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Cognitive reserve and β-amyloid pathology in Parkinson disease.
Parkinsonism Relat Disord 2015; 21(8):899-904PR

Abstract

INTRODUCTION

Dementia in Parkinson disease (PD) is associated with abnormal accumulation of proteins, including β-amyloid, in cortical regions. High cognitive reserve capacity may protect cognition from β-amyloid and delay the onset of dementia. We tested the cognitive reserve theory in PD by determining whether educational attainment, a proxy for cognitive reserve, modifies the correlation between cortical β-amyloid accumulation and cognitive impairment.

METHODS

PD participants (N = 155) underwent MRI to quantify brain volume and [(11)C] PiB PET imaging to quantify fibrillar β-amyloid deposition. Mean cortical binding potentials (MCBP) were calculated for each participant, with higher scores indicating more fibrillar β-amyloid. Global cognitive function was assessed using the Clinical Dementia Rating (CDR) and Mini-Mental State Examination (MMSE). Multiple linear regression analysis was used to determine whether education modified the relationship between MCBP and cognitive function after controlling for brain volume.

RESULTS

MCBP interacted with educational attainment to predict scores on each of the cognitive outcome measures (ps ≤ 0.02). Post-hoc analysis revealed that the effect of MCBP on cognitive function changed once the level of education reached 16 years. For participants with less than 16 years of education (n = 68), higher MCBP correlated with worse cognitive function, with MCBP accounting for 8-30% of the variance in MMSE and CDR scores (ps ≤ 0.02). For participants with at least 16 years of education (n = 87), MCBP did not correlate with MMSE or CDR scores (R(2)s < 0.02, ps ≥ 0.17).

CONCLUSION

These findings provide support for the cognitive reserve theory in PD and suggest that education may protect PD patients' cognition against cortical β-amyloid pathology.

Authors+Show Affiliations

Program in Occupational Therapy, Washington University School of Medicine, St. Louis, MO, USA; Occupational Therapist, Bethel Public Schools, Spanaway, WA, USA. Electronic address: carolynlucero33@gmail.com.Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: meghanc@npg.wustl.edu.Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: floresh@npg.wustl.edu.Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: maitib@neuro.wustl.edu.Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO, USA; Department of Anatomy & Neurobiology, Washington University School of Medicine, St. Louis, MO, USA; Program in Occupational Therapy, Washington University School of Medicine, St. Louis, MO, USA; Program in Physical Therapy, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: joel@npg.wustl.edu.Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Program in Occupational Therapy, Washington University School of Medicine, St. Louis, MO, USA; Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: erfoster@wustl.edu.

Pub Type(s)

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

Language

eng

PubMed ID

26037458

Citation

Lucero, Carolyn, et al. "Cognitive Reserve and Β-amyloid Pathology in Parkinson Disease." Parkinsonism & Related Disorders, vol. 21, no. 8, 2015, pp. 899-904.
Lucero C, Campbell MC, Flores H, et al. Cognitive reserve and β-amyloid pathology in Parkinson disease. Parkinsonism Relat Disord. 2015;21(8):899-904.
Lucero, C., Campbell, M. C., Flores, H., Maiti, B., Perlmutter, J. S., & Foster, E. R. (2015). Cognitive reserve and β-amyloid pathology in Parkinson disease. Parkinsonism & Related Disorders, 21(8), pp. 899-904. doi:10.1016/j.parkreldis.2015.05.020.
Lucero C, et al. Cognitive Reserve and Β-amyloid Pathology in Parkinson Disease. Parkinsonism Relat Disord. 2015;21(8):899-904. PubMed PMID: 26037458.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cognitive reserve and β-amyloid pathology in Parkinson disease. AU - Lucero,Carolyn, AU - Campbell,Meghan C, AU - Flores,Hubert, AU - Maiti,Baijayanta, AU - Perlmutter,Joel S, AU - Foster,Erin R, Y1 - 2015/05/27/ PY - 2015/03/02/received PY - 2015/05/13/revised PY - 2015/05/26/accepted PY - 2015/6/4/entrez PY - 2015/6/4/pubmed PY - 2016/5/7/medline KW - Cognition KW - Cognitive reserve KW - Dementia KW - Education KW - Parkinson's disease SP - 899 EP - 904 JF - Parkinsonism & related disorders JO - Parkinsonism Relat. Disord. VL - 21 IS - 8 N2 - INTRODUCTION: Dementia in Parkinson disease (PD) is associated with abnormal accumulation of proteins, including β-amyloid, in cortical regions. High cognitive reserve capacity may protect cognition from β-amyloid and delay the onset of dementia. We tested the cognitive reserve theory in PD by determining whether educational attainment, a proxy for cognitive reserve, modifies the correlation between cortical β-amyloid accumulation and cognitive impairment. METHODS: PD participants (N = 155) underwent MRI to quantify brain volume and [(11)C] PiB PET imaging to quantify fibrillar β-amyloid deposition. Mean cortical binding potentials (MCBP) were calculated for each participant, with higher scores indicating more fibrillar β-amyloid. Global cognitive function was assessed using the Clinical Dementia Rating (CDR) and Mini-Mental State Examination (MMSE). Multiple linear regression analysis was used to determine whether education modified the relationship between MCBP and cognitive function after controlling for brain volume. RESULTS: MCBP interacted with educational attainment to predict scores on each of the cognitive outcome measures (ps ≤ 0.02). Post-hoc analysis revealed that the effect of MCBP on cognitive function changed once the level of education reached 16 years. For participants with less than 16 years of education (n = 68), higher MCBP correlated with worse cognitive function, with MCBP accounting for 8-30% of the variance in MMSE and CDR scores (ps ≤ 0.02). For participants with at least 16 years of education (n = 87), MCBP did not correlate with MMSE or CDR scores (R(2)s < 0.02, ps ≥ 0.17). CONCLUSION: These findings provide support for the cognitive reserve theory in PD and suggest that education may protect PD patients' cognition against cortical β-amyloid pathology. SN - 1873-5126 UR - https://www.unboundmedicine.com/medline/citation/26037458/Cognitive_reserve_and_β_amyloid_pathology_in_Parkinson_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1353-8020(15)00238-2 DB - PRIME DP - Unbound Medicine ER -