Subjective cognitive decline predicts future deterioration in cognitively normal patients with Parkinson's disease

2014 ◽  
Vol 35 (7) ◽  
pp. 1739-1743 ◽  
Author(s):  
Jin Yong Hong ◽  
Mun Kyung Sunwoo ◽  
Seok Jong Chung ◽  
Jee Hyun Ham ◽  
Ji E. Lee ◽  
...  
Author(s):  
Iván Galtier ◽  
Antonieta Nieto ◽  
María Mata ◽  
Jesús N. Lorenzo ◽  
José Barroso

ABSTRACT Objective: Subjective cognitive decline (SCD) and mild cognitive impairment (MCI) in Parkinson’s disease (PD) are considered as the risk factors for dementia (PDD). Posterior cortically based functions, such as visuospatial and visuoperceptual (VS-VP) processing, have been described as predictors of PDD. However, no investigations have focused on the qualitative analysis of the Judgment of Line Orientation Test (JLOT) and the Facial Recognition Test (FRT) in PD-SCD and PD-MCI. The aim of this work was to study the VS-VP errors in JLOT and FRT. Moreover, these variables are considered as predictors of PDD. Method: Forty-two PD patients and 19 controls were evaluated with a neuropsychological protocol. Patients were classified as PD-SCD and PD-MCI. Analyses of errors were conducted following the procedure described by Ska, Poissant, and Joanette (1990). Follow-up assessment was conducted to a mean of 7.5 years after the baseline. Results: PD-MCI patients showed a poor performance in JLOT and FRT total score and made a greater proportion of severe intraquadrant (QO2) and interquadrant errors (IQO). PD-SCD showed a poor performance in FRT and made mild errors in JLOT. PD-MCI and QO2/IQO errors were independent risk factors for PDD during the follow-up. Moreover, the combination of both PD-MCI diagnosis and QO2/IQO errors was associated with a greater risk. Conclusions: PD-MCI patients presented a greater alteration in VS-VP processing observable by the presence of severe misjudgments. PD-SCD patients also showed mild difficulties in VS-SP functions. Finally, QO2/IQO errors in PD-MCI are a useful predictor of PDD, more than PD-MCI diagnosis alone.


2019 ◽  
Author(s):  
Edward N. Wilson ◽  
Michelle S. Swarovski ◽  
Patricia Linortner ◽  
Marian Shahid ◽  
Abigail J. Zuckerman ◽  
...  

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease (AD) and affects 1% of the population above 60 years old. Although PD commonly manifests with motor symptoms, a majority of patients with PD subsequently develop cognitive impairment which often progresses to dementia, a major cause of morbidity and disability. PD is characterized by α-synuclein accumulation that frequently associates with amyloid beta (Aβ) and tau fibrils, the hallmarks of AD neuropathologic changes; this co-occurrence suggests that onset of cognitive decline in PD may be associated with appearance of pathologic Aβ and/or tau. Recent studies have highlighted the appearance of the soluble form of the Triggering Receptor Expressed on Myeloid cells 2 (sTREM2) receptor in CSF during development of AD. Given the known association of microglial activation with advancing PD, we investigated whether CSF and/or plasma sTREM2 increased with progression to PD dementia. We examined 165 participants consisting of 17 cognitively normal elderly, 45 PD patients with no cognitive impairment, 86 with mild cognitive impairment, and 17 with dementia. Stratification of subjects by CSF Aβ and tau levels revealed that CSF sTREM2 concentrations were elevated in PD subgroups with abnormal tau, but not Aβ, CSF concentration. These findings indicate that CSF sTREM2 could serve as a surrogate immune biomarker of neuronal injury in PD that is associated with cognitive decline.One sentence summaryCSF sTREM2 correlates with CSF tau in PD


2014 ◽  
Vol 20 (9) ◽  
pp. 999-1003 ◽  
Author(s):  
Jin Yong Hong ◽  
Hyuk Jin Yun ◽  
Mun Kyung Sunwoo ◽  
Jee Hyun Ham ◽  
Jong-Min Lee ◽  
...  

Author(s):  
Anja Ophey ◽  
Fabian Krohm ◽  
Elke Kalbe ◽  
Andrea Greuel ◽  
Alexander Drzezga ◽  
...  

Abstract Background Subjective cognitive decline (SCD) may occur very early in the course of Parkinson’s disease (PD) before the onset of objective cognitive decline. Data on neural correlates and determinants of SCD in PD are rare. Objective The aim of the present study was to identify neural correlates as well as sociodemographic, clinical, and neuropsychological predictors of SCD in patients with PD. Methods We retrospectively analyzed 30 patients with PD without cognitive impairment (23% female, 66.90 ± 7.20 years, UPDRS-III: 19.83 ± 9.29), of which n = 12 patients were classified as having no SCD (control group, PD-CG) and n = 18 as having SCD (PD-SCD). Neuropsychological testing and 18-fluoro-2-deoxyglucose positron emission tomography (FDG-PET) were conducted. SCD was assessed using a questionnaire covering multiple cognitive domains. Results SCD subscores differed significantly between PD-CG and PD-SCD and correlated significantly with other scales measuring related concepts. FDG-PET whole-brain voxel-wise regression analysis revealed hypometabolism in middle frontal, middle temporal, and occipital areas, and the angular gyrus as neural correlates of SCD in PD. Next to this hypometabolism, depressive symptoms were an independent significant determinant of SCD in a stepwise regression analysis (adjusted R2 = 50.3%). Conclusion This study strengthens the hypothesis of SCD being an early manifestation of future cognitive decline in PD and, more generally, early pathological changes in PD. The early identification of the vulnerability for future cognitive decline constitutes the basis for successful prevention and delay of this non-motor symptom.


Author(s):  
H. Bejr‐kasem ◽  
F. Sampedro ◽  
J. Marín‐Lahoz ◽  
S. Martínez‐Horta ◽  
J. Pagonabarraga ◽  
...  

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Claudia Cicognola ◽  
Oskar Hansson ◽  
Philip Scheltens ◽  
Hlin Kvartsberg ◽  
Henrik Zetterberg ◽  
...  

Abstract Background Elevated cerebrospinal fluid (CSF) concentrations of total tau (T-tau) and phosphorylated tau at Thr181 (P-tau181) protein are typical of Alzheimer’s disease (AD). However, the T-tau assay measures only the mid-region of the protein, while tau in CSF is instead composed of a series of fragments. One fragment species in particular, N-224, shows increased levels in AD compared to controls. In this multicentre study, we performed a clinical validation of the N-224 assay in cohorts including patients with subjective cognitive decline (SCD), mild cognitive impairment (MCI), AD, non-AD dementias and controls. Methods Cohorts consisted of 30 SCD and 30 probable AD from the Amsterdam Dementia Cohort (cohort 1) and 539 controls, 195 SCD, 232 MCI, 137 AD and 253 non-AD from the Swedish BioFINDER study (cohort 2). All samples had AD core biomarkers (Aβ42, T-tau, P-tau181) measurements. N-224 was measured with an in-house ultrasensitive Simoa assay. Results N-224 levels were significantly higher in AD compared to SCD (cohort 1: p = 0.003) and in AD compared to all other diagnostic groups in cohort 2 (control, SCD, MCI and non-AD, p < 0.0001). Within the non-AD group, N-224 showed significantly lower concentrations compared to AD in Parkinson’s disease (PD, p < 0.0001), Parkinson’s disease dementia (PDD, p = 0.004), progressive supranuclear palsy (PSP, < 0.0001), multiple system atrophy (MSA, p = 0.002) and parkinsonisms not otherwise specified (NOS, p = 0.007). In cohort 1, higher concentrations of N-224 were associated to lower Mini-Mental State Examination (MMSE) scores (R2 = 0.318, β = 0.564, p ≤ 0.0001) and could accurately identify a pathological (< 24) MMSE score (p < 0.0001, AUC = 0.824). Conclusions N-224 tau can distinguish AD subjects from SCD and can discriminate subgroups of non-AD dementias from AD. Therefore, N-224 may be a useful addition to the tau biomarker toolbox for the study of tau species in CSF and for better understanding disease pathogenesis.


2021 ◽  
Vol 3 (1) ◽  
pp. e000112
Author(s):  
Mario H Flores-Torres ◽  
Katherine C Hughes ◽  
Samantha Molsberry ◽  
Xiang Gao ◽  
Jae H Kang ◽  
...  

ObjectiveSubtle cognitive deficits can occur during the prodromal phase of Parkinson’s disease (PD), commonly in conjunction with hyposmia. However, little is known about the association between cognitive function and other features suggestive of prodromal PD. We evaluated the association of non-motor prodromal PD features, including hyposmia, constipation and probable REM sleep behaviour disorder (pRBD), with objective measures of cognitive function and self-reported cognitive decline.MethodsThe study population comprised 804 men who responded to a telephone cognitive interview in 2016–2017. Participants included 680 individuals with hyposmia, of whom 45 had confirmed PD, and 124 men without hyposmia. Among these men, we evaluated objective cognitive function and subjective cognitive decline to determine whether the presence of non-motor features of prodromal PD was associated with cognitive functioning. Analyses were adjusted for age, physical activity, body mass index, smoking status and coffee consumption.ResultsIndividuals with non-motor features of prodromal PD had worse objective and subjective cognitive performance relative to men without non-motor features. Cognitive impairment was particularly prevalent among individuals with concurrent hyposmia, pRBD and constipation (multivariate-adjusted OR=3.80; 95% CI 1.52 to 9.47 for objective poor cognitive function; OR=8.71; 95% CI 3.18 to 23.83 for subjective cognitive decline). As expected, both objective (OR=7.91) and subjective (OR=17.42) cognitive impairment were also more common among men with confirmed PD.ConclusionsOur study suggests that cognition is commonly affected in individuals with non-motor prodromal PD features, particularly when multiple of these features are present.


2020 ◽  
Author(s):  
Shi Rong Wen ◽  
Guang Yang ◽  
Si Jia Xu ◽  
Yan Liu ◽  
Yu Jun Pan

Abstract Background: The predictive value of subjective cognitive decline in Parkinson's disease (PD-SCD) remains controversial. However, there is growing evidence that individuals with subjective cognitive decline (SCD) are associated with Alzheimer's disease pathology and are a higher risk for cognitive decline. The aim of the present study is to characterize PD-SCD and its progression, assess the effects of rehabilitation training programs on cognitive function in PD patients.Methods: Forty-two PD patients were evaluated with a neuropsychological protocol, and classified depending on the presence (PD-SCD+, n=22) or absence of SCD (PD-SCD-,n=20). After a mean follow-up of 3.0 years (2.0-4.0 years), we repeated the cognitive assessments with the same subjects. The rehabilitation training for individuals with PD for six months after the re-assessment.Results: The clinical characteristics and overall cognitive performance of the 2 groups did not differ from baseline. During the follow-up assessment, patients with PD-SCD exhibited a more significant annual decline in Chinese-Beijing version of Montreal Cognitive Assessment-Test (BJ-MoCA) and semantic fluency than patients without PD-SCD. Stepwise logistic regression analysis showed that the MMSE Scores(P=0.000), HAMD Scores (P=0.008), male (P=0.026), and the presence of SCD (P=0.022) were risk factors for language and related functions domain. There are significant improvements detected in 2 groups after rehabilitation training in terms of BJ-MoCA. Pairwise comparisons showed that language at post-intervention in the PD-SCD+ groups were significantly higher than at pre-intervention in the PD-SCD-.Conclusion: With the progression of the disease, the cognitive performance of patients with PD-SCD+ was worse than PD-SCD-. Meanwhile, the present data indicate that semantic fluency might be a key component to evaluate the cognitive subset of PD. Rehabilitation training is a viable intervention for PD that can improve several non-motor domains, produced larger improvements in cognition.


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