Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-9-12
pubmed:abstractText
Parkinson's disease is a primarily sporadic occurring neurodegenerative disorder of advanced age. However, in the last few years several genes have been identified that lead to a hereditary parkinsonian disorder with autosomal dominant or autosomal recessive inheritance. This includes autosomal dominant mutations in the alpha-synuclein, ubiquitin-C-terminal hydrolase-L1 (UCH-L1) and the leucine-rich repeat kinase (LRRK)2 genes and autosomal recessively inherited mutations in Parkin, PINK1, DJ-1 and the ATP13A2 genes. By taking the biochemical function of these genes and mutations into account, three underlying pathogenetic pathways can be identified: (i) altered protein quality control, (ii) oxidative stress and mitochondrial dysfunction, and (iii) disturbed kinase activity. It remains an open question whether alterations of these pathways lead to different entities of Parkinson's disease or whether they finally converge at a point that is the common pathogenetic denominator of Parkinson's disease. Finally cell death is executed by excitotoxicity, apoptosis and autophagy and appears to be facilitated by neuroinflammatory processes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0340-5354
pubmed:author
pubmed:issnType
Print
pubmed:volume
255 Suppl 5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-7
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Update on the pathogenesis of Parkinson's disease.
pubmed:affiliation
Dept. of Neurodegeneration and Restorative Research, Center for Neurological Medicine, University of Göttingen, Göttingen, Germany. jschulz4@gwdg.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't