COVID-19 outcomes in hospitalized Parkinson's disease patients in two pandemic waves in 2020: a nationwide cross-sectional study from Germany.

Background: The individualized clinical and public health management of the COVID-19 pandemic have changed over time, including care of people with PD. The objective was to investigate whether in-hospital COVID-19 outcomes and hospital care utilization of people with PD differed between the first two pandemic waves (W) 2020 in Germany.

Methods: We conducted a nationwide cross-sectional study of inpatients with confirmed COVID-19 and PD between March 1 and May 31 (W1), and October 1 and December 31 (W2), 2020 and 2019, using an administrative database.

Parkinson's Disease Multimodal Complex Treatment (PD-MCT): Analysis of Therapeutic Effects and Predictors for Improvement.

Parkinson's disease Multimodal Complex Treatment (PD-MCT) is a multidisciplinary inpatient treatment approach that has been demonstrated to improve motor function and quality of life in patients with Parkinson's disease (PD). In this study, we assessed the efficacy of PD-MCT and calculated predictors for improvement. We performed a prospective analysis in a non-randomized, open-label observational patient cohort.

Parkinson's Disease Multimodal Complex Treatment improves motor symptoms, depression and quality of life.

Parkinson's disease (PD) is the world's fastest growing neurological disorder disabling patients through a broad range of motor and non-motor symptoms. For the clinical management, a multidisciplinary approach has increasingly been shown to be beneficial. In Germany, inpatient Parkinson's Disease Multimodal Complex Treatment (PD-MCT) is a well-established and frequent approach, although data on its effectiveness are rare.

Dynamics of Parkinson's Disease Multimodal Complex Treatment in Germany from 2010⁻2016: Patient Characteristics, Access to Treatment, and Formation of Regional Centers.

Parkinson's disease (PD) is currently the world's fastest-growing neurological disorder. It is characterized by motor and non-motor symptoms which progressively lead to significant clinical impairment, causing a high burden of disease. In addition to pharmacological therapies, various non-pharmacological treatment options are available.

Novel Immunotherapeutic Approaches to Target Alpha-Synuclein and Related Neuroinflammation in Parkinson's Disease.

The etiology of Parkinson's disease (PD) is significantly influenced by disease-causing changes in the protein alpha-Synuclein (aSyn). It can trigger and promote intracellular stress and thereby impair the function of dopaminergic neurons. However, these damage mechanisms do not only extend to neuronal cells, but also affect most glial cell populations, such as astroglia and microglia, but also T lymphocytes, which can no longer maintain the homeostatic CNS milieu because they produce neuroinflammatory responses to aSyn pathology.

Impairment of Motor Function Correlates with Neurometabolite and Brain Iron Alterations in Parkinson's Disease.

We took advantage of magnetic resonance imaging (MRI) and spectroscopy (MRS) as non-invasive methods to quantify brain iron and neurometabolites, which were analyzed along with other predictors of motor dysfunction in Parkinson's disease (PD). Tapping hits, tremor amplitude, and the scores derived from part III of the Movement Disorder Society-Sponsored Revision of the Unified Parkinson Disease Rating Scale (MDS-UPDRS3 scores) were determined in 35 male PD patients and 35 controls. The iron-sensitive MRI relaxation rate R2* was measured in the globus pallidus and substantia nigra.

Emerging Immunotherapies for Parkinson Disease.

Symptomatic treatment options for Parkinson disease have steadily improved, and individualized therapeutic approaches are becoming established for every stage of the disease. However, disease-modifying therapy with a causal approach is still unavailable. The central causative role of alpha-synuclein pathology, including its progressive spread to most areas of the CNS, has been widely recognized, and a strong involvement of immune responses has recently been discovered.

Brainstem Raphe Alterations in TCS: A Biomarker for Depression and Apathy in Parkinson's Disease Patients.

Depression and apathy can both be present in patients with Parkinson's disease (PD) while e. g., essential tremor (ET) patients mostly only report depressive symptoms.

Association of exposure to manganese and iron with relaxation rates R1 and R2*- magnetic resonance imaging results from the WELDOX II study.

Objective: Magnetic resonance imaging is a non-invasive method that allows the indirect quantification of manganese (Mn) and iron (Fe) accumulation in the brain due to their paramagnetic features. The WELDOX II study aimed to explore the influence of airborne and systemic exposure to Mn and Fe on the brain deposition using the relaxation rates R1 and R2* as biomarkers of metal accumulation in regions of interest in 161 men, including active and former welders.

Material And Methods: We obtained data on the relaxation rates R1 and R2* in regions that included structures within the globus pallidus (GP), substantia nigra (SN), and white matter of the frontal lobe (FL) of both hemispheres, as well as Mn in whole blood (MnB), and serum ferritin (SF).

Association of exposure to manganese and iron with striatal and thalamic GABA and other neurometabolites - Neuroimaging results from the WELDOX II study.

Objective: Magnetic resonance spectroscopy (MRS) is a non-invasive method to quantify neurometabolite concentrations in the brain. Within the framework of the WELDOX II study, we investigated the association of exposure to manganese (Mn) and iron (Fe) with γ-aminobutyric acid (GABA) and other neurometabolites in the striatum and thalamus of 154 men.

Material And Methods: GABA-edited and short echo-time MRS at 3T was used to assess brain levels of GABA, glutamate, total creatine (tCr) and other neurometabolites.

Coronal Transcranial Sonography and M-Mode Tremor Frequency Determination in Parkinson's Disease and Essential Tremor.

Background And Purpose: The axial mesencephalic transcranial sonography plane is an established and sensitive diagnostic tool for the differentiation of Parkinson's disease and essential tremor. However, the substantia nigra can also be depicted in a second coronal examination plane, whose diagnostic value has not yet been evaluated. Furthermore, the M-mode tremor frequency determination represents another sonographic tool, which might yield additional diagnostic value.

Levodopa, placebo and rotigotine change biomarker levels for oxidative stress.

Introduction: Homocysteine increase and glutathione derivative cysteinyl-glycine fall are indirect biomarkers for oxidative stress, for instance due to dopamine D receptor stimulation.

Objectives: To investigate the influence of the D receptor agonists levodopa and rotigotine compared with placebo on homocysteine and cysteinyl-glycine in plasma of patients with Parkinson's disease.

Methods: Patients received 100 mg levodopa, 4 mg rotigotine or placebo.

Levodopa increases oxidative stress and repulsive guidance molecule A levels: a pilot study in patients with Parkinson's disease.

Exposure to free radicals influences synthesis, degradation and function of proteins, such as repulsive guidance molecule A. Decay of this protein is essential for neuronal maintenance and recovery. Levodopa elevates oxidative stress.

Fewer fluctuations, higher maximum concentration and better motor response of levodopa with catechol-O-methyltransferase inhibition.

Catechol-O-methyltransferase inhibitor addition to levodopa/carbidopa formulations improves motor symptoms and reduces levodopa fluctuations in patients with Parkinson's disease. Objectives were to investigate the effects of entacapone and tolcapone on plasma behaviour of levodopa, its metabolite 3-O-methyldopa and on motor impairment. 22 patients orally received levodopa/carbidopa first, then levodopa/carbidopa/entacapone and finally levodopa/carbidopa plus tolcapone within a 4.

Levodopa-related cysteinyl-glycine and cysteine reduction with and without catechol-O-methyltransferase inhibition in Parkinson's disease patients.

Oxidative stress is influenced by the thiol homeostasis, which regulates the redox milieu via glutathione. Components of glutathione metabolism are cysteine and cysteinyl-glycine. Both substrates decay following levodopa application or dopamine-related oxidative stress.

Methyl group-donating vitamins elevate 3-O-methyldopa in patients with Parkinson disease.

Background: Levodopa (LD)/dopa decarboxylase inhibitor application increases 3-O-methyldopa (3-OMD) concentrations in association with methyl group transfers, which demand for the conversion of methionine to homocysteine. This accompanying reaction is partially reversible by methyl group-donating vitamins.

Objective: The objective of this study was to investigate of the effect of methyl group-donating vitamins on 3-OMD synthesis in LD-treated patients with Parkinson disease.

Cysteine decrease following acute Levodopa intake in patients with Parkinson's disease.

The thiol homeostasis determines the redox milieu and thus scavenging of free radicals by antioxidants like glutathione (GSH). GSH is formed out of cysteine in combination with l-glycine and glutamine acid. An up regulation of free radical occurrence is looked upon as one key feature of chronic neurodegeneration.

Pain perception, pain drug therapy and health status in patients with Parkinson's disease.

Background: Parkinson's disease (PD) is traditionally characterized as a movement disorder; however, sensory perception problems including pain syndromes are also frequent. We performed a survey to analyze the relations between health status, pain perception and gender in 4,086 PD patients. Moreover, the participants should tick whether they took pain medications or not.

Levodopa induces synthesis of nerve growth factor and growth hormone in patients with Parkinson disease.

Background: Polyneuropathy is observed in treated patients with Parkinson disease. Peripheral axonal degeneration is related to nerve growth factor metabolism. The causes for this axonal degeneration and the role of levodopa itself are not known.

Inhibition of catechol-O-methyltransferase modifies acute homocysteine rise during repeated levodopa application in patients with Parkinson's disease.

Elevation of plasma total homocysteine concentrations were observed in levodopa/dopa decarboxylase inhibitor (DDI)-treated patients with Parkinson's disease (PD). Degradation of levodopa to 3-O-methyldopa via the enzyme catechol-O-methyltransferase (COMT) is a methyl group demanding reaction. It generates homocysteine from the methyl group donor methionine.

Cysteinyl-glycine reduction as marker for levodopa-induced oxidative stress in Parkinson's disease patients.

Oxidative stress is influenced by the thiol homeostasis, which determines the redox milieu. One of its components is Cysteinyl-glycine (Cys-Gly) generation, as its metabolic precursor is the free radicals scavenging glutathione. Levodopa is under suspicion to promote oxidative stress via the turnover of its metabolite dopamine in abundant mitochondria.

Elevation of total homocysteine levels in patients with Parkinson's disease treated with duodenal levodopa/carbidopa gel.

Levodopa/carbidopa (LD/CD) application elevates total plasma homocysteine (thcys). We determined thcys-, LD- and 3-O-methyldopa (3-OMD) concentrations in 28 patients with Parkinson's disease (PD) on a LD/CD duodenal gel treatment. We found a distinct thcys increase (29.

Impact of Oral Fast Release Amantadine on Movement Performance in Patients with Parkinson's Disease.

Application of oral fast release amantadine and levodopa may induce an improvement of motor symptoms in patients with Parkinson's disease (PD). The objective of this trial was to investigate the clinical efficacy of a fast release amantadine sulfate formulation on simple and complex movement performance and putative relations to the pharmacokinetic behavior in PD patients. We challenged two cohorts of 12 PD patients, who were taken off their regular antiparkinsonian treatment for at least 12 hours, with oral 300 mg amantadine sulfate.