Tags

Type your tag names separated by a space and hit enter

Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease.
Mov Disord 2016; 31(1):111-7MD

Abstract

INTRODUCTION

Although most previous cognitive studies of β-amyloidopathy in PD focused on cortical plaque deposition, recent postmortem studies point to an important role of striatal β-amyloid plaque deposition. The aim of this study was to investigate the relative contributions of striatal and cortical β-amyloidopathy to cognitive impairment in PD.

METHODS

Patients with PD (n = 62; age, 68.9 ± 6.4 years; H & Y stage: 2.7 ± 0.5; MoCA score: 25.2 ± 3.0) underwent [(11) C]Pittsburgh compound B β-amyloid, [(11) C]dihydrotetrabenazine monoaminergic, and [(11) C]methyl-4-piperidinyl propionate acetylcholinesterase brain PET imaging and neuropsychological assessment. [(11) C]Pittsburgh compound B β-amyloid data from young to middle-aged healthy subjects were used to define elevated [(11) C]Pittsburgh compound B binding in patients.

RESULTS

Elevated cortical and striatal β-amyloid deposition were present in 37% and 16%, respectively, of this predominantly nondemented cohort of patients with PD. Increased striatal β-amyloid deposition occurred in half of all subjects with increased cortical β-amyloid deposition. In contrast, increased striatal β-amyloid deposition did not occur in the absence of increased cortical β-amyloid deposition. Analysis of covariance using global composite cognitive z scores as the outcome parameter showed significant regressor effects for combined striatal and cortical β-amyloidopathy (F = 4.18; P = 0.02) after adjusting for covariate effects of cortical cholinergic activity (F = 5.67; P = 0.02), caudate nucleus monoaminergic binding, duration of disease, and age (total model: F = 3.55; P = 0.0048). Post-hoc analysis showed significantly lower cognitive z score for combined striatal and cortical β-amyloidopathy, compared to cortical-only β-amyloidopathy and non-β-amyloidopathy subgroups.

CONCLUSIONS

The combined presence of striatal and cortical β-amyloidopathy is associated with greater cognitive impairment than cortical β-amyloidopathy alone in PD.

Authors+Show Affiliations

Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA.Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA. Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA.Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA. University of Michigan Morris K. Udall Center, Ann Arbor, Michigan, USA.Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA.Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA.Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA. University of Michigan Morris K. Udall Center, Ann Arbor, Michigan, USA.Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA.Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. Neurology Service and GRECC, VAAAHS, Ann Arbor, Michigan, USA. University of Michigan Morris K. Udall Center, Ann Arbor, Michigan, USA.Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA. Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. Neurology Service and GRECC, VAAAHS, Ann Arbor, Michigan, USA. University of Michigan Morris K. Udall Center, Ann Arbor, Michigan, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

26380951

Citation

Shah, Neha, et al. "Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease." Movement Disorders : Official Journal of the Movement Disorder Society, vol. 31, no. 1, 2016, pp. 111-7.
Shah N, Frey KA, Müller ML, et al. Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease. Mov Disord. 2016;31(1):111-7.
Shah, N., Frey, K. A., Müller, M. L., Petrou, M., Kotagal, V., Koeppe, R. A., ... Bohnen, N. I. (2016). Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease. Movement Disorders : Official Journal of the Movement Disorder Society, 31(1), pp. 111-7. doi:10.1002/mds.26369.
Shah N, et al. Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease. Mov Disord. 2016;31(1):111-7. PubMed PMID: 26380951.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease. AU - Shah,Neha, AU - Frey,Kirk A, AU - Müller,Martijn L T M, AU - Petrou,Myria, AU - Kotagal,Vikas, AU - Koeppe,Robert A, AU - Scott,Peter J H, AU - Albin,Roger L, AU - Bohnen,Nicolaas I, Y1 - 2015/09/18/ PY - 2015/04/01/received PY - 2015/07/15/revised PY - 2015/07/17/accepted PY - 2015/9/19/entrez PY - 2015/9/19/pubmed PY - 2016/10/22/medline KW - PET KW - Parkinson's disease KW - acetylcholinesterase KW - cognitive impairment KW - cortex KW - dopamine KW - striatum KW - β-amyloid SP - 111 EP - 7 JF - Movement disorders : official journal of the Movement Disorder Society JO - Mov. Disord. VL - 31 IS - 1 N2 - INTRODUCTION: Although most previous cognitive studies of β-amyloidopathy in PD focused on cortical plaque deposition, recent postmortem studies point to an important role of striatal β-amyloid plaque deposition. The aim of this study was to investigate the relative contributions of striatal and cortical β-amyloidopathy to cognitive impairment in PD. METHODS: Patients with PD (n = 62; age, 68.9 ± 6.4 years; H & Y stage: 2.7 ± 0.5; MoCA score: 25.2 ± 3.0) underwent [(11) C]Pittsburgh compound B β-amyloid, [(11) C]dihydrotetrabenazine monoaminergic, and [(11) C]methyl-4-piperidinyl propionate acetylcholinesterase brain PET imaging and neuropsychological assessment. [(11) C]Pittsburgh compound B β-amyloid data from young to middle-aged healthy subjects were used to define elevated [(11) C]Pittsburgh compound B binding in patients. RESULTS: Elevated cortical and striatal β-amyloid deposition were present in 37% and 16%, respectively, of this predominantly nondemented cohort of patients with PD. Increased striatal β-amyloid deposition occurred in half of all subjects with increased cortical β-amyloid deposition. In contrast, increased striatal β-amyloid deposition did not occur in the absence of increased cortical β-amyloid deposition. Analysis of covariance using global composite cognitive z scores as the outcome parameter showed significant regressor effects for combined striatal and cortical β-amyloidopathy (F = 4.18; P = 0.02) after adjusting for covariate effects of cortical cholinergic activity (F = 5.67; P = 0.02), caudate nucleus monoaminergic binding, duration of disease, and age (total model: F = 3.55; P = 0.0048). Post-hoc analysis showed significantly lower cognitive z score for combined striatal and cortical β-amyloidopathy, compared to cortical-only β-amyloidopathy and non-β-amyloidopathy subgroups. CONCLUSIONS: The combined presence of striatal and cortical β-amyloidopathy is associated with greater cognitive impairment than cortical β-amyloidopathy alone in PD. SN - 1531-8257 UR - https://www.unboundmedicine.com/medline/citation/26380951/Striatal_and_Cortical_β_Amyloidopathy_and_Cognition_in_Parkinson's_Disease_ L2 - https://doi.org/10.1002/mds.26369 DB - PRIME DP - Unbound Medicine ER -