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)

The gastrointestinal microbiome is altered in Parkinson's disease and likely plays a key role in its pathophysiology, affecting symptoms and response to therapy and perhaps modifying progression or even disease initiation. Gut dysbiosis therefore has a significant potential as a therapeutic target in Parkinson's disease, a condition elusive to disease-modifying therapy thus far. The gastrointestinal environment hosts a complex ecology, and efforts to modulate the relative abundance or function of established microorganisms are still in their infancy. Still, these techniques are being rapidly developed and have important implications for our understanding of Parkinson's disease. Currently, modulation of the microbiome can be achieved through non-pharmacologic means such as diet, pharmacologically through probiotic, prebiotic, or antibiotic use and procedurally through fecal transplant. Novel techniques being explored include the use of small molecules or genetically engineered organisms, with vast potential. Here, we review how some of these approaches have been used to date, important areas of ongoing research, and how microbiome modulation may play a role in the clinical management of Parkinson's disease in the future.
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PMID:Modulation of the Microbiome in Parkinson's Disease: Diet, Drug, Stool Transplant, and Beyond. 3303 46

Aberrant performance of skilled action has long been noted in schizophrenia and relatedly, recent reports have demonstrated impaired use, performance, and perception of hand gestures in this group. Still, this deficit is not acknowledged as apraxia, which to the broader medical field, characterizes impairments in skilled actions. Understanding the relationship between apraxia and schizophrenia may shed an invaluable new perspective on disease mechanism, and highlight novel treatment opportunities as well. To examine this potential link, we reviewed the evidence for the types of praxis errors, associated psychopathology, and cerebral correlates of the praxis deficit in schizophrenia. Notably, the review indicated that gesture deficits are severe enough to be considered genuine apraxia in a substantial proportion of patients (about 25%). Further, other potential contributors (e.g., hypokinetic motor abnormalities, cognitive impairment) are indeed associated with gesture deficits in schizophrenia, but do not sufficiently explain the abnormality. Finally, patients with praxis deficits have altered brain structure and function including the left parieto-premotor praxis network and these neural correlates are specific to the praxis deficit. Therefore, we argue that the gestural disorder frequently observed in schizophrenia shares both the clinical and neurophysiological features of true apraxia, as in other neuropsychiatric disorders with impaired higher order motor control, such as Parkinson's disease.
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PMID:Gesture deficits and apraxia in schizophrenia. 3309 76


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