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Background: Hypomimia is a clinical feature of Parkinson’s disease (PD). Based on the embodied simulation theory, the impairment of facial mimicry may worsen facial emotion recognition; however, the empirical results are inconclusive. Objective: We aimed to explore the worsening of emotion recognition by hypomimia. We further explored the relationship between the hypomimia, emotion recognition, and social functioning. Methods: A total of 114 participants were recruited. The patients with PD and normal controls (NCs) were matched for demographic characteristics. All the participants completed the Mini-Mental State Examination and the Chinese Multi-modalities Emotion Recognition Test. In addition to the above tests, the patients were assessed with the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale and Parkinson’s Disease Social Functioning Scale (PDSFS). Results: Patients with PD with hypomimia had worse recognition of disgust than NCs (p = 0.018). The severity of hypomimia was predictive of the recognition of disgust (β= –0.275, p = 0.028). Facial emotion recognition was predictive of the PDSFS score of PD patients (β= 0.433, p = 0.001). We also found that recognizing disgust could mediate the relationship between hypomimia and the PDSFS score (β= 0.264, p = 0.045). Conclusion: Patients with hypomimia had the worst disgust facial recognition. Hypomimia may affect the social function of PD patients, which is related to recognizing the expression of disgust. Emotion recognition training may improve the social function of patients with PD.

This study aimed to understand the impact of sex on the neurocognitive function of patients with Parkinson’s disease (PD). Ninety-four participants with idiopathic PD and 167 age-matched healthy individuals as normal controls (NCs) were recruited and underwent comprehensive neuropsychological assessments. Sex differences were found in NCs, but not in patients with PD. Among male participants, patients with PD showed worse performance on the Digit Symbol Substitution (DSS) (p &lt, 0.001) test and Symbol Search (SS) (p &lt, 0.001) than NCs. Among female participants, patients with PD showed worse performance on the category score of the Modified Wisconsin Card Sorting Test (p &lt, 0.001), SS (p &lt, 0.001), and pentagon copying (p &lt, 0.001) than NCs. After controlling for the effects of age and years of education, Hoehn and Yahr stage was found to predict the performance of the Color Trails Test part A (βA = 0.241, pA = 0.036), Stroop Color and Word Test (β = −0.245, p = 0.036), and DSS (β = −0.258, p = 0.035) in men with PD. These results indicate the differential effect of sex on the neurocognitive function among healthy aging and PD populations. The disappearance of sex differences, which is present in healthy aging, in patients with PD suggests a gradual loss of the neuroprotective effect of estrogen after the initiation of the neurodegenerative process. This study also found mental flexibility and visuospatial function to be the susceptible cognitive domains in women with PD, while the disease severity could predict the working memory and processing speed in men with PD.

This study aimed to elucidate the role of sex in neurocognitive function in patients with Parkinson’s disease (PD). Ninety-four idiopathic PD and 167 healthy elderly as normal controls (NCs) were recruited and underwent comprehensive neuropsychological assessments. The sex difference were found in NCs but not in PD. In male, PD patients had worse performance on the Digit symbol substitution (DSS) (p

BACKGROUND Social functioning is crucial for the determinants of Parkinson's disease (PD) with dementia; however, there is no social functioning scale applicable to PD. OBJECTIVE This study aimed to develop a social functioning scale specific to PD (PDSFS) and provide a cut-off score to improve diagnosis accuracy. METHODS The items were developed through literature, interview patients, and PD expertise. After the pilot study, one hundred fifty-seven patients and 74 healthy participants were enrolled and completed the Mini-Mental State Examination, Clock Drawing Test, Activities of Daily Living, Neuropsychiatric Inventory, Adaptive Behavior Assessment System-Second Edition (ABAS-II) and part III of the Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS). RESULTS The final PDSFS has 23 items. The exploratory factor analysis revealed three factors, including "Family Life, Hobbies and Self-Care", "Interpersonal Relationship and Recreational Leisure", and "Social Bond". The internal consistency coefficient was 0.883, and the test-retest reliability was 0.774, respectively. The total score of the PDSFS was significantly related to the total score of ABAS-II (r = 0.609, p

The neuropathology of Parkinson’s disease (PD) involves the frontal-subcortical circuit, an area responsible for processing affective theory of mind (ToM). Patients with PD are expected to experience deficits in the affective ToM. This study aims to investigate whether the ability to infer emotion in others is affected in either young-onset Parkinson’s disease (YOPD) or middle-onset PD (MOPD) patients and to test whether the impairments in affective ToM are associated with the motor symptoms. The affective ToM, global mental abilities, and clinical symptoms were assessed in a total of 107 MOPD, 30 YOPD, and 30 normal controls (NCs). The MOPD patients exhibited deficits in affective ToM to the negative and neutral valences, when compared to the participants in the NCs and YOPD group. By conducting gender-stratified analysis, the deficits in affective ToM was only found in female participants. After adjusting for demographic variables, the multiple linear regression model revealed that affective ToM predicted motor symptoms, especially in female MOPD patients. The present study may aid in the development of medical care programs by advocating for a more comprehensive therapeutic plan that includes continuous disease progression monitoring and social skills training for female MOPD patients or their caregivers.

Monoamine neurotransmitters play essential roles in the regulation of arousal and sleep. Impaired metabolism of monoamine neurotransmitters could result in the accumulation of neurotoxic aldehyde metabolites and, hence, neuronal degeneration. Aldehyde dehydrogenases play an important role in the metabolism of the neurotoxic aldehyde metabolites, including the aldehyde metabolites of dopamine, serotonin, and noradrenaline. Deficient aldehyde dehydrogenase 2 (ALDH2) has been suggested to result in the accumulation of these biogenic aldehydes. An ALDH2 single nucleotide polymorphism (SNP), rs671 (A), results in significantly reduced ALDH2 enzyme activity. A total of 83 Parkinson’s disease (PD) patients were recruited in this study. In addition to the genotypes of rs671, the patients were assessed with the PD sleep scale-2nd version (PDSS-2) and the Epworth sleepiness scale (ESS) for symptoms of daytime and nocturnal sleep disturbances. The patients carrying rs671 (A) had more frequent dozing while lying down to rest in the afternoon (ESS item5) (F = 7.308, p = 0.008) than the rs671 (GG) patients. The patients with rs671 (A) reported a trend toward more frequent difficulty staying asleep than the patients with rs671 (GG). (F = 3.278, p = 0.074). The results indicate that patients carrying allele rs671 (A) are more likely to experience impairment in the regulation of arousal and sleep. The results also support the hypothesis that the accumulation of neurotoxic monoamine neurotransmitter aldehyde metabolites secondary to reduced ALDH2 enzyme activity may cause more severe monoaminergic neuronal loss and, hence, more severe symptoms in the regulation of wakefulness and sleep.

Executive dysfunction is common in Parkinson's disease (PD) patients. The catechol-O-methyltransferase (COMT) Val158Met polymorphism has been proposed to affect executive functions (EFs) in the prefrontal cortex. The present study attempted to explore the influence of the COMT polymorphism on EFs in patients with PD. Fifty-four PD patients were recruited and underwent neuropsychological assessments for three core EFs. The COMT polymorphism was genotyped using the TaqMan SNP Genotyping Assay. Participants were divided into three study groups: Val homozygotes, heterozygotes, and Met homozygotes. The three COMT genotype groups had significantly different performances in set-shifting [χ2 (2, 54) = 9.717, p = 0.008] and working memory tasks [χ2 (2, 54) = 7.806, p = 0.020]. Post-hoc analyses revealed that PD Val homozygotes performed significantly poorer in the set-shifting task than did either the PD Met homozygotes (z = -2.628, p = 0.009) or PD heterozygotes (z = -2.212, p = 0.027). Our explorative results suggest that the putative level of prefrontal dopamine influenced set-shifting through a "cane-shaped" dopamine level-response relationship. Our results have clinical implications, which may influence PD treatment with dopamine in the future because the optimal dopamine level to maximize EFs may vary based on the clinical course and COMT polymorphism status. Further study recruiting a larger number of participants is needed to confirm our preliminary findings.

Neurotransmitter degradation has been proposed to cause the accumulation of neurotoxic metabolites. The metabolism of these metabolites involves aldehyde dehydrogenase 2 (ALDH2). The Asian-specific single nucleotide polymorphism rs671 causes reduced enzyme activity. This study aims to explore whether Parkinson’s disease (PD) patients with reduced ALDH2 activity owing to the rs671 polymorphism are at risk for neuropsychological impairments. A total of 139 PD patients were recruited. Each participant was assessed for medical characteristics and their ALDH2 genotype. The Mini-Mental State Examination (MMSE), the Clinical Dementia Rating Scale and the Frontal Behavioral Inventory were used to measure neuropsychological functions. We found that the MMSE scores were significantly lower in patients with inactive ALDH2 (U = 1873.5, p = 0.02). The presence of cognitive impairments was significantly more frequent in the inactive ALDH2 group (46.0%) than in the active ALDH2 group (26.3%) (χ2 = 5.886, p = 0.01). The inactive group showed significant deterioration in hobbies and exhibited more severe “disorganization” and “hyper-sexuality” behaviours. The additive effects of the allele on the development of cognitive impairments in PD patients may be an important finding that provides further insight into the pathogenic mechanism of cognitive dysfunction in PD.

Objective Memory formation is proposed to be a dual process that involves the simultaneous memorisation of both detailed information (item-specific memory) and gist information (gist memory). Memory deficits have been reported in patients with Parkinson's disease (PD); however, few studies have explicitly addressed the nature of these deficits. To obtain a detailed understanding of memory dysfunction in patients with PD, it is of crucial importance to establish whether item-specific memory and gist memory performance are impaired. The aim of this study is to explore whether gist memory and item-specific memory performance are still intact in patients with PD, as well as to determine which psychological mechanisms are responsible for memory formation. Setting Two hospitals in northern Taiwan. Participants Thirty-nine patients with PD and 28 normal controls were recruited. Each participant received a gist-based recognition test following the Deese-Roediger-McDermott paradigm, as well as neuropsychological tests and measures of clinical characteristics. Results Gist memory was impaired in patients with advanced-stage disease (Hoehn and Yahr (H&Y) stage: III) (F2,64=3.58, p=0.033), whereas item-specific memory was preserved throughout all disease stages. Correlation analysis showed that item-specific memory was related to executive functions in normal controls and early-stage patients with PD (H&Y stage: I–II); however, item-specific memory was related to episodic memory, rather than to executive functions, in advanced-stage patients with PD. Moreover, gist memory was related to episodic memory, but only in early-stage patients with PD. Conclusions We discovered that impaired gist memory is found in advanced-stage, but not in early-stage, patients with PD. Our findings suggest that the techniques used to take advantage of the relatively preserved gist memory in early-stage patients with PD, as well as the preserved item-specific memory in patients with PD of all stages, could be useful for memory rehabilitation programmes.

Rwei-Ling Yu,1 Chun-Hsiang Tan,2 Ruey-Meei Wu3 1Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan; 2Wolfson Centre for Age Related Diseases, King’s College London, London, UK; 3Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan Objectives: The aims of this study were to explore nocturnal disturbances in patients with Parkinson’s disease (PD) and to assess their impact on quality of life (QoL).Methods: A total of 211 patients with PD were recruited for this study, and each participant was evaluated using the mini-mental state examination, PD sleep scale – second version (PDSS-2), pittsburgh sleep quality index (PSQI), PD QoL questionnaire (PDQ), Epworth sleepiness scale, Hoehn and Yahr (H&Y) staging, and unified Parkinson’s disease rating scale (UPDRS). Multiple regression analyses were performed to determine the contribution of the predictive variables on QoL.Results: There were 56.4% males (mean age: 64.08years; disease duration: 6.02years; H&Y stage: 2.25; and UPDRS: 33.01) in this study. Our patients’ actual sleep time was 5.96±1.16hours and the average sleep efficiency was 82.93%±12.79%. Up to 64.4% of patients were classified as “poor” sleepers and 23.8% suffered from daytime sleepiness. The final stepwise regression model revealed that UPDRS parts I and II, the sleep disturbance and daytime dysfunction components of the PSQI, the PD symptoms at night subscale of the PDSS-2, and the levodopa equivalent dose were significant predictors of the PDQ score (R2=53, F7,165=28.746; P