The relationship between associative learning, transfer generalization, and homocysteine levels in mild cognitive impairment

Previous studies have shown that high total homocysteine levels are associated with Alzheimer's disease (AD) and mild cognitive impairment (MCI). In this study, we test the relationship between cognitive function and total homocysteine levels in healthy subjects (Global Dementia Rating, CDR = 0) and individuals with MCI (CDR = 0.5). We have used a cognitive task that tests learning and generalization of rules, processes that have been previously shown to rely on the integrity of the striatal and hippocampal regions, respectively. We found that total homocysteine levels are higher in MCI individuals than in healthy controls. Unlike what we expected, we found no difference between MCI subjects and healthy controls in learning and generalization. We conducted further analysis after diving MCI subjects in two groups, depending on their Global Deterioration Scale (GDS) scores: individuals with very mild cognitive decline (vMCD, GDS = 2) and mild cognitive decline (MCD, GDS = 3). There was no difference among the two MCI and healthy control groups in learning performance. However, we found that individuals with MCD make more generalization errors than healthy controls and individuals with vMCD. We found no difference in the number of generalization errors between healthy controls and MCI individuals with vMCD. In addition, interestingly, we found that total homocysteine levels correlate positively with generalization errors, but not with learning errors. Our results are in agreement with prior results showing a link between hippocampal function, generalization performance, and total homocysteine levels. Importantly, our study is perhaps among the first to test the relationship between learning (and generalization) of rules and homocysteine levels in healthy controls and individuals with MCI

Estudio comparativo sobre la deterioración de aceites por calentamiento en microonda y convencional

Refined cottonseed oil and hydrogenated palm oil were heated by two methods, i.e., conventionally by gas-cooker and microwaves. Quality assurance methods such as refractive index, color, diene content, acid value, peroxide value, TBA value, iodine value, petroleum ether insoluble oxidized fatty acid content and degree of polymerization were determined. Exposing the oil samples to various heating times and microwave oven power caused some hydrolysis to free fatty acids, accelerated the formation of hydroperoxides and secondary oxidation products. The values from each test increased with both the power settings of microware oven and time of heating. In general, the development of rancidity for refined cottonseed oil heated by microwaves was twice faster than that produced by conventional heating. Also, the chemical values for refined cottonseed oil were much higher than that of hydrogenated palm oil in all cases.Se han calentado aceites de semilla de algodón y de palma hidrogenado mediante dos métodos: convencionalmente en cocina de gas y microonda. Se han determinado como métodos de garantía de calidad el índice de refracción, color, contenido en dienos, índice de acidez, índice de peróxido, índice de TBA, índice de iodo, contenido en ácidos grasos oxidados insolubles en éter de petróleo y grado de polimerización. La exposición de las muestras de aceite a varios tiempos de calentamiento y potencia del horno microonda causó hidrólisis hacia ácidos grasos libres, aceleró la formación de hidroperóxidos y productos de oxidación secundarios. Los valores para cada test aumentaron con los ajustes de potencia del horno microonda y el tiempo de calentamiento. En general, el desarrollo de la rancidez para aceite de semilla de algodón refinado calentado por microonda fue 2 veces más rápido que el producido por calentamiento convencional. También, los índices químicos para aceites de semilla de algodón refinado fueron mucho mayores que los de aceite de palma hidrogenado en todos los casos

Neural substrates and potential treatments for levodopa-induced dyskinesias in Parkinson's disease

Parkinson's disease (PD) is primarily a motor disorder that involves the gradual loss of motor function. Symptoms are observed initially in the extremities, such as hands and arms, while advanced stages of the disease can effect blinking, swallowing, speaking, and breathing. PD is a neurodegenerative disease, with dopaminergic neuronal loss occurring in the substantia nigra pars compacta, thus disrupting basal ganglia functions. This leads to downstream effects on other neurotransmitter systems such as glutamate, gamma-aminobutyric acid, and serotonin. To date, one of the main treatments for PD is levodopa. While it is generally very effective, prolonged treatments lead to levodopa-induced dyskinesia (LID). LID encompasses a family of symptoms ranging from uncontrolled repetitive movements to sustained muscle contractions. In many cases, the symptoms of LID can cause more grief than PD itself. The purpose of this review is to discuss the possible clinical features, cognitive correlates, neural substrates, as well as potential psychopharmacological and surgical (including nondopaminergic and deep brain stimulation) treatments of LID

The effects of clinical motor variables and medication dosage on working memory in Parkison's disease

In this study, we investigate the interrelationship between clinical variables and working memory (WM) in Parkinson's disease (PD). Specifically, the aim of the study was to investigate the relationship between disease duration, dopaminergic medication dosage, and motor disability (UPDRS score) with WM in individuals with PD. Accordingly, we recruited three groups of subjects: unmedicated PD patients, medicated PD patients, and healthy controls. All subjects were tested on three WM tasks: short-delay WM, long-delay WM, and the n-back task. Further, PD encompasses a spectrum that can be classified either into akinesia/rigidity or resting tremor as the predominant motor presentation of the disease. In addition to studying medication effects, we tested WM performance in tremor-dominant and akinesia-dominant patients. We further correlated WM performance with disease duration and medication dosage. We found no difference between medicated and unmedicated patients in the short-delay WM task, but medicated patients outperformed unmedicated patients in the long-delay WM and n-back tasks. Interestingly, we also found that akinesia-dominant patients were more impaired than tremor-dominant patients at various WM measures, which is in agreement with prior studies of the relationship between akinesia symptom and basal ganglia dysfunction. Moreover, the results show that disease duration inversely correlates with more demanding WM tasks (long-delay WM and n-back tasks), but medication dosage positively correlates with demanding WM performance. In sum, our results show that WM impairment in PD patients depend on cognitive domain (simple vs. demanding WM task), subtype of PD patients (tremor- vs. akinesia-dominant), as well as disease duration and medication dosage. Our results have implications for the interrelationship between motor and cognitive processes in PD, and for understanding the role of cognitive training in treating motor symptoms in PD

Factors underlying probabilistic and deterministic stimulus-response learning performance in medicated and unmedicated patients with Parkinson's disease

Objective: Prior studies have not tested individual differences or effects of medication dosage on stimulus-response learning in patients with Parkinson's disease (PD). In the current study, we investigated the effects of motor variables (including tremor, akinesia, and disease duration) as well as dopaminergic medication dosage on learning in unmedicated PD patients, medicated PD patients, and healthy controls. Method: We tested all subjects on probabilistic and deterministic learning tasks, and also collected awareness measures data using postexperimental questionnaires. Importantly, we tested learning performance in tremor-dominant and akinesia-dominant PD patients, and further correlated learning performance with disease duration and medication dosage. Results: Results show that akinesia-dominant patients were more impaired than tremor-dominant patients at probabilistic rewardbut not punishment-based learning, which is in agreement with prior studies of the relationship between akinesia and basal ganglia dysfunction. We also found no difference between medicated and unmedicated PD patients in reward- or punishment-based deterministic learning, but medicated patients were better than unmedicated patients at reward-based probabilistic learning. Our results show that awareness measures explain differences among probabilistic and deterministic learning performance. Moreover, we found that disease duration and motor severity are inversely correlated, and medication dosage is positively correlated, with reward-based probabilistic learning. Conclusion: Our results suggest that stimulus-response learning performance in patients with PD depends on the type of learning (probabilistic vs. deterministic), medication status (on vs. off medication, dopaminergic medication dosage), disease duration as well as motor severity and subtype in PD patients (tremor- vs. akinesia-dominant)