Parkinson's Score Research Articles

Purpose in Life and Its Association to Parkinsonism.

Purpose in life has been associated with diverse health outcomes; however, few studies have examined its associations with progressive motor decline in older adults. We tested if higher purpose would be associated with lower likelihood of incident parkinsonism as well as with lower levels and slower rates of increase in parkinsonian signs. Participants were 2,626 older adults from the Rush Memory and Aging Project and Minority Aging Research Study followed for an average of 7.2 years (standard deviation [SD] = 4.6). Purpose was measured using the purpose in life subscale of the modified Ryff's and Keyes's measure of psychological well-being. Four parkinsonian signs (i.e., parkinsonian gait, rigidity, bradykinesia, and tremor) were assessed using the United Parkinson's Disease Rating Scale. We examined purpose with risk of developing incident parkinsonism using Cox proportional hazards models. We also used linear mixed-effect models to assess the association between purpose and parkinsonian sign trajectories. After including demographics, health conditions, and health behaviors in the model, for a 1-SD increase in purpose, the hazards ratio for incident parkinsonism was 0.88 (95% confidence interval [CI] 0.80, 0.97). A 1-SD increase in purpose was associated with a -0.19 (95% CI -0.24, -0.15) point lower score in the global parkinsonian summary score at baseline but no differences in rate of change were evident. Higher purpose was associated with lower hazards of incident parkinsonism and lower levels of parkinsonian signs at baseline. Associations were seen even after adjustment for a wide range of covariates. Findings suggest higher purpose may contribute to maintenance of healthy physical function among older adults.

Study on the Correlation between Blood Urea Nitrogen, Creatinine Level, Proteinuria and Parkinson's Disease.

Parkinson's disease (PD) is related to renal insufficiency. The purpose of this study was to explore the correlation between PD and blood urea nitrogen, creatinine, and proteinuria. The case-control study method was adopted in this study. In total, 200 patients with PD who were hospitalized in the Department of Neurology of the Second Affiliated Hospital of Anhui Medical University were selected as the PD group, and 110 healthy patients during the same period were selected as the control group. The differences in clinical data and laboratory results between the two groups were compared. Logistic regression analysis, ROC curve, and Spearman correlation analysis were used to determine the correlation between PD and blood urea nitrogen, creatinine, and urine protein. The levels of cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL-C), and apolipoprotein B in the PD group were lower than those in the control group. The levels of creatinine, urea nitrogen, and proteinuria in the PD group were higher than those in the control group. Multivariate logistic regression analysis showed that elevated blood urea nitrogen, creatinine, and urine protein levels were risk factors for PD, and elevated LDL-C levels were protective factors for PD. The blood urea nitrogen level of patients with PD was positively correlated with the course of PD, Hoehn-Yahr staging, and UPDRS exercise score (r = 0.309, 0.434, and 0.540, respectively; P < 0.01). Serum creatinine level was positively correlated with the course of PD, Hoehn-Yahr staging, and UPDRS exercise score (r = 0.139, 0.320, and 0.290, respectively; P < 0.01). Blood urea nitrogen, creatinine levels, and proteinuria can be regarded as the onset of PD and a biomarker of disease progression.

Relation of Motor Impairments to Neuropathologic Changes of Limbic-Predominant Age-Related TDP-43 Encephalopathy in Older Adults.

Limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy neuropathologic change (LATE-NC) is common and is a major contributor to cognitive decline and Alzheimer dementia in older adults. The objective of the current study was to examine whether LATE-NC was also associated with declining motor function in older adults. Participants were from 2 longitudinal clinical pathologic studies of aging who did not have dementia at the time of enrollment. Postmortem pathologic examination included immunohistochemical staining for TDP-43 in 8 brain regions, which was summarized as a dichotomous variable indicating advanced LATE-NC stages at which TDP-43 pathology had accumulated in the hippocampus, entorhinal, or neocortical regions. Annual motor testing included maximal inspiratory and expiratory pressures (summarized as respiratory muscle strength), grip and pinch strength (summarized as hand strength), finger tapping speed and the Purdue Pegboard Test (summarized as hand dexterity), and walking 8 feet and turning 360° (summarized as gait function). The severity of parkinsonism was also assessed and summarized as a global parkinsonism score. Global cognition was a summary of standardized scores of 19 neuropsychological tests. We used linear mixed-effect models to examine the associations of LATE-NC with longitudinal changes of motor decline and used multivariate random coefficient models to simultaneously examine the associations of LATE-NC with cognitive and motor decline. Among 1,483 participants (mean age at death 90.1 [SD = 6.4] years, 70% women, mean follow-up 7.4 [SD = 3.8] years), LATE-NC was present in 34.0% (n = 504). In separate linear mixed-effect models controlling for demographics and other brain pathologies, LATE-NC was associated with faster decline in respiratory muscle strength (estimate = -0.857, SE = 0.322, p = 0.008) and hand strength (estimate = -0.005, SE = 0.002, p = 0.005) but was not related to hand dexterity, gait function, or parkinsonism. In multivariate random coefficient models including respiratory muscle strength, hand strength, and global cognition as the outcomes, LATE-NC remained associated with a faster respiratory muscle strength decline rate (estimate = -0.021, SE = 0.009, p = 0.023), but the association with hand strength was no longer significant (estimate = -0.002, SE = 0.003, p = 0.390). Motor impairment, specifically respiratory muscle weakness, may be an unrecognized comorbidity of LATE-NC that highlights the potential association of TDP-43 proteinopathy with noncognitive phenotypes in aging adults.

Vagus nerve cross-sectional area decreases in Parkinson's disease

IntroductionMorphological alterations of the vagus nerve (VN) in Parkinson's disease (PD) are discussed controversially. Several studies reported no difference in VN cross-sectional area (CSA) in PD patients in nerve ultrasound, others found a reduced CSA interpreted as atrophy of the VN and involvement of the dorsal nucleus of VN. MethodsIn a prospective comparative cross-sectional study, CSA of the VN bilaterally and the right ulnar nerve, clinical PD scales, non-motor symptoms and autonomic tests were compared between 49 PD patients and 24 healthy controls. Nerve ultrasound was performed by two independent investigators, patients and controls were compared at Bonferroni corrected p < 0.025 using results of both investigators and averaged results. Blinding included CSA measurements and PD scores, but not PD diagnosis. ResultsBilateral averaged VN CSA was significantly lower in PD patients than in controls (Right VN PD mean 2.70 mm2 SD 0.69, controls 3.30 mm2 SD 0.49, p < 0.001. Left VN PD mean 2.45 mm2 SD 0.57, controls 2.77 mm2 SD 0.46, p = 0.012). No difference was found in the ulnar nerve. There was a weak negative correlation between the right VN CSA and the Unified Parkinson Disease Rating Scale (−0.08 mm2 per 10 points). The area under the receiver operating characteristic curve for the right VN was 0.78 (p < 0.001). ConclusionThe present results support the hypothesis of atrophy of the VN in PD. Reduction of VN CSA is a weak marker of disease progression. Nerve ultrasound of the VN might represent a supplementary method in diagnosis of PD.

Effects of Cerebrovascular and Lewy Body Pathology on Parkinsonian Signs in Community-Dwelling Older Adults.

The roles of Lewy body (LB) and separately of cerebrovascular disease (CVD) pathologies in the severity of parkinsonian signs are well recognized in old age. We investigated whether the 2 pathologies act synergistically to further potentiate the severity of parkinsonism beyond their separate effects. We used postmortem data of decedents from 3 longitudinal community-based studies of aging who underwent annual clinical evaluation to assess parkinsonian signs using 26 items of the motor portion of a modified Unified Parkinson Disease Rating Scale. A summary score was developed from each item score to construct a global parkinsonian score, with a higher score indicating more severe parkinsonism. A detailed neuropathologic evaluation was performed to identify LB, Alzheimer disease pathology, nigral neuronal loss, atherosclerosis, macroscopic infarcts, and other CVD pathologies (arteriolosclerosis, cerebral amyloid angiopathy, and microscopic infarcts). A series of regression models with terms for LB, CVD pathology, and the interaction of LB with CVD pathologies was fit for global parkinsonism proximate to death and for individual parkinsonian signs scores including, parkinsonian gait, rigidity, tremor, and bradykinesia. In 1,753 participants (mean age at death = 89 years; 68% women), LB was observed in 26% of participants, and CVD pathologies were present in more than two-thirds of participants. LB and 3 CVD pathologies (atherosclerosis, arteriolosclerosis, and macroscopic infarcts) were each independently associated with the severity of global parkinsonism proximate to death (LB: β = 0.318, SE = 0.08, p < 0.001; atherosclerosis: β = 0.373, SE = 0.079, p < 0.001; arteriolosclerosis: β = 0.253, SE = 0.078, p = 0.001; macroscopic infarcts: β = 0.333, SE = 0.077, p < 0.001). A linear regression model adjusted for demographics, CVD, and neurodegenerative pathologies showed interaction between LB and macroscopic infarcts (β = 0.463, SE = 0.168, p = 0.006), with LBs being associated with worse global parkinsonism when macroinfarcts are present. Similar interactions were found for atherosclerosis and LBs (β = 0.371, SE = 0.173, p = 0.032) and for parkinsonian gait as the outcome (macroscopic infarcts: β = 0.662, SE = 0.239, p = 0.005; atherosclerosis: β = 0.509, SE = 0.246, p = 0.038). Findings were not affected when the 66 participants with a clinical diagnosis of Parkinson disease were excluded. By contrast, there were no interactions between LB and other CVD pathologies or between atherosclerosis and macroscopic infarcts for global parkinsonism proximate to death. These findings suggest that atherosclerosis and macroscopic infarcts interact with LB pathology to increase the severity of parkinsonism beyond their additive effects in older persons.

Primary motor area-related injury of anterior central gyrus in Parkinson's disease with dyskinesia: A study based on MRS and Q-space

IntroductionBy using magnetic resonance spectroscopy (MRS) and Q-Space imaging technology, this research analyzes the imaging characteristics of white matter fibers in the primary motor cortex and posterior limbs of the subcortical internal capsule in parkinsonian patients with motor disorders. The correlation among the changes in axonal function and structure in the cerebral cortex and subcortical cortex and motor disorder is further revealed. MethodsFirst, motor function and clinical condition of 20 patients with Parkinson's disease is assessed the third section of the Unified Parkinson's Scale and H&Y Parkinson's Clinical Staging Scale. Magnetic resonance (MR) scanning is performed with 1H-MRS. Secondly, the range maps of N-acetylaspartic acid (NAA), Choline (Cho), and Creatine (Cr) in the region of interest (the primary motor area of anterior central cortex gyrus, i.e. M1 region) are obtained, and the ratios of NAA/Cr and Cho are calculated. Third, Q-Space MR diffusion imaging technique is used to collect Q-Space images, and a Dsi-studio workstation is used to post-process the images. The fraction anisotropic (FA), generalized fraction anisotropic (GFA), and apparent diffusion coefficient (ADC) parameters of Q-Space in the primary motor cortex and the region of interest in the posterior limb of the internal capsule are obtained. Finally, the parameters of MRS and Q-Space in the experimental group and the control group are further analyzed by SPSS statistical software. ResultsAfter assessing with Parkinson's score scale, there is obvious motor dysfunction in the experimental group. The average clinical stage of H&Y is 3.0 ± 0.31. In the analysis of MRS data, the ratio of NAA/Cr in the primary motor area of the anterior central gyrus in the experimental group is significantly lower than that in the control group (P < 0.05). In the ADC map obtained by Q-Space imaging technique, the ADC value in the primary motor area of the anterior central gyrus in the experimental group is higher than that in the control group (P < 0.05), and the difference is statistically significant (P < 0.05). There is no significant difference between the experimental group and the control group (P > 0.05) in FA and GFA values of the posterior limb of capsule to characterize the characteristics of white matter fibers. ConclusionsIn parkinsonian patients with motor dysfunction, there are apparent functional and structural changes in the primary motor area neurons and peripheral white matter of the anterior central gyrus, and no obvious damage to the axonal structure of the descending fibers in the cortex.

The impact of iron deposition on the fear circuit of the brain in patients with Parkinson's disease and anxiety.

Anxiety is one of the most common psychiatric symptoms of Parkinson's disease (PD), and brain iron deposition is considered to be one of the pathological mechanisms of PD. The objective of this study was to explore alterations in brain iron deposition in PD patients with anxiety compared to PD patients without anxiety, especially in the fear circuit. Sixteen PD patients with anxiety, 23 PD patients without anxiety, and 26 healthy elderly controls were enrolled prospectively. All subjects underwent neuropsychological assessments and brain magnetic resonance imaging (MRI) examinations. Voxel-based morphometry (VBM) was used to study morphological brain differences between the groups. Quantitative susceptibility mapping (QSM), an MRI technique capable of quantifying susceptibility changes in brain tissue, was used to compare susceptibility changes in the whole brain among the three groups. The correlations between brain susceptibility changes and anxiety scores quantified using the Hamilton Anxiety Rating Scale (HAMA) were compared and analyzed. PD patients with anxiety had a longer duration of PD and higher HAMA scores than PD patients without anxiety. No morphological brain differences were observed between the groups. In contrast, voxel-based and ROI-based QSM analyses showed that PD patients with anxiety had significantly increased QSM values in the medial prefrontal cortex, anterior cingulate cortex, hippocampus, precuneus, and angular cortex. Furthermore, the QSM values of some of these brain regions were positively correlated with the HAMA scores (medial prefrontal cortex: r = 0.255, p = 0.04; anterior cingulate cortex: r = 0.381, p < 0.01; hippocampus: r = 0.496, p < 0.01). Our findings support the idea that anxiety in PD is associated with iron burden in the brain fear circuit, providing a possible new approach to explaining the potential neural mechanism of anxiety in PD.

Pathological α-synuclein accumulation, CSF metabolites changes and brain microstructures in cynomolgus monkeys treated with 6-hydroxydopamine

The lack of evidence indicating the accumulation of phosphorylated α-synuclein (P-α-syn), a neuropathological hallmark of Parkinson disease (PD), limits the application of 6-OHDA animal models. In cynomolgus monkeys received unilateral 6-hydroxydopamine (6-OHDA) injection, we identified nigrostriatal dysfunction related behavioral defects, such as the increase of PD score, decrease of locomotor activities, and exhibition of typical rotations. We found the dopaminergic neurons were significantly reduced and had fragmented morphology in substantia nigra (SN). Furthermore, insoluble P-α-syn aggregates were observed. The P-α-syn aggregates were extracellular distributed and had typical morphology of inclusion. Immunofluorescence staining showed that the P-α-syn colocalized with ubiquitin (Ub) and p62. We also found there were more actived astrocytes and microglial in SN and striatum, reflecting neuroinflammations increase in nigrostriatal pathway. At last, to determine the long-term consequence of dopamine (DA) neuron loss induced by 6-OHDA injection, the changes of cerebrospinal fluid (CSF) neurotransmitters over time as well as the brain microstructure alternations were examined. The dopamine-related metabolites were decreased after 6-OHDA injection reflecting dopaminergic neuron loss. The levels of γ-aminobutyric acid (GABA) and acetylcholine (Ach) showed an increasing trend but not significant. By diffusion tensor Magnetic Resonance Imaging (MRI) image scans, the fractional anisotropy (FA) value in the ipsilateral SN and caudate was found to reduce, which indicated neural fiber injury. Therefore, these results suggested that α-syn pathology might participate in process of 6-OHDA injuring DA neurons, and may expand the application of 6-OHDA monkeys on investigations into the pathogenesis of PD.

Increased Expression of Alpha-, Beta-, and Gamma-Synucleins in Brainstem Regions of a Non-Human Primate Model of Parkinson's Disease.

Parkinson’s disease (PD) is characterized by cell loss in the substantia nigra and the presence of alpha-synuclein (α-syn)-containing neuronal Lewy bodies. While α-syn has received major interest in the pathogenesis of PD, the function of beta- and gamma-synucleins (β-syn and γ-syn, respectively) is not really known. Yet, these proteins are members of the same family and also concentrated in neuronal terminals. The current preclinical study investigated the expression levels of α-, β-, and γ-synucleins in brainstem regions involved in PD physiopathology. We analyzed synuclein expression in the substantia nigra, raphe nuclei, pedunculopontine nucleus, and locus coeruleus from control and parkinsonian (by MPTP) macaques. MPTP-intoxicated monkeys developed a more or less severe parkinsonian score and were sacrificed after a variable post-MPTP period ranging from 1 to 20 months. The expression of the three synucleins was increased in the substantia nigra after MPTP, and this increase correlates positively, although not very strongly, with cell loss and motor score and not with the time elapsed after intoxication. In the dorsal raphe nucleus, the expression of the three synucleins was also increased, but only α- and γ-Syn are linked to the motor score and associated cell loss. Finally, although no change in synuclein expression was demonstrated in the locus coeruleus after MPTP, we found increased expression levels of γ-Syn, which are only correlated with cell loss in the pedunculopontine nucleus. Altogether, our data suggest that these proteins may play a key role in brainstem regions and mesencephalic tegmentum. Given the involvement of these brain regions in non-motor symptoms of PD, these data also strengthen the relevance of the MPTP macaque model of PD, which exhibits pathological changes beyond nigral DA cell loss and α-synucleinopathy.

Decreased vestibular efficacy contributes to abnormal balance in Parkinson's disease

Background and purposeAbnormal balance is poorly responsive to dopaminergic therapy in Parkinson's disease (PD). Decreased vestibular efficacy may contribute to imbalance in PD. The purpose of this study was to investigate the relationship between vestibular measures of dynamic posturography and imbalance in PD while accounting for confounder variables. Methods106 patients with PD underwent dynamic posturography for the 6 conditions of the sensory integration test (SOT) using the Neurocom Equitest device. All SOT measures, nigrostriatal dopaminergic denervation ((+)-[11C]DTBZ PET), brain acetylcholinesterase ([11C]PMP PET), age, duration of disease, cognitive and parkinsonian motor scores, and ankle vibration sensitivity were used as regressors in a stepwise logistic regression model comparing PD patients with versus without imbalance defined as Hoehn and Yahr (HY) stage 2.5 or higher. ResultsThe presence of imbalance was significantly associated with vestibular ratio COP RMS (P = 0.002) independently from visual ratio COP velocity (P = 0.012), thalamic acetylcholinesterase activity (P = 0.0032), cognition (P = 0.006), motor severity (P = 0.0039), age (P = 0.001), ankle vibration sensitivity (P = 0.0008), and borderline findings for somatosensory ratio COP velocity (P = 0.074) and visual ratio COP RMS (P = 0.078). Nigrostriatal dopaminergic denervation did not achieve significance. ConclusionsThe inability to efficaciously utilize vestibular information to retain upright stance is a determinant of imbalance in PD independent from visual and somatosensory processing changes and nigrostriatal dopaminergic losses. Thalamic, but not cortical, cholinergic denervation incrementally predicted balance abnormality. Further research is needed to investigate an intrinsic role of the cholinergic thalamus in multi-sensory, in particular vestibular, processing functions of postural control in PD.

Estimating Parkinsonism Severity in Natural Gait Videos of Older Adults With Dementia.

Drug-induced parkinsonism affects many older adults with dementia, often causing gait disturbances. New advances in vision-based human pose- estimation have opened possibilities for frequent and unobtrusive analysis of gait in long-term care settings. This work leverages spatial-temporal graph convolutional network (ST-GCN) architectures and training procedures to predict clinical scores of parkinsonism in gait from video of individuals with dementia. We propose a two-stage training approach consisting of a self-supervised pretraining stage that encourages the ST-GCN model to learn about gait patterns before predicting clinical scores in the finetuning stage. The proposed ST-GCN models are evaluated on joint trajectories extracted from video and are compared against traditional (ordinal, linear, random forest) regression models and temporal convolutional network baselines. Three 2D human pose-estimation libraries (OpenPose, Detectron, AlphaPose) and the Microsoft Kinect (2D and 3D) are used to extract joint trajectories of 4787 natural walking bouts from 53 older adults with dementia. A subset of 399 walks from 14 participants is annotated with scores of parkinsonism severity on the gait criteria of the Unified Parkinson's Disease Rating Scale (UPDRS) and the Simpson-Angus Scale (SAS). Our results demonstrate that ST-GCN models operating on 3D joint trajectories extracted from the Kinect consistently outperform all other models and feature sets. Prediction of parkinsonism scores in natural walking bouts of unseen participants remains a challenging task, with the best models achieving macro-averaged F1-scores of 0.53 ± 0.03 and 0.40 ± 0.02 for UPDRS-gait and SAS-gait, respectively. Pre-trained model and demo code for this work is available.1.

Neuroprotective effects of curcumin via autophagy induction in 6-hydroxydopamine Parkinson's models

Curcumin, a polyphenolic compound extracted from curcuma longa, acts as a nontoxic matter with anti-oxidant and anti-inflammatory effects as well as antiproliferative activities. Here, our research aimed to explore the neuroprotective effects of curcumin both in the 6-hydroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease (PD) in vivo and 6-OHDA-lesioned PC12 cells in vitro. In vitro, 6-OHDA caused a distinct decrease in cell viability of PC12 cells (150 μM). With the incubation of curcumin (1 μM), 6-OHDA-induced apoptosis was suppressed, increasing the autophagy markers (LC3-II/LC3-I, Beclin-1) and inhibiting phosphor-AKT/AKT, phosphor-mTOR/mTOR. In vivo, curcumin (50 mg/kg) reduced the accumulation of a-synuclein and led to higher parkinsonian disability scores in 6-OHDA-lesioned PD rats, contributing to induction of autophagy through inhibiting AKT/mTOR signal pathway. Moreover, treatment with autophagy inhibitors, such as 3-MA and chloroquine, abolished the neuroprotective effects of curcumin as evidence by compromised autophagy and declined motor behavior in PD rats. In conclusion, the present study demonstrated that curcumin repressed PC12 cell death in vitro and improved parkinsonian disability scores in vivo by inhibiting AKT/mTOR signaling pathway which mediated by autophagy, indicating a potential value of curcumin in the therapeutic intervention of Parkinson's disease.

Current Status of Acceptance of Disability and the Correlation With the Life Quality in Parkinson's Disease in Southwest China.

BackgroundAcceptance of disability (AOD) is a process that a patient must undergo to cope with altered abilities, but its effect in Parkinson's disease (PD) remains unclear. The present study aimed to determine the level of AOD, examine the influence of sociodemographic variables and disease characteristics on the AOD level, and evaluate the relation between AOD level and quality of life in a cohort of PD patients from Southwest of China.MethodsA total of 336 PD patients were consecutively recruited from November 2018 to October 2020. At enrollment, demographic and clinical data were obtained using a questionnaire, and the Acceptance of Disability Scale-Revised (AODS-R) scale was used to measure the AOD level.ResultsThe mean total score of AOD is 87.28, indicating a moderate level of disability acceptance in PD patients. Statistical analysis showed that understanding of PD, family support, and UPDRS-II score were major factors affecting AOD level, and patients with low AOD levels were more likely to have poorer quality of life.ConclusionAOD is a serious problem in PD patients in Southwest China, especially among individuals with insufficient family support and a lack of recognition of the disease. AOD was also associated with motor function and daily living ability, thus suggesting that evaluation of the AOD and promotion of the awareness may be helpful to improve the quality of life in patients with PD.

Blood neurofilament light, Parkinson’s disease, Parkinsonism, and physical function in a longitudinal population study

AbstractBackgroundBlood biomarkers of parkinsonism and Parkinson’s disease (PD) may allow for earlier identification of these conditions and improved longitudinal investigation of PD pathogenesis. Neurofilament light (Nf‐L), a neuronal cytoplasmic protein, is a biomarker of neurodegeneration measurable in CSF or blood. We examined the longitudinal association of serum Nf‐L with clinically diagnosed PD, parkinsonian signs, and physical functioning change over 16 years in a population‐based sample of Black and White older adults.MethodsData came from 1,327 older participants from the Chicago Health and Aging Project (CHAP), a longitudinal population‐based study of common chronic conditions of aging. Clinical evaluations included assessing parkinsonian signs in four domains, bradykinesia, parkinsonian gait, rigidity, and tremors using a structured version of the United Parkinson’s Disease Rating Scale. PD was diagnosed by board certified neurologists. Parkinsonian signs were reported as the four domain scores and a global parkinsonian score (combination of domain scores). Physical function was assessed by performance‐based tests. Serum Nf‐L was measured with an ultrasensitive immunoassay.ResultsAfter adjusting for demographic characteristics, the APOE‐e4 allele, and cognitive function, a 2‐fold higher concentration of serum Nf‐L was associated with the development of clinical PD (OR = 2.54, 95% CI: 1.70, 3.81), and global parkinsonian scores (OR = 2.44, 95% CI: 1.94, 2.94). This association was significant over five years before diagnosis. Compared to participants below 18.5 pg/mL of serum Nf‐L at baseline, participants in between 18.5–25.4 pg/mL, 25.4–37.3 pg/mL, and above 37.3 pg/mL had a higher odds ratio of clinical PD at all time intervals ranging from the time of diagnosis to greater than five years before diagnosis. A higher concentration of serum Nf‐L was associated with a faster decline in physical functioning over the duration of the study. In participants with 2‐fold higher concentrations of serum Nf‐L, the annual rate of decline in physical functioning increased by 0.15 units (95% CI: 0.21, 0.08).ConclusionsSerum Nf‐L predicted the development of clinically diagnosed PD, parkinsonian signs, and physical functioning decline in a population‐based sample. Our findings suggest that Nf‐L may serve as a potential biomarker for physical functioning outcomes in older adults.

Dietary Patterns and Individual Parkinsonian Signs Among Biracial Population of Older Adults

Abstract Objectives Loss of motor function, including parkinsonian signs, is common among older adults. Given limited treatment options, we investigated individual parkinsonian signs in accordance with two dietary patterns -Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) and Mediterranean diet (MedDiet) in older adults. Methods This cross-sectional observational study included 1496 Chicago Health and Aging Project participants aged 78.5 ± 6.4, 40% female, and 50% Blacks (a subsample of the community cohort, with dietary information (assessed by a validated food frequency questionnaire) and parkinsonian signs assessments done within 2.5 years). The four parkinsonian signs (bradykinesia, gait, tremors, and rigidity) were evaluated using a 26-item modified version of the United Parkinson's Disease Rating Scale (UPDRS) and were averaged to construct a global parkinsonian sign score. Linear (global parkinsonian signs, bradykinesia, and gait score) and logistic (tremors and rigidity (present/absent)) regression models were adjusted for age, sex, race, education, smoking, physical activity, and calories. We further adjusted the models for cardiovascular conditions (diabetes, hypertension, stroke, myocardial infarction). Diet was assessed both as continuous and in tertiles. Results MIND (T3 vs. T1: β = −0.39, P &amp;lt; 0.0001) and MedDiet (T3 vs. T1: β = −0.41, P &amp;lt; 0.0001) scores were associated with a lower global parkinsonian sign score in separate models. Those in the highest tertile of MIND and MedDiet had lower bradykinesia (MIND: T3 vs. T1: β = −0.44, P = 0.0002; MedDiet: T3 vs. T1: β = −0.38, P = 0.003) and gait (MIND: T3 vs. T1: β = −0.48, P = 0.0003; MedDiet: T3 vs. T1: β = −0.61, P &amp;lt; 0.0001) score than those in the lowest tertile. The MIND diet was associated with lower odds of tremors (T3 vs. T1: OR = 0.70, 95% CI:0.51, 0.95) and rigidity (T3 vs. T1: OR = 0.65, 95% CI:0.47, 0.89). However, MedDiet was associated with lower odds of rigidity (T3 vs. T1: OR = 0.45, 95% CI:0.32, 0.64) but not tremor. All associations were retained when further controlled for cardiovascular conditions. Conclusions MIND and MedDiet may benefit motor outcomes such as individual parkinsonian signs, including bradykinesia, gait, and rigidity in the aging population. Future studies with longitudinal follow-up are needed. Funding Sources Michael J Fox Foundation, R01AG021972, R01AG011101

The relationship between attention and static balance disturbance in patients with Parkinson’s disease

Balance disturbance is one of the main complications of the Parkinson's disease (PD). As studies have shown that impairments in some cognitive processescan lead to balance problems, we investigated the relationship between focused and divided attention and static balance in patients with PD and a healthycontrol group. We included 111 patients with PD (M age = 49.41, SD = 6.33 years) and 142 healthy individuals (M age = 50.62, SD = 6.07 years). All participants wereevaluated with the Trails Making Test A and B (TMT), and all participants' balance was evaluated with a Wii Balance Board, from which we measured theantero-posterior (AP), medio-lateral (ML), and total center of pressure (COP) velocity. We compared the two groups in terms of TMT-A, TMT-B, and COPvelocity tests in both eyes-open and eyes-closed conditions with independent t-tests, and we calculated Pearson's correlation coefficients between thebalance board-derived outcomes and the TMT scores. The two groups differed significantly on TMT-A and TMT-B scores, in total and ML COP velocity in both eyes-closed and eyes-open conditions, and in APCOP velocity only in eyes-open condition. Among patients with PD, TMT-A and TMT-B scores were positively correlated with total, ML, and AP COPvelocity, in both eyes-open and eyes-closed conditions. Associated attention deficits may be among the causes of balance disturbances in patients with PD, though both attention and balance may have a commonroot in brain circuitry.

Vascular Parkinsonism (VP) score: A simple clinical scale to differentiate vascular from degenerative parkinsonism

Background: Vascular parkinsonism(VP) constitutes (5-8) % of all parkinsonian disorders. Despite several existing diagnostic criteria for VP, there is no standard clinical grading scale for VP analogous to those for vascular dementia, like the Hachinski score.

Does gender differences have a role in determining sleep quality in Parkinson's disease?

Sleep disturbances in Parkinson's disease (PD) are common. Non -motor symptoms including sleep disturbance have gender difference in PD. The objective is to determine gender differences in PD in relation to the sleep quality. 156 patients with PD with males (n = 119) and females (n = 37) were included. The sleep quality and sleep disturbances were assessed using Pittsburgh sleep quality index (PSQI), Parkinson's disease Sleep Scale (PDSS) and Epworth Sleep Scale (ESS). Females with PD had higher frequency with insomnia (56.7%) as compared to males with PD (44.5%) (p = 0.05), nightmares (32.4%) as compared to males with PD (16.8%) (p = 0.04), greater PSQI component score of habitual sleep efficiency (p = 0.008), sleep disturbance (p = 0.03) and daytime dysfunction (p = 0.02), greater global PSQI score (p = 0.03), higher percentage of patients with global PSQI score > 5 (64.8%) than males with PD (41.1%) (p = 0.01), suggesting poor quality of sleep in females with PD. Higher total ESS score (p = 0.03), higher frequency of females with PD with total ESS score > 10 (45.9%) than in males with PD (26.9%) (p = 0.02), and lower total PDSS score (p = 0.009). On correlation analysis, the global PSQI score in females with PD had strong positive correlation with duration of PD, HAM-A and HAM-D scores and negative correlation with MMSE scores. Females with PD had a poor sleep quality with higher frequency of insomnia, nightmares, and daytime sleepiness. The longer duration of PD, higher scores of anxiety and depression scale and lower MMSE scores are associated with poor sleep quality in females with PD.

Recognition of emotions expressed on the face impairments in Parkinson’s disease

Background: Facial emotion recognition (FER) is a complex process, involving many brain circuits, including the basal ganglia that its motor involvement causes Parkinson's disease (PD). The previous studies used different tools for assessment of FER in PD. There is a discrepancy between the results of these studies due to different tools. In this study, we used a modified version of the Multimodal Emotion Recognition Test (MERT) to compare patients with PD to healthy controls (HCs). Methods: It was a cross-sectional study with primary objective of the mean percentage of the correct answers in MERT. Subjects had to name the emotions presented with different modalities. Results: 30 subjects were recruited and assessed in each group. The mean total MERT score was significantly lower in subjects with PD compared to HCs (35.0% vs. 44.5%). FER was significantly better when emotions were presented by video and worse when presented by still pictures. Both subjects with PD and HCs had lower MERT scores in recognizing negative emotions. There was no significant correlation between the duration and severity of PD and MERT score. Conclusion: Our study provided more pieces of evidence for impairment of FER in PD for recognizing emotions like sadness, disgust, and fear compared to happy expressions.

Dietary antioxidants associated with slower progression of parkinsonian signs in older adults

ABSTRACT Background and Objective: Progressive loss of motor function including parkinsonian signs is common in older adults. As diet may contribute to the motor decline, we tested the hypothesis that dietary intake of antioxidant nutrients (carotenoids, vitamin E and vitamin C) is related to the progression of parkinsonian signs in older adults. Research Design and Methods: A total of 682 participants without a clinical diagnosis of Parkinson’s Disease from the Rush Memory and Aging Project, were assessed annually over an average of 5.7 (±3.0) years using a 26-item modified version of the United Parkinson’s Disease Rating Scale. The scale assesses the severity of four parkinsonian signs (bradykinesia, gait, tremors, and rigidity) that were averaged to construct a global parkinsonian sign score. Nutrient intakes were assessed at baseline using a validated food frequency questionnaire. The associations between quintiles of antioxidant nutrient intakes and progression of parkinsonian signs were assessed using mixed effects models adjusted for age, sex, education, smoking. Results: In separate adjusted models, a slower rate of progressive parkinsonian signs was observed among those in the highest intake quintiles of total carotenoids (β= −0.06, 95%CI: −0.10 to −0.02,), beta-carotene from foods (β= −0.04, 95% CI:−0.08 to −0.0021), lutein-zeaxanthin (β= −0.05, 95%CI:−0.09 to −0.02), vitamin E from foods (β= −0.04, 95%CI:−0.08 to −0.01,) and vitamin C from foods (β= −0.06, 95%CI:−0.10 to −0.02), when compared to those in the lowest quintiles of intake. Conclusion: A higher level of dietary antioxidant nutrients may slow the rate of parkinsonian sign progression in older adults.