusory associations between conditioned stimuli and reward, respectively. This effect was present when associations were assessed by means of faster responding after conditioned stimuli signaling reward (implicit salience) and overt rating of stimulus-reward links (explicit salience). However, unusual feelings and experiences, which are subclinical manifestations of psychotic-like symptoms, were specifically related to irrelevant and illusory stimulus-reward associations (aberrant salience) in PD patients receiving dopamine agonists. The learning of relevant and real stimulus-reward associations (adaptive salience) was not related to unusual experiences. These results suggest that dopamine agonists may increase psychotic-like experiences in young patients with PD, possibly by facilitating dopaminergic transmission in the ventral striatum, which results in aberrant associations between conditioned stimuli and reward

Saturated Fat and Cardiovascular Disease: A Review of Current Evidence

Cardiovascular disease (CVD) is one of the leading causes of death throughout the world. Saturated fatty acids (SFA) have long been implicated in the development of CVD. The evidence to support this hypothesis came from studies which examined the effects of SFA intake on total cholesterol (TC). However, relying on TC as the sole primary outcome may not be sufficient and understanding the effect of SFA on the concentrations of other lipid fractions is necessary. SFA are known to increase low-density lipoprotein cholesterol (LDL-C) and consequently dietary guidelines recommend reducing SFA intakes in order to decrease LDL-C and CVD risk. However, recent evidence suggests that not all SFAs possess the same atherogenic properties but this development has not yet been reflected in dietary recommendations. This review summarizes recent evidence on the relationship between SFA intake and CVD risk. It also explores current dietary guidelines specific to SFA intake and outlines why future guidelines may need to be food- rather than nutrient-specific. Overall, the evidence presented in this review suggests that not all SFA are created equal and the food sources of SFA, as well as individual characteristics of the SFA, such as chain length, should be considered in dietary recommendations