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)

To characterize the relationship between bruxism and dystonia, 79 patients (28 men and 51 women) with cranial-cervical dystonia were studied. Sixty-two patients (78.5%), 22 men and 40 women, had bruxism. The mean age at onset of dystonia in patients with bruxism was 52.4 +/- 12.6 years (range 14-80), similar to patients with cranial-cervical dystonia without bruxism. Involuntary oromandibular movements (46 patients) and blepharospasm (34 patients) were the most common initial symptoms among patients with dystonia. About one-fourth of bruxism patients had associated dental problems including TMD (21%) and tooth wear (5%). A majority (58%) of the bruxism patients had diurnal bruxism and 12% had nocturnal bruxism. The bruxism patients were compared to 100 patients with Parkinson's disease (PD), cervical dystonia, cranial dystonia, and normal controls, respectively. The prevalence of bruxism was much higher in the cranial-cervical dystonia patients when compared to normal controls (P < 0.001); however, this difference was not significant between other diseased groups and controls. Medications and botulinum toxin injections, used in the treatment of focal dystonia also provided effective relief of bruxism.
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PMID:Bruxism and cranial-cervical dystonia: is there a relationship? 1065 Apr 7

Dysregulation of genes that control cell-cycle progression and DNA repair is a hallmark of tumorigenesis. It is becoming increasingly apparent, however, that these defects also contribute to degeneration of post-mitotic neurons under certain conditions. The gene for ataxia-telangiectasia mutated (ATM) is a prototype for this dual mechanism of action, with loss-of-function mutations causing not only selective degeneration of cerebellar neurons but also increased susceptibility to breast cancer and hematologic malignancy. Increased dosage of amyloid precursor protein in Down syndrome (trisomy 21) predisposes to dementia of Alzheimer type and may also contribute to acute leukemia and transient myeloproliferative disorder. The gene parkin, loss-of-function mutations in which account for about half of cases of early-onset Parkinson disease, has been identified as a candidate tumor suppressor gene by several groups. Parkin is deleted or downregulated in several tumor types, and its re-expression sensitizes derivative cell lines to inhibitors of cell-cycle progression. The overlap of molecular pathways implicated in cancer and neurodegeneration challenges long-held notions about differentiated cellular states and may open the door to novel therapeutic approaches to both groups of disorders.
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PMID:Tumorigenesis and neurodegeneration: two sides of the same coin? 1862 69