Publication:
The neurobiological basis of cognitive impairment in Parkinson's disease

dc.contributor.author Halliday, Glenda en_US
dc.contributor.author Leverenz, James B. en_US
dc.contributor.author Schneider, Jay S. en_US
dc.contributor.author Adler, Charles H. en_US
dc.date.accessioned 2021-11-25T12:30:50Z
dc.date.available 2021-11-25T12:30:50Z
dc.date.issued 2014 en_US
dc.description.abstract The recent formalization of clinical criteria for PD with dementia (PD-D) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PD-D occurs on the background of severe dopamine deficits with the main pathological drivers of cognitive decline being a synergistic effect between α-synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the α-synuclein gene, lead to a clear increased risk of PD-D, while others, such as parkin mutations, are associated with a reduced risk of PD-D. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD-MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low dose MPTP treatment in primates recapitulates PD-MCI over time, enhancing the current biological concept of PD-MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. While dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies and genetic factors in PD-MCI remain to be fully elucidated. en_US
dc.identifier.issn 0885-3185 en_US
dc.identifier.uri http://hdl.handle.net/1959.4/54026
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/3.0/au/ en_US
dc.source Legacy MARC en_US
dc.subject.other neuropathology en_US
dc.subject.other Parkinson's disease dementia en_US
dc.subject.other genetic risk en_US
dc.subject.other neurotransmitters en_US
dc.subject.other preclinical models en_US
dc.title The neurobiological basis of cognitive impairment in Parkinson's disease en_US
dc.type Journal Article en
dcterms.accessRights open access
dspace.entity.type Publication en_US
unsw.accessRights.uri https://purl.org/coar/access_right/c_abf2
unsw.description.publisherStatement This is the pre-peer reviewed version of the article, which has been published in final form at http://dx.doi.org/10.1002/mds.25857 en_US
unsw.identifier.doiPublisher http://dx.doi.org/10.1002/mds.25857 en_US
unsw.relation.faculty Medicine & Health
unsw.relation.ispartofissue 5 en_US
unsw.relation.ispartofjournal Movement Disorders en_US
unsw.relation.ispartofpagefrompageto 634-650 en_US
unsw.relation.ispartofvolume 29 en_US
unsw.relation.originalPublicationAffiliation Halliday, Glenda, Neuroscience Research Australia, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Leverenz, James B., Lou Ruvo Center for Brain Health, Cleveland Clinic Foundation, Cleveland, OH, United States en_US
unsw.relation.originalPublicationAffiliation Schneider, Jay S., Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, United States en_US
unsw.relation.originalPublicationAffiliation Adler, Charles H., Department of Neurology, Mayo Clinic, Scottsdale, Arizona, United States en_US
unsw.relation.school Neuroscience Research Australia *
unsw.subject.fieldofresearchcode 110903 Central Nervous System en_US
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
Author's pre-print.pdf
Size:
393.37 KB
Format:
application/pdf
Description:
Resource type