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dc.contributor.authorBrowne, Patrick
dc.contributor.authorDaly, Lorna
dc.contributor.authorCounihan, Timothy
dc.date.accessioned2015-07-06T08:58:45Zen
dc.date.available2015-07-06T08:58:45Zen
dc.date.issued2014-09en
dc.identifier.urihttp://hdl.handle.net/10147/558981en
dc.description.abstractParkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease, and affects about 1% of the population over 65 year of age. Although the incidence of PD rises with advancing age, juvenile onset PD (onset under 40 years of age) is well recognised and is associated with identifiable genetic mutations in a significant proportion of cases. The cause of PD remains unknown. One possibility is that affected individuals may have inherited a predisposition to developing PD and that some environmental exposure may trigger the start of neuronal degeneration. The recent identification of a number of genetic mutations in families with several affected members, has enhanced our understanding of the pathogenesis of neuronal degeneration in PD. These gene mutations result in a number of possible abnormalities including abnormal protein folding/aggregation, defective protein clearance, defective cell resistance to oxidative stress, mitochondrial dysfunction – such abnormalities may contribute to pathogenesis.
dc.language.isoenen
dc.publisherNursing in General Practiceen
dc.subjectPARKINSON'S DISEASEen
dc.subjectNEUROLOGICAL DISEASEen
dc.titleParkinson’s disease – a brief practical approachen
dc.typeArticleen
dc.identifier.journalNursing in General Practiceen
dc.description.fundingNo fundingen
dc.description.provinceConnachten
dc.description.peer-reviewpeer-reviewen
refterms.dateFOA2018-08-26T21:07:52Z
html.description.abstractParkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease, and affects about 1% of the population over 65 year of age. Although the incidence of PD rises with advancing age, juvenile onset PD (onset under 40 years of age) is well recognised and is associated with identifiable genetic mutations in a significant proportion of cases. The cause of PD remains unknown. One possibility is that affected individuals may have inherited a predisposition to developing PD and that some environmental exposure may trigger the start of neuronal degeneration. The recent identification of a number of genetic mutations in families with several affected members, has enhanced our understanding of the pathogenesis of neuronal degeneration in PD. These gene mutations result in a number of possible abnormalities including abnormal protein folding/aggregation, defective protein clearance, defective cell resistance to oxidative stress, mitochondrial dysfunction – such abnormalities may contribute to pathogenesis.


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