Association of Hemispheric Asymmetry of Dopamine-Transporter Binding with Risk of Parkinsonian Depression.

Background: Depression is the most common psychiatric disorder diagnosed in patients with Parkinson's disease (PD). A direct role in PD depression for loss of dopaminergic terminals and dopamine-transporter (DAT) expression in the striatum is revealed by many studies.

Objectives: The objective was to discern the relationship between DAT neuroimaging and risk of depression in PD.

Is there a halo-enzymopathy in Parkinson's disease?

Laboratory studies identified changes in the metabolism of halogens in the serum and cerebrospinal fluid (CSF) of patients with Parkinson's disease, which indicates the presence of "accelerated self-halogenation" of CSF and/or an increase in haloperoxidases, specifically serum thyroperoxidase and CSF lactoperoxidase. Furthermore, an excess of some halogenated derivatives, such as advanced oxygenation protein products (AOPP), has been detected in the CSF and serum. "Accelerated self-halogenation" and increased levels of haloperoxidases and AOPP proteins indicate that halogenative stress is present in Parkinson's disease.

Salivary ATP13A2 is a potential marker of therapy-induced motor complications and is expressed by inclusions in submandibulary glands in Parkinson ´s disease.

Background: ATP13A2 holds promise as biomarker for Parkinsońs disease (PD). No study has examined how salivary ATP13A2 is related to motor features in idiopathic PD.

Methods: Salivary ATP13A2 concentration was evaluated with ELISA, and statistical correlations of ATP13A2 level with PD parameters were examined.

Myeloperoxidase and Advanced Oxidation Protein Products in the Cerebrospinal Fluid in Women and Men with Parkinson's Disease.

Background: Myeloperoxidase (MPO) and advanced oxidation protein products, or AOPP (a type of MPO-derived chlorinated adducts), have been implicated in Parkinson´s disease (PD). Human MPO also show sex-based differences in PD. The objective was to study the relationship of MPO and AOPP in the cerebrospinal fluid (CSF) with motor features of idiopathic PD in male and female patients.

Microorganisms associated with increased risk of Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disorder that affects more than 7 million people worldwide. Its aetiology is unknown, although the hypothesis of a genetic susceptibility to environmental agents is accepted. These environmental agents include fungi, bacteria, and viruses.

Endocannabinoid-mediated synaptic plasticity and substance use disorders.

Drugs impact brain reward circuits, causing dependence and addiction, in a condition currently described as substance use disorders. Mechanisms of synaptic plasticity in these circuits are crucial in the development of addictive behaviour, and endocannabinoids, particularly anandamide and 2-arachidonyl-glycerol, participate in normal neuroplasticity. Substance use disorders are known to be associated with disruption of endocannabinoid-mediated synaptic plasticity, among other phenomena.

ATP13A2 levels in serum and cerebrospinal fluid in patients with idiopathic Parkinson's disease.

Background: The enzyme ATP13A2 holds promise as biomarker in Parkinson's disease (PD). No study has examined the content of ATP13A2 in serum and cerebrospinal fluid (CSF) in idiopathic PD cohorts, or how ATP13A2 relates to the clinical features of the disease.

Methods: ATP13A2 concentration was evaluated with ELISA and immunoblotting.

Native α-Synuclein, 3-Nitrotyrosine Proteins, and Patterns of Nitro-α-Synuclein-Immunoreactive Inclusions in Saliva and Submandibulary Gland in Parkinson's Disease.

Salivary α-synuclein (aSyn) and its nitrated form, or 3-nitrotyrosine-α-synuclein (3-NT-αSyn), hold promise as biomarkers for idiopathic Parkinson's disease (IPD). Nitrative stress that is characterized by an excess of 3-nitrotyrosine proteins (3-NT-proteins) has been proposed as a pathogenic mechanism in IPD. The objective is to study the pathological role of native αSyn, 3-NT-αSyn, and 3-NT-proteins in the saliva and submandibulary glands of patients with IPD.

A Cross-Sectional Study of Foot Growth and Its Correlation with Anthropometric Parameters in a Representative Cohort of Schoolchildren from Southern Spain.

: The relationship between growth of the foot and other anthropometric parameters during body development until puberty has been scarcely studied. Some studies propose that growth of the foot in length may be an early index of puberty. The objective of this cross-sectional study was to analyze the relationship between the growth of the foot in length and width with other anthropometric parameters, in prepubertal and early pubertal schoolchildren (Tanner stage II).

Cerebrospinal fluid lactoperoxidase level is enhanced in idiopathic Parkinson's disease, and correlates with levodopa equivalent daily dose.

Lactoperoxidase (LPO) is proposed to play a role in the pathogenesis of Parkinson's disease (PD). This enzyme has been reported to be enhanced in the cerebrospinal fluid (CSF) in parkinsonian patients. The objective was to look at the relationship of LPO in the CSF and serum with clinical features of idiopathic PD.

A Rare Paronychia with Superinfection with and : The Importance of Early Microbiological Diagnosis.

is an anaerobic, gram-negative bacillus which naturally thrives in the human vagina, and is usually related to vaginal tract infections. However, this microorganism can also cause infections in other body locations. Infections with are frequently severe due to the risk of osteomyelitis and the lack of good protocols for adequate therapeutic management.

Microorganisms that are related with increased risk for Parkinson's disease.

Parkinson's disease is a neurodegenerative disorder that affects more than 7 million people worldwide. Its aetiology is unknown, although the hypothesis of a genetic susceptibility to environmental agents is accepted. These environmental agents include fungi, bacteria, and viruses.

Is there a halo-enzymopathy in Parkinson's disease?

Laboratory studies identified changes in the metabolism of halogens in the serum and cerebrospinal fluid (CSF) of patients with Parkinson's disease, which indicates the presence of «accelerated self-halogenation» of CSF and/or an increase in haloperoxidases, specifically serum thyroperoxidase and CSF lactoperoxidase. Furthermore, an excess of some halogenated derivatives, such as advanced oxygenation protein products (AOPP), has been detected in the CSF and serum. «Accelerated self-halogenation» and increased levels of haloperoxidases and AOPP proteins indicate that halogenative stress is present in Parkinson's disease.

Endocannabinoid-mediated synaptic plasticity and substance use disorders.

Drugs impact brain reward circuits, causing dependence and addiction, in a condition currently described as substance use disorders. Mechanisms of synaptic plasticity in these circuits are crucial in the development of addictive behaviour, and endocannabinoids, particularly anandamide and 2-arachidonyl-glycerol, participate in normal neuroplasticity. Substance use disorders are known to be associated with disruption of endocannabinoid-mediated synaptic plasticity, among other phenomena.

Oleoylethanolamide and Palmitoylethanolamide Protect Cultured Cortical Neurons Against Hypoxia.

Perinatal hypoxic-ischemic (HI) encephalopathy is defined as a neurological syndrome where the newborn suffers from acute ischemia and hypoxia during the perinatal period. New therapies are needed. The acylethanolamides, oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), possess neuroprotective properties, and they could be effective against perinatal HI.

Palmitoylethanolamide prevents neuroinflammation, reduces astrogliosis and preserves recognition and spatial memory following induction of neonatal anoxia-ischemia.

Rational: Neonatal anoxia-ischemia (AI) particularly affects the central nervous system. Despite the many treatments that have been tested, none of them has proven to be completely successful. Palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) are acylethanolamides that do not bind to CB1 or CB2 receptors and thus they do not present cannabinoid activity.

Excess amounts of 3-iodo-l-tyrosine induce Parkinson-like features in experimental approaches of Parkinsonism.

3-iodo-l-tyrosine might play a role in Parkinson's disease since this molecule is able, at high concentration, to inhibit tyrosine-hydroxylase activity, the rate-limiting enzyme in dopamine biosynthesis. The possible Parkinson-like effects of 3-iodo-l-tyrosine were tested on three experimental approaches in mice: cultured substantia nigra neurons, the enteric nervous system of the jejunum after intra-peritoneal infusions, and the nigrostriatal system following unilateral intrabrain injections. 3-iodo-l-tyrosine, a physiological molecule, was used at concentrations higher than its serum levels in humans.

Analysis of neurotrophic and antioxidant factors related to midbrain dopamine neuronal loss and brain inflammation in the cerebrospinal fluid of the elderly.

Midbrain dopamine neuronal loss and neuroinflammation are two phenomena that are associated with brain senescence. Neurotrophic factor changes and oxidative stress could subserve these phenomena. Aging-related brain changes can be well monitored through the cerebrospinal fluid (CSF).

Effects of acute and repeated cocaine on markers for neural plasticity within the mesolimbic system in rats.

Rationale: Repeated cocaine is known to induce morphological changes in dopaminergic circuits that are known to participate on cocaine-induced addictive changes.

Objective: The objective of the present study was to discern if acute or repeated regimens of daily cocaine (10 mg/kg) lead to reliable changes in the expression of some protein markers for neural plasticity such as synaptophysin, p21-Arc, alpha-tubulin (α-tubulin), and stathmin, in the mesolimbic dopaminergic circuit. Well-known changes in tyrosine hydroxylase and protein kinase A were used for confirming biochemical effects of repeated cocaine.

The transient receptor potential vanilloid-1 is localized at excitatory synapses in the mouse dentate gyrus.

The transient receptor potential vanilloid type 1 (TRPV1) is a non-selective cation channel that plays an important role in pain perception and modulates neurotransmitter release and synaptic plasticity in the brain. TRPV1 function must lay on its anatomical distribution in the peripheral and central nervous system regions involved in the physiological roles of the channel. However, the anatomical localization of TRPV1 is well established in the periphery, but in the brain it is a matter of debate.

The systemic administration of oleoylethanolamide exerts neuroprotection of the nigrostriatal system in experimental Parkinsonism.

Oleoylethanolamide (OEA) is an agonist of the peroxisome proliferator-activated receptor α (PPARα) and has been described to exhibit neuroprotective properties when administered locally in animal models of several neurological disorder models, including stroke and Parkinson's disease. However, there is little information regarding the effectiveness of systemic administration of OEA on Parkinson's disease. In the present study, OEA-mediated neuroprotection has been tested on in vivo and in vitro models of 6-hydroxydopamine (6-OH-DA)-induced degeneration.

Oleoylethanolamide dose-dependently attenuates cocaine-induced behaviours through a PPARα receptor-independent mechanism.

Oleoylethanolamide (OEA) is an acylethanolamide that acts as an agonist of nuclear peroxisome proliferator-activated receptor alpha (PPARα) to exert their biological functions, which include the regulation of appetite and metabolism. Increasing evidence also suggests that OEA may participate in the control of reward-related behaviours. However, direct experimental evidence for the role of the OEA-PPARα receptor interaction in drug-mediated behaviours, such as cocaine-induced behavioural phenotypes, is lacking.

Alteration of neuropathic and visceral pain in female C57BL/6J mice lacking the PPAR-α gene.

Rationale: Peroxisome proliferator-activated receptors (PPARs) participate in the control of chronic neuropathic and inflammatory pain, and these receptors could play a role on acute pain.

Objectives: We used null (PPAR-α -/-) and wild-type female mice and the PPAR-α blocker GW6471 to evaluate (1) the role of PPAR-α on neuropathic pain, (2) the involvement of PPAR-α on visceral and acute thermal nociception, and (3) tissue levels of pro-inflammatory factors.

Methods: Neuropathic pain was induced by sciatic nerve ligature.

Mice lacking the peroxisome proliferator-activated receptor α gene present reduced number of dopamine neurons in the substantia nigra without altering motor behavior or dopamine neuron decline over life.

Peroxisome proliferator-activated receptor alpha (PPAR-α), which is expressed by neurons of the nigrostriatal circuit, plays a prominent role in oxidative stress and neuroinflammation. The objectives were: (i) to discern if levels of antioxidant molecules and pro-inflammatory cytokines, along with PPAR-γ expression are modified in the nigrostriatal region of null PPAR-α mice, (ii) to discern whether dopaminergic neuronal features of the substantia nigra pars compacta (SNpc) and dorsal striatum are affected in null mice, and (iii) to establish if aging-induced decline of nigral neurons is different in null PPAR-α mice relative to wild-type littermates. A substantial decrease in antioxidant molecules was found in SNpc of null mice, by using ELISA.

Sensitization to cocaine is inhibited after intra-accumbal GR103691 or rimonabant, but it is enhanced after co-infusion indicating functional interaction between accumbens D(3) and CB1 receptors.

Rationale: Dopamine D(3) receptors and cannabinoid CB(1) receptors are both expressed in the nucleus accumbens, and they have been involved in motor sensitization to cocaine. The objectives were: (1) to study the effects of blockade of these receptors on sensitization to repeated cocaine, by using GR103691, D(3) receptor blocker, and rimonabant, CB(1) receptor ligand, and (2) to discern if both receptors interact by co-infusing them.

Materials And Methods: Cocaine (10 mg/kg) was injected daily for 3 days (induction phase) and later on day 8 (expression phase), and locomotor activity was measured during 2 h after cocaine.