Diabetes mellitus and Parkinson's disease: dangerous liaisons between insulin and dopamine.

The relationship between diabetes mellitus and Parkinson's disease has been described in several epidemiological studies over the 1960s to date. Molecular studies have shown the possible functional link between insulin and dopamine, as there is strong evidence demonstrating the action of dopamine in pancreatic islets, as well as the insulin effects on feeding and cognition through central nervous system mechanism, largely independent of glucose utilization. Therapies used for the treatment of type 2 diabetes mellitus appear to be promising candidates for symptomatic and/or disease-modifying action in neurodegenerative diseases including Parkinson's disease, while an old dopamine agonist, bromocriptine, has been repositioned for the type 2 diabetes mellitus treatment.

Identification of circulating microRNAs for the differential diagnosis of Parkinson's disease and Multiple System Atrophy.

Parkinson's disease (PD) is a progressive neurodegenerative disorder which may be misdiagnosed with atypical conditions such as Multiple System Atrophy (MSA), due to overlapping clinical features. MicroRNAs (miRNAs) are small non-coding RNAs with a key role in post-transcriptional gene regulation. We hypothesized that identification of a distinct set of circulating miRNAs (cmiRNAs) could distinguish patients affected by PD from MSA and healthy individuals.

The MTHFR C677T polymorphism modifies age at onset in Parkinson's disease.

Hyperhomocysteinemia is a risk factor for Parkinson's disease (PD) and may result from genetic mutations or/and environmental factors. 5,10-methylenetetrahydrofolate reductase (MTHFR) is a folate-dependent enzyme that catalyzed remethylation of homocysteine (Hcy) and the MTHFR C677T polymorphism makes the MTHFR enzyme thermolabile causing hyperhomocysteinemia. In this study we analyzed whether two functional polymorphisms of MTHFR gene, A1298C and C677T, affect age of onset in PD.

Preliminary kinetic characterization of a copper amine oxidase from rat liver mitochondria matrix.

Kinetic measurements of a novel copper-dependent amine oxidase, purified from rat liver mitochondria matrix, were carried out using various substrates in a large pH (5.6-10.2) and ionic strength range (5-200 mM), in order to study the docking of substrates to the enzyme and, as a consequence, to verify the physicochemical characteristics of the active site.

Novel copper amine oxidase activity from rat liver mitochondria matrix.

Copper containing amine oxidases (Cu-AO) represent a heterogeneous class of enzymes classified as EC 1.4.3.

Oxidative metabolism of dopamine: a colour reaction from human midbrain analysed by mass spectrometry.

In order to identify the protein responsible for a dopamine peroxidizing activity, previously described in human normal and parkinsonian substantia nigra by our group, we developed non-denaturing polyacrylamide gel electrophoresis conditions, mimicking the characteristic colour in vitro reaction, resulting from cyclic oxidation of dopamine (DA). After separating protein mixtures from human normal midbrain homogenates on two sets of identical native gels, one gel set was subjected to specific activity staining by using DA and hydrogen peroxide. An activity red/orange band appeared in midbrain tissue lanes, similarly to the lane where commercial horseradish peroxidase (HRP) was present as control of peroxidative activity.

A proteomic approach in the study of an animal model of Parkinson's disease.

Background: The aetiology of Parkinson's disease (PD), an age-related disorder characterized by a progressive degeneration of dopaminergic neurons of the substantia nigra (SN) pars compacta, remains unclear. Current treatments, such as administration of L-DOPA, are only symptomatic and do not stop or delay the progressive loss of neurons. In fact, it has been suggested that the dopamine precursor L-DOPA, increases generation of reactive oxygen species (ROS) leading to further neuronal damage.

The biochemical basis of Parkinson's disease: the role of catecholamine o-quinones: a review-discussion.

This paper reviews the possible role of catecholamine o-quinones (oQs) in the genesis of Parkinson's disease (PD). This disease is characterized by damage caused to the pigmented catecholaminergic cells in various areas of the brain. The pigment involved is neuromelanin that is the end product of catecholamine oxidation by the o-quinone route.

Increased dopamine peroxidation in postmortem Parkinsonian brain.

We have previously reported the presence, in human midbrain, of an enzymatic activity which catalyzes the formation of dopaminochrome from dopamine (DA) and hydrogen peroxide. Here, we report, for the first time, an increased DA peroxidizing activity in the midbrain and basal ganglia of autoptic Parkinsonian brains. The crude activity was determined spectrophotometrically in extracts of paraffin-embedded slices obtained from autopsied brain.