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These studies show that the emergence of PDD occurs on the background of severe dopamine deficits with, the main pathological drivers of cognitive decline being a synergistic effect between alpha\u2010synuclein 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 <jats:italic>\u03b1\u2010synuclein<\/jats:italic> gene, lead to a clear increased risk of PDD, whereas others, such as <jats:italic>parkin<\/jats:italic> mutations, are associated with a reduced risk of PDD. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD\u2010MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low\u2010dose MPTP treatment in primates recapitulates PD\u2010MCI over time, enhancing the current biological concept of PD\u2010MCI 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. Whereas 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\u2010MCI remains to be fully elucidated. \u00a9 2014 International Parkinson and Movement Disorder Society<\/jats:p>","DOI":"10.1002\/mds.25857","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T10:27:39Z","timestamp":1398162459000},"page":"634-650","source":"Crossref","is-referenced-by-count":348,"title":["The neurobiological basis of cognitive impairment in Parkinson's disease"],"prefix":"10.1002","volume":"29","author":[{"given":"Glenda M.","family":"Halliday","sequence":"first","affiliation":[{"name":"Neuroscience Research Australia and the University of New South Wales  Sydney Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James B.","family":"Leverenz","sequence":"additional","affiliation":[{"name":"Lou Ruvo Center for Brain Health, Cleveland Clinic Foundation Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay S.","family":"Schneider","sequence":"additional","affiliation":[{"name":"Department of Pathology Anatomy and Cell Biology, Thomas Jefferson University Philadelphia Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles H.","family":"Adler","sequence":"additional","affiliation":[{"name":"Department of Neurology Mayo Clinic Scottsdale Arizona USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,4,22]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(09)70238-8"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2009.05118.x"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.25249"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.21507"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.24893"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.25655"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-010-0755-1"},{"key":"e_1_2_10_9_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.54.10.1916"},{"key":"e_1_2_10_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.parkreldis.2005.09.001"},{"key":"e_1_2_10_11_1","doi-asserted-by":"publisher","DOI":"10.1097\/WAD.0b013e31819c5ef4"},{"key":"e_1_2_10_12_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-009-0620-2"},{"key":"e_1_2_10_13_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.23659"},{"key":"e_1_2_10_14_1","doi-asserted-by":"publisher","DOI":"10.1007\/s004019900168"},{"key":"e_1_2_10_15_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.59.1.102"},{"key":"e_1_2_10_16_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.20635"},{"key":"e_1_2_10_17_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awq059"},{"key":"e_1_2_10_18_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/aws234"},{"key":"e_1_2_10_19_1","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.74.7.852"},{"key":"e_1_2_10_20_1","doi-asserted-by":"publisher","DOI":"10.1007\/s004010100390"},{"key":"e_1_2_10_21_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.21956"},{"key":"e_1_2_10_22_1","doi-asserted-by":"publisher","DOI":"10.1007\/s004010050843"},{"key":"e_1_2_10_23_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awr031"},{"key":"e_1_2_10_24_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0297-11.2011"},{"key":"e_1_2_10_25_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuint.2008.08.004"},{"key":"e_1_2_10_26_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.25112"},{"key":"e_1_2_10_27_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-008-0344-8"},{"key":"e_1_2_10_28_1","doi-asserted-by":"publisher","DOI":"10.1097\/NEN.0b013e3181d88e63"},{"key":"e_1_2_10_29_1","first-page":"255","article-title":"Amyloid angiopathy in idiopathic Parkinson's disease. 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