Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ever since the first description of Parkinson's disease, it has not only been associated with the classical triad of akinesia, rigor and tremor but also with autonomic regulation disorders. However, the studies published on this subject show differing and partly contradictory results. A large number of studies demonstrate a distinct autonomic disorder. On the other hand there are authors who question an affliction of the autonomic nervous system and others who attribute the autonomic disorder to Parkinson specific medication. To make matters worse, the various pathogeneses of Parkinson's syndrome within the patients collectives have not been sufficiently differentiated and nomenclature of the multisystem degeneration was handled in different ways. Taking our examinations of the various autonomic functions and the underlying literature into critical consideration, we come to the conclusion that regulation disorders of the cardiovascular system, gastrointestinal and urinary tract, as well as sweat and thermoregulation are often seen in the idiopathic Parkinson's disease. In our opinion the idiopathic Parkinson's syndrome must be attributed to the multisystem degenerations. Autonomic dysfunction occurs in different intensities in the disease.
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PMID:[Disorders of autonomic regulation in Parkinson syndrome]. 778 20

The phenotype of 16 members of a family affected by a late-onset, dominant, progressive, motor and autonomic disorder is described. The VAPB (Pro56Ser) mutation was detected in Brazilian families with different phenotypes of motor neuron disorders. In this family, proximal and axial muscle weakness and atrophy, associated with abdominal protrusion, defined the motor phenotype. Death occurred in 10-15 years due to respiratory insufficiency. Tone and tendon reflexes were decreased and a distal tremor was common. Sensation was preserved. Autonomic abnormalities were also present, including choking, chronic intestinal constipation, sexual dysfunction, and sudomotor abnormalities, and on nerve morphology there was involvement of unmyelinated fibers. Electromyography disclosed ongoing denervation and reinnervation. Isolated dysfunction of motor and autonomic neurons is unusual among the spinal muscular atrophies. On this basis, this condition seems to represent a new category of disease.
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PMID:Expanding the phenotypes of the Pro56Ser VAPB mutation: proximal SMA with dysautonomia. 1696 88

Parkinson's disease (PD) is one of common neurodegenerative diseases, which shows motor symptoms including tremor, bradykinesia, rigidity and postural instability. It also involves non-motor symptoms such as cognitive impairment, mental manifestation, autonomic disorder and sensory disturbance. Although treatments to improve the motor disability in PD are being assessed at present, the main challenge remains that is the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find approaches that can inhibit the progression of dopaminergic neurodegeneration. Astrocytes are known to play an important role in the maintenance of the neuronal environment and exert neuroprotective effects. Additionally, astrocyte dysfunction increases the susceptibility of neurons to cytotoxicity. We have demonstrated neuroprotective approaches in parkinsonian models in various studies targeting astrocytes. In this article, we summarize the neuroprotective function of astrocytes in the brain, involvement of astrocyte dysfunction in neurodegeneration, and experimental approaches to dopaminergic neuroprotection. We review findings reported in several papers including our own studies. We also address target molecules and pivotal pathways in astrocytes for dopaminergic neuroprotection. The review discusses new promising therapeutic strategies to prevent dopaminergic neurodegeneration in PD.
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PMID:Therapeutic Strategy of Targeting Astrocytes for Neuroprotection in Parkinson's Disease. 2869 20