Abstract

Cognitive impairment is a common feature in Parkinson's disease (PD) and other α-synucleinopathies as 80% of PD patients develop dementia within 20 years. Early cognitive changes in PD patients present as a dysexecutive syndrome, broadly characterized as a disruption of the fronto-striatal dopamine network. Cognitive deficits in other domains (recognition memory, attention processes and visuospatial abilities) become apparent with the progression of PD and development of dementia. In dementia with Lewy bodies (DLB) the cognitive impairment develops early or even precedes parkinsonism and it is more pronounced in visuospatial skills and memory. Cognitive impairment in the rarer α-synucleinopathies (multiple system atrophy and pure autonomic failure) is less well studied. Metabolic brain imaging with positron emission tomography and [18F]-fluorodeoxyglucose (FDG-PET) is a well-established diagnostic method in neurodegenerative diseases, including dementias. Changes in glucose metabolism precede those seen on structural magnetic resonance imaging (MRI). Reduction in glucose metabolism and atrophy have been suggested to represent consecutive changes of neurodegeneration and are linked to specific cognitive disorders (e.g., dysexecutive syndrome, memory impairment, visuospatial deficits etc.). Advances in the statistical analysis of FDG-PET images enabling a network analysis broadened our understanding of neurodegenerative brain processes. A specific cognitive pattern related to PD was identified by applying voxel-based network modeling approach. The magnitude of this pattern correlated significantly with patients' cognitive skills. Specific metabolic brain changes were observed also in patients with DLB as well as in a prodromal phase of α-synucleinopathy: REM sleep behavior disorder. Metabolic brain imaging with FDG-PET is a reliable biomarker of neurodegenerative brain diseases throughout their course, precisely reflecting their topographic distribution, stage and functional impact.

Highlights

  • Parkinson’s disease (PD) is a chronic neurodegenerative disease affecting 2–3% of the population older than 65 years

  • It is recognized that the full spectrum of cognitive decline, ranging from subjective cognitive decline (SCD) through mild cognitive impairment (MCI) to dementia can be observed in PD patients [4]

  • We reviewed studies investigating MCI in PD, its progression to PD dementia (PDD) and studies addressing the correlation between metabolic changes and neuropsychological deficits

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Summary

Introduction

Parkinson’s disease (PD) is a chronic neurodegenerative disease affecting 2–3% of the population older than 65 years. It is primarily a movement disorder characterized by bradykinesia, rigidity, postural impairment, and resting tremor. Since James Parkinson’s An Essay on the Shaking Palsy [2], which still remains largely valid, new knowledge has been gained, on non-motor symptoms, some of which may precede motor signs by decades [3]. Cognitive decline, which was not described by James Parkinson, is one of the most debilitating non-motor symptoms and it may drastically decrease patient’s and caregiver’s quality of life. It is recognized that the full spectrum of cognitive decline, ranging from subjective cognitive decline (SCD) through mild cognitive impairment (MCI) to dementia can be observed in PD patients [4]

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