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)

Acetylcholine plays an important role in regulation of nervous system development and function. We are developing zebrafish (Danio rerio) as a model system to study the role of specific neuronal nicotinic acetylcholine receptor (nAChR) subtypes in development and the effects of nicotine on the developing vertebrate nervous system. We previously characterized the expression of several zebrafish nAChR subunits. To further develop the zebrafish model, here we report a study on the molecular characterization of two additional nAChR subunit genes, designated chrna6 and chrna4. Both zebrafish nAChRs have a high degree of sequence identity to nAChRs expressed in a variety of mammalian species. Reverse transcription polymerase chain reaction was used to show that both nAChR subunit RNAs were expressed early in zebrafish development, with the chrna4 transcript present at 3 hours postfertilization (hpf) and the chrna6 RNA present at 10 hpf. In situ hybridization was used to localize chrna6 and chrna4 RNA expression in 24, 48, 72, and 96 hpf zebrafish. The chrna6 and chrna4 RNAs were each expressed in a unique pattern, which changed during development. At various ages, chrna6 was expressed in Rohon-Beard sensory neurons, trigeminal ganglion, retina, and the pineal gland. Most notably, chrna6 was expressed in catecholaminergic neurons in the midbrain, but was also present in noncatecholaminergic cells in both midbrain and hindbrain. The expression of chrna6 RNA in catecholaminergic cells supports the use of zebrafish as a valid model system to better understand the molecular basis of cholinergic regulation of dopaminergic signaling and the role of alpha6-containing nAChRs in Parkinson's disease. The most notable chrna4 expression was in neural crest cells at 24 hpf and reticulospinal neurons in hindbrain at 48 hpf. chrna4 RNA exhibited a widespread and robust expression pattern in the midbrain in 72 hpf and 96 hpf zebrafish.
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PMID:Cloning and spatiotemporal expression of zebrafish neuronal nicotinic acetylcholine receptor alpha 6 and alpha 4 subunit RNAs. 1930 90

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

Although psychiatric comorbidity in Parkinson's Disease (PD) has often been studied, the individual psychiatric symptoms have rarely been evaluated from a clinimetric point of view in an attempt to measure how much the symptoms have been bothering or distressing the PD patients. The current study is therefore aimed at evaluating from a clinimetric viewpoint the severity of psychiatric symptoms affecting PD patients by using the Hopkins Symptom Checklist (SCL-90-R) to show its measurement-driven construct validity (scalability). The conventional nine SCL-90-R subscales (somatization, obsessive-compulsive, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideas, and psychoticism), as well as the clinical most valid subscales from the SCL-28 version (depression, anxiety, interpersonal sensitivity, and neurasthenia) were analysed according to a clinimetric approach by comparing PD patients with a control group from a general population study. Scalability was tested by the non-parametric item response theory model by use of a Mokken analysis. Among the various SCL-90-R or SCL-28 subscales we identified from the clinimetric analysis that the somatization, anxiety, phobic anxiety, psychoticism, and neurasthenia (apathy), as well as the SCL-90-R GSI, were the most impaired psychiatric syndromes reaching a clinically significant effect size above 0.80, whereas the total SCL-28 GSI obtained an effect size of just 0.80. Our clinimetric analysis has shown that patients with PD not only are bothered with diverse somatic symptoms, but also with specific secondary psychiatric comorbidities which are clinically severe markers of impairment in the day-to-day function implying a negative cooping approach.
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PMID:Evaluating psychiatric symptoms in Parkinson's Disease by a clinimetric analysis of the Hopkins Symptom Checklist (SCL-90-R). 2910 Sep 73

A number of rating scales for the assessment of apathy in Parkinson's disease (PD) were developed. Unfortunately, previous studies focused mainly on psychometric criteria rather than on clinimetric principles to develop these assessment instruments. In the clinimetric approach, the clinical validity of a rating scale, rather than its statistical significance, has the priority. The aim of the present systematic review was to capture the clinimetric properties of these rating scales and to identify the measures, which display clinical validity for the assessment of apathy in PD. The systematic search was conducted on Scopus, PsycINFO, PubMed, Web of Science, ScienceDirect, and Medline following the PRISMA guidelines. A total of 44 studies were included and analyzed in this systematic review. The apathy rating scales, which were found to be psychometrically robust and reliable, were actually clinically questionable. The apathy measures, which displayed clinimetric properties, were the Starkstein Apathy Scale (SAS), the 5-item version of the World Health Organization Well-Being Index (WHO-5), the Neurasthenia Scale and the Lille Apathy Rating Scale (LARS). The SAS was found to be clinically valid at a macro-analytic level, particularly when used either to exclude the presence of symptoms of apathy or to evaluate the side effects of medications. The WHO-5 and the Neurasthenia Scale were found to be clinically valid only at a micro-analytic level and can be used as screening measures for the assessment of the severity of symptoms of apathy. The LARS was a clinically valid instrument to be used for the diagnosis of apathy.
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PMID:Clinimetric approach to rating scales for the assessment of apathy in Parkinson's disease: A systematic review. 3105 22