ArticleOpen Access Journal of Parkinson ’ s disease & Alzheimer ’ s disease (original) (raw)
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Movement Disorders, 2013
A B S T R AC T : Mild cognitive impairment (MCI) can occur early in the course of Parkinson's disease (PD), and its presence increases the risk of developing dementia. Determining the cortical changes associated with MCI in PD, thus, may be useful in predicting the future development of dementia. To address this objective, 37 patients with PD, divided into 2 groups according to the presence or absence MCI (18 with and 19 without) and 16 matched controls, underwent anatomic magnetic resonance imaging. Corticometry analyses were performed to measure the changes in cortical thickness and surface area as well as their correlation with disease duration. Compared with healthy controls, the PD-MCI group exhibited increased atrophy and changes of local surface area in the bilateral occipital, left temporal, and frontal cortices; whereas the PD non-MCI group exhibited only unilateral thinning and decreased surface area in the occipital lobe and in the frontal cortex. In addition, a comparison between the PD-MCI and PD non-MCI groups revealed increased local surface area in the occipital lobe, temporal lobe, and postcentral gyrus for the cognitively impaired patients. It is noteworthy that, in the PD-MCI group, cortical thickness had a significant negative correlation with disease duration in the precentral, supramarginal, occipital, and superior temporal cortices; whereas, in the PD non-MCI group, such a correlation was absent. The findings from this study reveal that, at the same stage of PD evolution, the presence of MCI is associated with a higher level of cortical changes, suggesting that cortical degeneration is increased in patients with PD because of the presence of MCI. V C 2013 Movement Disorder Society
Cognitive Impairment and Dementia in Parkinson’s Disease
European Journal of Neurology, 2010
Over the last decade, the importance of cognitive impairment and dementia in Parkinson's disease (PDD) has been increasingly recognized. Investigators have proposed criteria for PD dementia, and mild cognitive impairment. Risk profiles associated with the development of dementia based on demographic, neurological, neuropsychological, imaging, and genetic investigations have been delineated. The FDA has approved a treatment for PDD, and efforts now are directed toward intervention at earlier stages of cognitive impairment.
Cognitive impairment in nondemented Parkinson's disease
Movement Disorders, 2011
A substantial percentage of patients with newly diagnosed Parkinson's disease without dementia are reported to be affected by cognitive impairment (CI). In practice, however, CI is underrecognized, as the signs may not be apparent in early-stage disease and many routine assessment tools lack the sensitivity to detect subtle cognitive dysfunction. Patients with PD and mild CI (MCI) may have a higher risk of developing dementia than cognitively intact PD patients; however, it is not currently known which patients with CI are at increased risk of developing dementia. This review summarizes current knowledge about CI in nondemented PD; it discusses the structural and functional changes associated with CI and addresses areas of unmet needs. We focus on questions that should be addressed in future studies to achieve consensus on its characteristics and definition, pathophysiology, epidemiology, diagnosis and assessment, and treatment and management.
Parkinson's disease-cognitive rating scale: A new cognitive scale specific for Parkinson's disease
Movement Disorders, 2008
Cognitive defects associated with cortical pathology may be a marker of dementia in Parkinson's disease (PD). There is a need to improve the diagnostic criteria of PD dementia (PDD) and to clarify the cognitive impairment patterns associated with PD. Current neuropsychological batteries designed for PD are focused on fronto-subcortical deficits but are not sensitive for cortical dysfunction. We developed a new scale, the Parkinson's Disease-Cognitive Rating Scale (PD-CRS), that was designed to cover the full spectrum of cognitive defects associated with PD. We prospectively studied 92 PD patients [30 cognitively intact (CogInt), 30 mild cognitive impairment (MCI), 32 PDD] and 61 matched controls who completed the PD-CRS and neuropsychological tests assessing the cognitive domains included in the PD-CRS. Acceptability, construct validity, reliability, and the discriminative properties of the PD-CRS were examined. The PD-CRS included items assessing fronto-subcortical defects and items assessing cortical dysfunction. Construct validity, test-retest and inter-rater reliability of PD-CRS total scores showed an intraclass correlation coefficient >0.70. The PD-CRS showed an excellent test accuracy to diagnose PDD (sensitivity 94%, specificity 94%). The PD-CRS total scores and confrontation naming item scores-assessing ''cortical'' dysfunction-independently differentiated PDD from non-demented PD. Alternating verbal fluency and delayed verbal memory independently differentiated the MCI group from both controls and CogInt. The PD-CRS appeared to be a reliable and valid PDspecific battery that accurately diagnosed PDD and detected subtle fronto-subcortical deficits. Performance on the PD-CRS showed that PDD is characterized by the addition of cortical dysfunction upon a predominant and progressive fronto-subcortical impairment.
Parkinson’s Disease–Mild Cognitive Impairment (PD-MCI): A Useful Summary of Update Knowledge
Frontiers in Aging Neuroscience, 2019
Mild cognitive impairment (MCI) is a common feature in Parkinson's Disease (PD), even at the time of diagnosis. Some levels of heterogeneity in nature and severity of cognitive impairment and risk of conversion to Parkinson's Disease Dementia (PDD) exist. This brief overview summarized the current understanding of MCI in PD, by considering the following major points: historical development of the clinical entity, evaluation, epidemiology, predictors and outcomes, neuroimaging findings, pathophysiology, treatment, and pharmacological and non-pharmacological intervention. MCI in PD represents a concept in evolution and plays a pivotal role in advancing our understanding of the disease mechanisms, with the ultimate goal of building effective strategies to prevent conversion into PDD. Challenges for future research are also discussed.
A review article in Cognitive deficits in Parkinson’s Disease
Journal of Experimental and Clinical Neurosciences
Parkinson's disease (PD) is a common, progressive, disabling, neurodegenerative disorder, that apart from well-known motor symptoms, reveals a wide spectrum of non-motor features, that are now widely accepted as part of the clinical aspect, and cognitive decline is a very important part of these non-motor presentations. The diagnosis of cognitive decline in PD can be extremely challenging, remaining largely based on clinical and cognitive assessments. Expert work groups have issued diagnostic criteria and methods for PD dementia and cognitive impairment. This manuscript has gathered relevant data in order to obtain an updated review regarding cognitive deficit in PD, from mild stages to dementia. This article has summarized clinical features, diagnostic methods, and therapeutic issues of cognitive decline in PD.
Neurocognitive Signatures of Parkinson's and Alzheimer's Disease Ph.D. Dissertation
2012
Budapest 2012 5.3. Transfer and flexibility of stimulus-response associations in AD 65. 5.3.1. Habit learning in AD, striatal automaticity, and hippocampal pattern completion 65. 5.3.2. Is feedback-guided stimulus-response learning an implicit memory process? 67. 5.4. Visuospatial functions discriminate between AD and FTD 70. 6. Conclusions 74. 7. Summary 76. 8. References 80. 9. List of own publications related to the thesis 98. 10. List of own publications independent of the thesis 99. Acknowledgement 101. ABBREVIATIONS AD-Alzheimer's disease ANCOVAanalyses of covariance ANOVAanalyses of variance CBDScorticobasal degeneration syndrome CDT-Clock Drawing Test DDSdopamine dysregulation syndrome DRS-Dementia Rating Scale FTDfrontotemporal dementia FTD-bvfrontotemporal dementia behavioral variant GDS-Global Deterioration Scale HAM-A-Hamilton Anxiety Rating Scale HAM-D-Hamilton Depression Rating Scale HSD-Honestly Significant Difference test MANOVAmultivariate analyses of variance MMSE-Mini-Mental State Examination MRI-Magnetic Resonance Imaging NINCDS-ADRDA-National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association PAprogressive aphasia PD-Parkinson's disease PETpositron emission tomography PNFAprimer non-fluent aphasia PSPprogressive supranuclear palsy SDsemantic dementia TCI-Temperament and Character Inventory TPQ-Tridimensional Personality Questionnaire UPDRS-Unified Parkinson's Disease Rating Scale WAIS-R-Wechsler Adult Intelligence Scale 1.2. Beyond the motor symptoms: reinforcement learning in PD 1.2.1. Basic pathology: from molecules to cognition PD was described by James Parkinson in 1817, although a similar symptomatic delineation can be found in the work of Ferenc Pápai Páriz from 1690 with all four cardinal symptoms: resting tremor, rigidity, bradykinesia, and gait disturbances (Bereczki, 2010). The classic neuroanatomical definition of PD is based on the loss of neuromelanine-positive dopaminergic cells in substantia nigra pars compacta, leading to the disturbance of the nigrostriatal pathway (Lees et al., 2009). Neuronal loss may be induced by accumulated alpha-synuclein in these cells that comprises the core of the Lewy-bodies. Damaging alpha-synuclein may occur via phosphorylation by intracellular kinases, truncation by proteases, modification by free radicals, reactive nitrogen species, toxins, overproduction (gene duplication), and decreased elimination by parkin and synphilin (Venda et al., 2010). However, alpha-synuclein is not the sole player in mitochondrial damage and abnormal ubiquitine-proteosomal functions; other relevant factors are Parkin (PARK2), PINK1 [phosphatase and tensin homolog-induced putative kinase 1] (PARK6), DJ-1 (PARK7), LRRK2 [leucine-rich repeat kinase 2] and dardarin (PARK8) (Mellick et al., 2010). From our point of view, alpha-synuclein and its interactive proteins are especially important because this molecule, acting as a presynaptic regulator of dopamine release, may bridge neurodegeneration and cognition (Kéri et al., 2010). Regarding the functional localization of PD, the hypothesis of selective nigrostriatal dysfunction seems to be problematic given that it can hardly explain several non-motor symptoms of PD: olfactory, sleep, and vegetative abnormalities, blunted affect, changes in personality traits (e.g., decreased novelty seeking and increased neuroticism), and atypical responses to dopaminergic medications in some patients (e.g., impulse control disorders and psychotic symptoms) (Bassetti, 2011). Consistent with post-mortem studies showing that the loss of dopaminergic neurons in the substantia nigra is just an intermediate step in neurodegeneration, Jubault et al. (2009) demonstrated in vivo imaging evidence for an early volume loss in the medulla oblongata/pontine tegmentum, which is followed by neurodegeneration in substantia nigra/amygdala, and then in the cortex. Although dopaminergic deficit is a hallmark of PD, the loss of this neurotransmitter is not evenly distributed in the striatum. Specifically, there is a more pronounced reduction of dopamine in the dorsal than in the ventral striatum (Kish et al., 1988). Therefore, therapies that restore dopamine level in the dorsal striatum result in dopamine "overdose" in the ventral striatum, which may lead to impaired performance on some cognitive tasks (