The antagonistic interaction between adenosine and dopamine receptors could have important pathophysiological and therapeutic implications in Parkinson's disease (PD). The primary aim of this study was to investigate the expression, affinity, and density of A(1), A(2A), A(2B), and A(3) adenosine receptors (ARs) and D(2) dopamine receptors (D(2)Rs) in PD. An increase in A(2A)AR density in putamen was found. The presence and functionality of ARs in human lymphocyte and neutrophil membranes from patients with PD revealed a specific A(2A)AR alteration compared with healthy subjects. A statistically significant linear correlation among the A(2A)AR density, functionality, or tumor necrosis factor-alpha (TNF-alpha) levels and Unified Parkinson's Disease Rating Scale (UPDRS) motor score was reported. Adenosine concentration and TNF-alpha levels were increased in plasma of patients with PD. In rat adrenal pheochromocytoma (PC12) cells, a widely useful model, adenosine antagonists decreased dopamine uptake, and an opposite effect was mediated by A(2A) agonists. This is the first report showing the presence of an A(2A)AR alteration in putamen in PD that mirrors a similar up-regulation in human peripheral blood cells. Moreover, the correlation found between A(2A)AR density or A(2A) agonist potency and UPDRS motor score highlights the central role of A(2A)ARs in the pharmacological treatment of PD.

These incidence and prevalence rates are the highest to date that have been estimated for a large community in southern Europe, and they constitute some of the highest rates in the world. Based on other surveys, these results reinforce the position of Sardinia as a higher and rising prevalence area for MS compared with other Mediterranean populations. Genetic and social-historic data strengthen the hypothesis of the environmental role and genetic factors among Sardinians in determining the notable difference in MS frequency between Sardinians and other Mediterraneans.

It is widely accepted that oxidative stress increases with age, and that age is a major risk factor for several neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. An inbalanced overproduction of reactive oxygen species can induce neuronal damage, leading to neuronal death by necrosis or apoptosis. Antioxidants are consequently considered to be a promising approaches to neuroprotection. Although experimental data are consistent in demonstrating a neuroprotective effects of antioxidants in vitro and in animal models, the clinical evidence that antioxidants agents may prevent or slow the course of these diseases is still relatively unsatisfactory, and unsufficient to strongly modify the clinical practice. This review summarizes the available data from experimental studies and clinical trials on antioxidant neuroprotection in Parkinson's and Alzheimer's disease.

Our study confirms the circadian rhythm of stroke reported in previous studies. There is a chronological pattern of ischemic stroke in the morning, which appears to be independent of the presence of risk factors and of clinical stroke subtypes. The role of circadian variability of blood pressure (present in patients with and without hypertension) and a concurrent morning hypercoagulability are suggested as possible determinants of this pattern. Preventive pharmacological interventions aimed at specifically targeting the morning rise in risk factors could be advantageous in reducing the overall risk of ischemic stroke.