title: Amyloid is linked to cognitive decline in patients with Parkinson disease without dementia.
abstract: OBJECTIVE
  To determine whether amyloid burden, as indexed by Pittsburgh compound B (PiB) retention, identifies patients with Parkinson disease with mild cognitive impairment (PD-MCI) compared to those with normal cognition (PD-nl). A related aim is to determine whether amyloid burden predicts cognitive decline in a cohort of subjects with PD without dementia.
  
  
  METHODS
  In this prospective cohort study, we examined 46 subjects with PD without dementia, of whom 35 had normal cognition and 11 met criteria for PD-MCI at study baseline. All subjects underwent standardized neurologic and neuropsychological examinations and PiB PET at baseline, and clinical examinations were conducted annually for up to 5 years.
  
  
  RESULTS
  At baseline, precuneus PiB retention did not distinguish PD-MCI from PD-nl. Subjects with PD-MCI declined more rapidly than PD-nl subjects on cognitive tests of memory, executive function, and activation retrieval. Of the 35 PD-nl subjects, 8 progressed to PD-MCI and 1 to dementia; of the 11 PD-MCI subjects, 5 converted to dementia. Both higher PiB retention and a diagnosis of PD-MCI predicted a greater hazard of conversion to a more severe diagnosis. Baseline PiB retention predicted worsening in executive function over time. The APOE ε4 allele also related to worsening in executive function, as well as visuospatial function, activation retrieval, and performance on the Mini-Mental State Examination. In contrast to its relation to cognitive decline, PiB retention did not affect progression of motor impairment.
  
  
  CONCLUSIONS
  At baseline measurements, amyloid burden does not distinguish between cognitively impaired and unimpaired subjects with PD without dementia, but our data suggest that amyloid contributes to cognitive, but not motor, decline over time.
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Boston, USA.
authors.forename: Stephen N
authors.initials: SN
authors.lastname: Gomperts
authors.forename: Joseph J
authors.initials: JJ
authors.lastname: Locascio
authors.forename: Dorene
authors.initials: D
authors.lastname: Rentz
authors.forename: Andrea
authors.initials: A
authors.lastname: Santarlasci
authors.forename: Marta
authors.initials: M
authors.lastname: Marquie
authors.forename: Keith A
authors.initials: KA
authors.lastname: Johnson
authors.forename: John H
authors.initials: JH
authors.lastname: Growdon
mesh_terms: D000368:Aged; D000682:Amyloid / Q000378:metabolism*; D000814:Aniline Compounds; D053327:Apolipoprotein E4 / Q000235:genetics / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002250:Carbon Radioisotopes; D060825:Cognitive Dysfunction / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000523:psychology*; D003704:Dementia / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism*; D018450:Disease Progression; D005260:Female; D059907:Functional Neuroimaging / Q000379:methods / Q000523:psychology*; D006801:Humans; D008297:Male; D009483:Neuropsychological Tests / Q000706:statistics & numerical data; D010296:Parietal Lobe / Q000378:metabolism; D010300:Parkinson Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000235:genetics / Q000378:metabolism* / Q000523:psychology*; D049268:Positron-Emission Tomography / Q000379:methods / Q000523:psychology; D011446:Prospective Studies; D013844:Thiazoles
chemical_list: C475519:2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole; D000682:Amyloid; D000814:Aniline Compounds; D053327:Apolipoprotein E4; D015415:Biomarkers; D002250:Carbon Radioisotopes; D013844:Thiazoles