Combined 18F-fluorodeoxyglucose positron emission tomography and event-related potentials study of the cognitive impairment mechanisms in Parkinson’s disease

Хоменко, Ю. Г.; Pronina, M. V.; Kataeva, G. V.; Kropotov, Juri D.; Irishina, Yulia; Susin, D. S.

doi:10.1016/j.jocn.2019.11.044

Cited by 3 publications

(1 citation statement)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PD-MCI patients exhibited hypometabolism in the frontal and parietal regions compared with PD-NC ones, while it was higher in PDD patients than in those with MCI, mainly in the posterior cortical areas [ 360 , 361 ]. Correlations of reduced metabolism in the areas with event-related potentials confirmed the important role of EF disorders [ 362 ]. Patients with atypical brain hypometabolism showed a higher incidence of dementia (60% vs. 3%) and hallucinations (56% vs. 7%) [ 363 ].…”

Section: Brain Positron Emission Tomography Studies In Pd-cimentioning

confidence: 85%

Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks

Jellinger

2023

IJMS

View full text Add to dashboard Cite

Cognitive impairment (CI) is a characteristic non-motor feature of Parkinson disease (PD) that poses a severe burden on the patients and caregivers, yet relatively little is known about its pathobiology. Cognitive deficits are evident throughout the course of PD, with around 25% of subtle cognitive decline and mild CI (MCI) at the time of diagnosis and up to 83% of patients developing dementia after 20 years. The heterogeneity of cognitive phenotypes suggests that a common neuropathological process, characterized by progressive degeneration of the dopaminergic striatonigral system and of many other neuronal systems, results not only in structural deficits but also extensive changes of functional neuronal network activities and neurotransmitter dysfunctions. Modern neuroimaging studies revealed multilocular cortical and subcortical atrophies and alterations in intrinsic neuronal connectivities. The decreased functional connectivity (FC) of the default mode network (DMN) in the bilateral prefrontal cortex is affected already before the development of clinical CI and in the absence of structural changes. Longitudinal cognitive decline is associated with frontostriatal and limbic affections, white matter microlesions and changes between multiple functional neuronal networks, including thalamo-insular, frontoparietal and attention networks, the cholinergic forebrain and the noradrenergic system. Superimposed Alzheimer-related (and other concomitant) pathologies due to interactions between α-synuclein, tau-protein and β-amyloid contribute to dementia pathogenesis in both PD and dementia with Lewy bodies (DLB). To further elucidate the interaction of the pathomechanisms responsible for CI in PD, well-designed longitudinal clinico-pathological studies are warranted that are supported by fluid and sophisticated imaging biomarkers as a basis for better early diagnosis and future disease-modifying therapies.

show abstract