Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A moderate daily intake of 3-4 cups of coffee has convincing protective effects against development of type 2 diabetes and Parkinson's disease. The literature also indicates that moderate coffee intake reduces the risk of stroke, the overall risk of cancer, Alzheimer's disease, suicide and depression. However, pregnant women, people suffering from anxiety disorder and persons with a low calcium intake should restrain from moderate or high intake of coffee due to uncertainty regarding potential negative effects on pregnancy, anxiety and risk of osteoporosis, respectively.
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PMID:[Coffee can protect against disease]. 2300 23

Transcranial magnetic stimulation has become an important field for both research in neuroscience and for therapy since Barker in 1985 showed that it was possible to stimulate the human motor cortex with an electromagnet. Today for instance, transcranial magnetic stimulation can be used to measure nerve conduction velocities and to create virtual lesions in the brain. The latter option creates the possibility to inactivate parts of the brain temporarily without permanent damage. In 2008, the American Food and Drugs Administration approved repetitive transcranial magnetic stimulation as a therapy for major depression under strict conditions. Repetitive transcranial magnetic stimulation has not yet been cleared for treatment of other diseases, including schizophrenia, anxiety disorders, obesity and Parkinson's disease, but results seem promising. Transcranial magnetic stimulation, however, was not invented at the end of the 20th century. The discovery of electromagnetism, the enthusiasm for electricity and electrotherapy, and the interest in Beard's concept of neurasthenia already resulted in the first electromagnetic treatments in the late 19th and early 20th century. In this article, we provide a history of electromagnetic stimulation circa 1900. From the data, we conclude that Mesmer's late 18th century ideas of 'animal magnetism' and the 19th century absence of physiological proof had a negative influence on the acceptance of this therapy during the first decades of the 20th century. Electromagnetism disappeared from neurological textbooks in the early 20th century to recur at the end of that century.
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PMID:Magnetic flimmers: 'light in the electromagnetic darkness'. 2304 45

This study examined the rates of anxiety and depressive disorders, physical illnesses, and health service use in male patients 55 years or older with a diagnosis of Parkinson disease who were seen at least twice at the 10 medical centers in the Veterans Affairs Healthcare Network of the South Central region of the United States. Of the 273 male patients diagnosed between October 1, 1997, and September 30, 2009, 62 (22.7%) had a depressive disorder. The overall prevalence of anxiety disorders was 12.8%; patients with comorbid depression had a 5-fold greater prevalence of anxiety disorders than those without depression (35.5% vs 6.2%, P<.0001). Patients with comorbid depression also had increased prevalence of all physical illnesses examined and more outpatient clinic and mental health visits. Patients with Parkinson disease and comorbid depression are more likely to have anxiety disorders and several physical illnesses, to be using antipsychotic and dementia medicines, and to have increased health service utilization than those without depression.
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PMID:Anxiety disorders, physical illnesses, and health care utilization in older male veterans with Parkinson disease and comorbid depression. 2319 99

There is no sense organ specifically dedicated to time perception, as there is for other senses such as hearing and vision. However, this subjective sense of time is fundamental to our conception of reality and it creates the temporal course of events in our lives. Here, we explored neurobiological relations from the clinical perspective, examining timing ability in patients with different neurological and psychiatric conditions (e.g. Parkinson's disease, depression, bipolar disorder, anxiety disorders and schizophrenia). The neural bases of present distortions in time perception and temporal information processing still remain poorly understood. We reviewed: a) how the brain is capable of encoding time in different environments and multiple tasks, b) different models of interval timing, c) brain structures and neurotransmitters associated with time perception, d) the relationship between memory and time perception, e) neural mechanisms underlying different theories in neural and mental processes, and f) the relationship between different mental diseases and time perception. Bibliographic research was conducted based on publications over the past thirteen years written in English in the databases Scielo, Pubmed/MEDLINE, ISI Web of Knowledge. The time perceptions research are executed to evaluate time perception in mental diseases and can provide evidence for future clinical applications.
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PMID:Time perception distortion in neuropsychiatric and neurological disorders. 2384 80

It is widely accepted that autism is associated with disordered emotion processing and, in particular, with deficits of emotional reciprocity such as impaired emotion recognition and reduced empathy. However, a close examination of the literature reveals wide heterogeneity within the autistic population with respect to emotional competence. Here we argue that, where observed, emotional impairments are due to alexithymia-a condition that frequently co-occurs with autism-rather than a feature of autism per se. Alexithymia is a condition characterized by a reduced ability to identify and describe one's own emotion, but which results in reduced empathy and an impaired ability to recognize the emotions of others. We briefly review studies of emotion processing in alexithymia, and in autism, before describing a recent series of studies directly testing this 'alexithymia hypothesis'. If found to be correct, the alexithymia hypothesis has wide-reaching implications for the study of autism, and how we might best support subgroups of autistic individuals with, and without, accompanying alexithymia. Finally, we note the presence of elevated rates of alexithymia, and inconsistent reports of emotional impairments, in eating disorders, schizophrenia, substance abuse, Parkinson's Disease, multiple sclerosis and anxiety disorders. We speculate that examining the contribution of alexithymia to the emotional symptoms of these disorders may bear fruit in the same way that it is starting to do in autism.
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PMID:Mixed emotions: the contribution of alexithymia to the emotional symptoms of autism. 2388 Aug 81

The purpose of this article is to provide an overview of some of the important information related to safety and tolerability of duloxetine. Duloxetine, a potent reuptake inhibitor of serotonin and noradrenaline, is effective for the treatment of major depressive disorder, anxiety disorder, and painful diabetic neuropathy (PDN). Duloxetine is safe and well-tolerated across indications, with few reported serious side effects. Common adverse events are consistent with the pharmacology of the molecule and are mainly referable to the gastrointestinal and the nervous systems. Duloxetine should not be used in combination with CYP 1A2 inhibitors or nonselective, irreversible monoamine oxidase inhibitors. Duloxetine has a generally favorable side effect profile and dosing is simple. Nausea is the most common side effect, but it occurs less frequently if treatment is initiated at 30 mg . day-1 and titrated after one week to 60 mg . day-1, an efficacious dosage at which pain relief can occur within one week. Clinical trials have demonstrated the analgesic efficacy of duloxetine for PDN and fibromyalgia in addition to improvements in quality-of-life measurements. Furthermore trials for osteoarthritis, headache, and the pain associated with Parkinson disease may provide insight into alternative uses for duloxetine.
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PMID:[Duloxetine for chronic pain management: pharmacology and clinical use]. 2390 4

Evidence is rapidly accumulating that rare, recurrent copy number variants represent large effect risk factors for neuropsychiatric disorders. 22q11.2 deletion syndrome (22q11DS) (velocardiofacial syndrome or DiGeorge syndrome) is the most common known contiguous gene deletion syndrome and is associated with diverse neuropsychiatric disorders across the life span. One of the most intriguing aspects of the syndrome is the variability in clinical and cognitive presentation: children with 22q11DS have high prevalence of autism spectrum, attention deficit, and anxiety disorders, as well as psychotic-like features, and up to 30% of adolescents and adults develop schizophrenia-like psychosis. Recently, cases of early-onset Parkinson's disease in adults have been reported, collectively suggesting a role for disrupted dopaminergic neurotransmission in the observed neuropsychiatric phenotypes. There is also some evidence that 22q11DS-associated autism spectrum disorder and schizophrenia represent two unrelated phenotypic manifestations, consistent with a neuropsychiatric pleiotropy model. This genetic lesion thus provides a unique model for the discovery of specific genomic risk and (potentially) protective factors for neuropsychiatric disease. Here, we provide an overview of neuropsychiatric findings to date, which highlight the value of this syndrome in mapping the developmental trajectory of dimensional phenotypes that traverse multiple diagnostic categories. Potential sources of genetic variability that may contribute to the disorder's heterogeneous presentation are reviewed. Because of its known genetic etiology, animal models can readily be developed that recapitulate specific aspects of the syndrome. Future research directions involve translational models and potential for drug screenable targets in the context of this human model system.
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PMID:The 22q11.2 deletion syndrome as a window into complex neuropsychiatric disorders over the lifespan. 2399 25

The nuclei of the human amygdaloid complex can be distinguished from each other on the basis of their cytoarchitecture, chemistry and connections, all of which process the information needed for the different functions (ranging from attention to memory and emotion) of the amygdala. This complex receives dopaminergic input that exerts modulatory effects over its intrinsic network and is critical for reward-related learning and fear conditioning. To determine the specific distribution of the dopaminergic input through the different nuclei and nuclear subdivisions of this structure we used stereological tools to quantify the fibers containing the dopamine transporter (used to signal the dopaminergic phenotype) in post-mortem samples from control individuals. Dopaminergic axons targeted every nucleus of the amygdaloid complex, and the density of dopamine transporter-containing axons varied considerably among its nuclear groups. The central group showed the greatest density of dopamine transporter-positive fibers, more than double the density of the basolateral group, the second most densely innervated structure. The dopamine transporter-positive innervation is very scant in the corticomedial group. The density of dopamine transporter-positive fibers did not vary among the nuclei of the basolateral group - i.e. basal, lateral and accessory basal nuclei - although there were significant density gradients among the subdivisions of these nuclei. These detailed quantitative data on dopamine transporter-positive innervation in the human amygdaloid complex can offer a useful reference in future studies aimed at analysing putative dysfunctions of this system in diseases involving brain dopamine, such as certain anxiety disorders, Parkinson's disease and schizophrenia.
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PMID:Distribution of dopamine transporter immunoreactive fibers in the human amygdaloid complex. 2410 48

Repeated sessions of transcranial magnetic stimulation (rTMS) are capable of changing and modulating neural activity beyond the period of stimulation. Because many neurological disorders are thought to involve abnormal or dysfunctional neuronal activity, it is hypothesised that the therapeutic action of rTMS may occur through modulating and reversing abnormal activity and facilitating neuroplasticity.Numerous clinical studies have investigated the safety and efficacy of rTMS treatment for a wide variety of conditions including depression, anxiety disorders including obsessive compulsive disorder, Parkinson's disease, stroke, tinnitus, affective disorders, schizophrenia and chronic pain. Despite some promising results, rTMS is not currently widely used to assist in recovery from neurotrama. In this review, we argue that the therapeutic promise of rTMS is limited because the mechanisms of action of rTMS are not completely understood and therefore it is difficult to determine which treatment protocols are appropriate for specific neurological conditions. We use the application of rTMS in motor functional recovery from cerebral ischemic stroke to illustrate the difficulties in interpreting and assessing the therapeutic potential of rTMS for neurotrauma in terms of the presumed mechanisms of action of rTMS. Future directions for research will also be discussed.
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PMID:Repetitive transcranial magnetic stimulation for stroke rehabilitation-potential therapy or misplaced hope? 2459 27

The high rate of coexistent emotional disorders in neurological diseases is challenging. As a rule this coexistence comprises a more dramatic subjective suffering, reduced psychological coping, possible negative interferences with somatic treatments and rehabilitation, an impaired quality of life and higher grades of psychosocial disability. It may also lead to an overall increased risk of somatic morbidity and even mortality in the further course of illness. The complex interrelations may be favorably integrated within a biopsychosocial model. Psychological and psychosocial stressors can be appreciated on their own discrete levels but have to be reflected in their neurobiological correlates. Both neurological and emotional disorders frequently share decisive pathogenetic mechanisms, i.e. the underlying process of neurological disease may contribute to major affective problems also in a somatopsychic direction. From a perspective of multimorbidity the prevalence and clinical relevance of coexistent depressive and anxiety disorders, common pathogenetic mechanisms and implications for treatment will be described for stroke and Parkinson's disease, as selected neurological disorders.
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PMID:[Coexistent depressive and anxiety disorders in neurological diseases: from a perspective of multimorbidity]. 2461 47


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