Cognitive Impairment In Parkinson's Disease Research Articles

Relation of serum level of tumor necrosis factor-alpha to cognitive functions in patients with Parkinson\u2019s disease

BackgroundInflammation is suggested to play a role in the development of non-motor Parkinson’s disease (PD) symptoms. We aimed to investigate the association between serum tumor necrosis factor-alpha (TNF-α) levels and cognition in PD patients. Thirty patients with PD and 30 healthy controls were included. Evaluation and staging of PD were done using Unified PD Rating Scale. Cognitive assessment was done using Addenbrooke’s Cognitive Examination (ACE-III) and trail making B tests. Measurement of serum levels of TNF-α was done.ResultsPatients had significantly worser cognitive scores than controls except for language subclass of ACE score. Mean serum TNF-α level was significantly greater in PD patients as compared to controls. TNF-α serum level was significantly negatively correlated with ACE visuospatial function. Sensitivity and specificity of TNF-α to detect cognitive dysfunction in PD using ACE III and trail making B tests were (73.1, 75%), (57.1, 56.2%), respectively, whereas sensitivity and specificity of TNF-α to detect severity of PD using H&Y staging in PD were 50%.ConclusionPatients with PD frequently have cognitive impairment. Elevated serum TNF-α levels in patients with PD, and association of this cytokine to visuospatial impairment, implicate this pro-inflammatory cytokine in the neurobiology of cognitive impairment in PD.

Ambroxol reverses tau and α-synuclein accumulation in a cholinergic N370S GBA1 mutation model.

Cognitive impairment is a common non-motor complication of Parkinson’s disease (PD). Glucocerebrosidase gene (GBA1) variants are found in 10–15% of PD cases and are numerically the most important risk factor for PD and dementia with Lewy bodies. Accumulation of α-synuclein and tau pathology is thought to underlie cognitive impairment in PD and likely involves cholinergic as well as dopaminergic neurons. Neural crest stem cells were isolated from both PD patients with the common heterozygous N370S GBA1 mutation and normal subjects without GBA1 mutations. The stem cells were used to generate a cholinergic neuronal cell model. The effects of the GBA1 variant on glucocerebrosidase (GCase) protein and activity, and cathepsin D, tau and α-synuclein protein levels in cholinergic neurons were examined. Ambroxol, a GCase chaperone, was used to investigate whether GCase enhancement was able to reverse the effects of the GBA1 variant on cholinergic neurons. Significant reductions in GCase protein and activity, as well as in cathepsin D levels, were found in GBA1 mutant (N370S/WT) cholinergic neurons. Both tau and α-synuclein levels were significantly increased in GBA1 mutant (N370S/WT) cholinergic neurons. Ambroxol significantly enhanced GCase activity and decreased both tau and α-synuclein levels in cholinergic neurons. GBA1 mutations interfere with the metabolism of α-synuclein and tau proteins and induce higher levels of α-synuclein and tau proteins in cholinergic neurons. The GCase pathway provides a potential therapeutic target for neurodegenerative disorders related to pathological α-synuclein or tau accumulation.

Magnetic Resonance Imaging Markers for Cognitive Impairment in Parkinson's Disease: Current View.

Cognitive impairment (CI) ranging from mild cognitive impairment (MCI) to dementia is a common and disturbing complication in patients with Parkinson’s disease (PD). Numerous studies have focused on neuropathological mechanisms underlying CI in PD, along with the identification of specific biomarkers for CI. Magnetic resonance imaging (MRI), a promising method, has been adopted to examine the changes in the brain and identify the candidate biomarkers associated with CI. In this review, we have summarized the potential biomarkers for CI in PD which have been identified through multi-modal MRI studies. Structural MRI technology is widely used in biomarker research. Specific patterns of gray matter atrophy are promising predictors of the evolution of CI in patients with PD. Moreover, other MRI techniques, such as MRI related to small-vessel disease, neuromelanin-sensitive MRI, quantitative susceptibility mapping, MR diffusion imaging, MRI related to cerebrovascular abnormality, resting-state functional MRI, and proton magnetic resonance spectroscopy, can provide imaging features with a good degree of prediction for CI. In the future, novel combined biomarkers should be developed using the recognized analysis tools and predictive algorithms in both cross-sectional and longitudinal studies.

Altered Cholinergic Innervation in De Novo Parkinson's Disease with and Without Cognitive Impairment.

BackgroundAltered cholinergic innervation plays a putative role in cognitive impairment in Parkinson's disease (PD) at least in advanced stages. Identification of the relationship between cognitive impairment and cholinergic innervation early in the disease will provide better insight into disease prognosis and possible early intervention.ObjectiveThe aim was to assess regional cholinergic innervation status in de novo patients with PD, with and without cognitive impairment.MethodsFifty‐seven newly diagnosed, treatment‐naive, PD patients (32 men, mean age 64.6 ± 8.2 years) and 10 healthy controls (5 men, mean age 54.6 ± 6.0 years) were included. All participants underwent cholinergic [18F]fluoroethoxybenzovesamicol positron emission tomography and detailed neuropsychological assessment. PD patients were classified as either cognitively normal (PD‐NC) or mild cognitive impairment (PD‐MCI). Whole brain voxel‐based group comparisons were performed.ResultsResults show bidirectional cholinergic innervation changes in PD. Both PD‐NC and PD‐MCI groups showed significant cortical cholinergic denervation compared to controls (P < 0.05, false discovery rate corrected), primarily in the posterior cortical regions. Higher‐than‐normal binding was most prominent in PD‐NC in both cortical and subcortical regions, including the cerebellum, cingulate cortex, putamen, gyrus rectus, hippocampus, and amygdala.ConclusionAltered cholinergic innervation is already present in de novo patients with PD. Posterior cortical cholinergic losses were present in all patients independent of cognitive status. Higher‐than‐normal binding in cerebellar, frontal, and subcortical regions in cognitively intact patients may reflect compensatory cholinergic upregulation in early‐stage PD. Limited or failing cholinergic upregulation may play an important role in early, clinically evident cognitive impairment in PD. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Analysis of Brain Activity Changes in Patients with Parkinson's Disease Based on Resting-State Functional Magnetic Resonance Imaging.

This paper uses resting-state functional magnetic resonance imaging to observe the changes in local consistency of brain activity in patients with Parkinson's disease (PD). Both healthy volunteers and Parkinson's disease patients were scanned for resting brain functional imaging, and the collected raw data were processed using resting functional magnetic resonance data processing toolkit software. This study adopted the use of Regional Homogeneity (ReHo). The postprocessing method of RS-fMRI is to study the spontaneous brain activity changes of patients with Parkinson's disease and cognitive impairment and to explore the changes in the function of their brain regions in the hope of providing help for the treatment of Parkinson's disease cognitive impairment. The results showed that, compared with the normal control group, the brain regions with increased ReHo values in the PD group were the right central anterior gyrus, the right lingual gyrus, the left middle occipital gyrus, and the bilateral anterior cuneiform lobes. The results show that PD patients have abnormal brain nerve activities in the resting state, and these abnormal brain nerve activities may be related to PD cognitive and behavioral dysfunction.

Hydrogen Sulfide Attenuates the Cognitive Dysfunction in Parkinson's Disease Rats via Promoting Hippocampal Microglia M2 Polarization by Enhancement of Hippocampal Warburg Effect.

Identification of innovative therapeutic targets for the treatment of cognitive impairment in Parkinson's disease (PD) is urgently needed. Hydrogen sulfide (H2S) plays an important role in cognitive function. Therefore, this work is aimed at investigating whether H2S attenuates the cognitive impairment in PD and the underlying mechanisms. In the rotenone- (ROT-) established PD rat model, NaHS (a donor of H2S) attenuated the cognitive impairment and promoted microglia polarization from M1 towards M2 in the hippocampus of PD rats. NaHS also dramatically upregulated the Warburg effect in the hippocampus of PD rats. 2-Deoxyglucose (2-DG, an inhibitor of the Warburg effect) abolished NaHS-upregulated Warburg effect in the hippocampus of PD rats. Moreover, the inhibited hippocampal Warburg effect by 2-DG abrogated H2S-excited the enhancement of hippocampal microglia M2 polarization and the improvement of cognitive function in ROT-exposed rats. Our data demonstrated that H2S inhibits the cognitive dysfunction in PD via promoting microglia M2 polarization by enhancement of hippocampal Warburg effect.

Quantitative Electroencephalography as a Biomarker for Cognitive Dysfunction in Parkinson's Disease.

Background: Quantitative electroencephalography (qEEG) has been suggested as a biomarker for cognitive decline in Parkinson’s disease (PD).Objective: Determine if applying a wavelet-based qEEG algorithm to 21-electrode, resting-state EEG recordings obtained in a routine clinical setting has utility for predicting cognitive impairment in PD.Methods: PD subjects, evaluated by disease stage and motor score, were compared to healthy controls (N = 20 each). PD subjects with normal (PDN, MoCA 26–30, N = 6) and impaired (PDD, MoCA ≤ 25, N = 14) cognition were compared. The wavelet-transform based time-frequency algorithm assessed the instantaneous predominant frequency (IPF) at 60 ms intervals throughout entire recordings. We then determined the relative time spent by the IPF in the four standard EEG frequency bands (RTF) at each scalp location. The resting occipital rhythm (ROR) was assessed using standard power spectral analysis.Results: Comparing PD subjects to healthy controls, mean values are decreased for ROR and RTF-Beta, greater for RTF-Theta and similar for RTF-Delta and RTF-Alpha. In logistic regression models, arithmetic combinations of RTF values [e.g., (RTF-Alpha) + (RTF-Beta)/(RTF-Delta + RTF-Theta)] and RTF-Alpha values at occipital or parietal locations are most able to discriminate between PD and controls. A principal component (PC) from principal component analysis (PCA) using RTF-band values in all subjects is associated with PD status (p = 0.004, β = 0.31, AUC = 0.780). Its loadings show positive contribution from RTF-Theta at all scalp locations, and negative contributions from RTF-Beta at occipital, parietal, central, and temporal locations. Compared to cognitively normal PD subjects, cognitively impaired PD subjects have lower median RTF-Alpha and RTF-Beta values, greater RTF-Theta values and similar RTF-Delta values. A PC from PCA using RTF-band values in PD subjects is associated with cognitive status (p = 0.002, β = 0.922, AUC = 0.89). Its loadings show positive contributions from RTF-Theta at all scalp locations, negative contributions from RTF-Beta at central locations, and negative contributions from RTF-Delta at central, frontal and temporal locations. Age, disease duration and/or sex are not significant covariates. No PC was associated with motor score or disease stage.Significance: Analyzing standard EEG recordings obtained in a community practice setting using a wavelet-based qEEG algorithm shows promise as a PD biomarker and for predicting cognitive impairment in PD.

Cognition and serotonin in Parkinson's disease.

Cognitive impairment affects up to 80% of patients with Parkinson's disease (PD) and is associated with poor quality of life. PD cognitive dysfunction includes poor working memory, impairments in executive function and difficulty in set-shifting. The pathophysiology underlying cognitive impairment in PD is still poorly understood, but there is evidence to support involvements of the cholinergic, dopaminergic, and noradrenergic systems. Only rivastigmine, an acetyl- and butyrylcholinesterase inhibitor, is efficacious for the treatment of PD dementia, which limits management of cognitive impairment in PD. Whereas the role of the serotonergic system in PD cognition is less understood, through its interactions with other neurotransmitters systems, namely, the cholinergic system, it may be implicated in cognitive processes. In this chapter, we provide an overview of the pharmacological, clinical and pathological evidence that implicates the serotonergic system in mediating cognition in PD.

Management of Psychiatric Disorders in Patients with Parkinson's Diseases.

Parkinson’s disease (PD) is a heterogeneous progressive neurodegenerative disorder, with a triad of motor symptoms with akinesia/bradykinesia, resting tremor (4–6 Hz), and rigidity. It is the second most common neurodegenerative disease after Alzheimer’s disease. The overall management of PD depends on the status of symptoms, functioning of the patients, impairment, disability, and its impact on quality of life. Depression, anxiety disorders, apathy, anhedonia, psychosis, cognitive impairments, dementia, and impulse control disorders (ICDs) are the common psychiatric symptoms/disorders comorbid with PD. Depression remains the most common psychiatric disorder reported to be comorbid with PD. Several pharmacological and nonpharmacological management strategies are used for the treatment of comorbid psychiatric disorders in PD. Selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors are used to treat depression in patients with PD. The best evidence of efficacy in PD psychosis is for clozapine and pimavanserin. The treatment for cognitive impairments in PD remains poorly researched. Rivastigmine is the only approved treatment for PD as per the Food and Drug Administration. Pramipexole, a dopamine agonist (DA), is reported to cause improvement in the symptoms of decreased willingness in apathy. The treatment approaches for different sleep disorders in PD are different. Identifying the cause, reviewing the patient’s ongoing medications, and evaluating the impact of comorbid medical conditions and sleep hygiene are common to all conditions related to sleep disorders. The first approach for treating ICD symptoms is the reduction or discontinuation of DAs. The psychiatric symptoms in patients with PD are highly prevalent, and their management should be included in the basic treatment algorithm for PD. This paper summarizes common psychiatric symptoms/disorders in PD and their management approaches.

Real-life consequences of cognitive dysfunction in Parkinson's disease.

While motor symptoms are the most recognized features of Parkinson's disease (PD), cognitive dysfunction is a key determinant of consequences of PD in real-life. In this chapter we review important domains where cognitive dysfunction negatively impacts the lives of people with PD (PwPD), such as difficulties in occupational and social life, and instrumental ADLs such as driving. Early loss of employment has important effects for PwPD, their families, and society. PwPD experience higher rates of family and social discord as well as important changes in their social roles. These processes are largely mediated through cognitive dysfunction, particularly difficulties processing and understanding emotions, decreased attention, and executive dysfunction. Cognitive dysfunction is also an important mediator of driving impairments, which contributes to decreased independence in PwPD. Finally, we briefly review the costs associated with cognitive impairment in PD. Both indirect and direct costs for PwPD with cognitive impairment are substantially higher than for PwPD with normal cognition.

Alterations in Large-Scale Intrinsic Connectivity Networks in the Parkinson's Disease-Associated Cognitive Impairment Continuum: A Systematic Review.

Cognitive impairment is common in the course of Parkinson's disease (PD) and displays a continuum from subjective cognitive impairment to dementia. Illuminating the pathophysiological processes associated with the continuum may help create follow-up and new treatment approaches. In this context, large-scale intrinsic connectivity networks are widely investigated to elucidate the neural processes underlying PD and are promising as non-invasive biomarkers. This systematic review aims to examine the alterations in large-scale intrinsic connectivity networks in the continuum of PD-associated cognitive impairment. ScienceDirect, Web of Science, and PubMed databases were searched with the specified keywords. The studies obtained as a result of this review were investigated by the PRISMA criteria, which were taken as a basis for the systematic review and writing of meta-analyses. A total of 974 studies were obtained from three databases. Twenty studies were included in the systematic review based on predetermined eligibility criteria. Among the large-scale connectivity networks examined in these studies, it was found that sensory-motor networks decreased their connectivity in the continuum of PD-associated cognitive impairment, and there were conflicting results in terms of cognitive networks. Well-designed longitudinal studies are needed to clarify the alterations in the intrinsic connectivity networks in the PD cognitive impairment continuum. In these studies, it is necessary to define the cognitive disorder groups well, to control the connectivity changes that may occur due to dopaminergic treatment, and to evaluate Parkinson's patients with subjective cognitive impairment and dementia within the continuum.

Mapping Actuarial Criteria for Parkinson's Disease-Mild Cognitive Impairment onto Data-Driven Cognitive Phenotypes.

Prevalence rates for mild cognitive impairment in Parkinson’s disease (PD-MCI) remain variable, obscuring the diagnosis’ predictive utility of greater dementia risk. A primary factor of this variability is inconsistent operationalization of normative cutoffs for cognitive impairment. We aimed to determine which cutoff was optimal for classifying individuals as PD-MCI by comparing classifications against data-driven PD cognitive phenotypes. Participants with idiopathic PD (n = 494; mean age 64.7 ± 9) completed comprehensive neuropsychological testing. Cluster analyses (K-means, Hierarchical) identified cognitive phenotypes using domain-specific composites. PD-MCI criteria were assessed using separate cutoffs (−1, −1.5, −2 SD) on ≥2 tests in a domain. Cutoffs were compared using PD-MCI prevalence rates, MCI subtype frequencies (single/multi-domain, executive function (EF)/non-EF impairment), and validity against the cluster-derived cognitive phenotypes (using chi-square tests/binary logistic regressions). Cluster analyses resulted in similar three-cluster solutions: Cognitively Average (n = 154), Low EF (n = 227), and Prominent EF/Memory Impairment (n = 113). The −1.5 SD cutoff produced the best model of cluster membership (PD-MCI classification accuracy = 87.9%) and resulted in the best alignment between PD-MCI classification and the empirical cognitive profile containing impairments associated with greater dementia risk. Similar to previous Alzheimer’s work, these findings highlight the utility of comparing empirical and actuarial approaches to establish concurrent validity of cognitive impairment in PD.

Alterations in white matter fiber in Parkinson disease across different cognitive stages

Cognitive impairment in Parkinson disease (PD) leads to substantial disability. Unlike external manifestations such as tremor, the decay of cognitive function is often an underlying process, and its neuroanatomic substrates are not yet fully elucidated. Knowledge regarding cognitive-related alterations in white matter (WM) pathways helps us understand the mechanisms of cognitive decline in patients with PD. Previous voxel-based analyses with Diffusion tensor imaging (DTI) metrics, such as fractional anisotropy (FA) and mean diffusivity (MD) have uncovered white matter differences in groupwise, but the conclusions were inconsistent. That was partially due to white matter fibers that are known to affect cognition, such as the corpus callosum (CC) and superior longitudinal fasciculus that cross in voxel, and are hard to interpreted by the abovementioned metrics. Furthermore, cognitive decay is a continuous process, it is difficult to reflect the continuous changes of white matter fibers between groups comparison. In the present work, we chose the constrained spherical deconvolution (CSD) and the fixel model, which avoided the effect of crossing fibers. To compare the white matter fiber in different cognitive stages of patients with PD, the results found that the CC, the cingulum bundle (CB), and the corticospinal tract (CST) showed the same trend in the decline of cognitive function, and this change may lead to the impairment of cognitive function. Our findings can help physicians determine the cognitive stage of PD from the perspective of white matter fiber and provide a reference for clinical trials and predictions.

Thalamic Dorsomedial Nucleus Free Water Correlates with Cognitive Decline in Parkinson's Disease.

Brain diffusion tensor imaging (DTI) has been shown to reflect cognitive changes in early Parkinson's disease (PD) but the diffusion-based measure free water (FW) has not been previously assessed. To assess if FW in the thalamic nuclei primarily involved with cognition (ie, the dorsomedial [DMN] and anterior [AN] nuclei), the nucleus basalis of Meynert (nbM), and the hippocampus correlates with and is associated with longitudinal cognitive decline and distinguishes cognitive status at baseline in early PD. Also, to explore how FW compares with conventional DTI, FW-corrected DTI, and volumetric assessments for these outcomes. Imaging data and Montreal Cognitive Assessment (MoCA) scores from the Parkinson's Progression Markers Initiative database were analyzed using partial correlations and ANCOVA. Primary outcome multiple comparisons were corrected for false discovery rate (q value). Thalamic DMN FW changes over 1year correlated with MoCA changes over both 1 and 3 years (partial correlations -0.222, q = 0.040, n = 130; and - 0.229, q = 0.040, n = 123, respectively; mean PD duration at baseline = 6.85months). NbM FW changes over 1 year only correlated with MoCA changes over 3 years (-0.222, q = 0.040). Baseline hippocampal FW was associated with cognitive impairment at 3 years (q = 0.040) and baseline nbM FW distinguished PD-normal cognition (MoCA ≥26) from PD-cognitive impairment (MoCA ≤25), (q = 0.008). The exploratory comparisons showed FW to be the most robust assessment modality for all outcomes. Thalamic DMN FW is a promising cognition progression biomarker in early PD that may assist in identifying cognition protective therapies in clinical trials. FW is a robust assessment modality for these outcomes. © 2021 International Parkinson and Movement Disorder Society.

Does the Montreal Cognitive Assessment (MoCA) identify cognitive impairment profiles in Parkinson’s disease? An exploratory study

An important proportion of patients with Parkinson’s Disease (PD) present signs of cognitive impairment, although this is heterogeneous. In an attempt to classify this, the dual syndrome hypothesis distinguishes between two profiles: one defined by attentional and executive problems with damage in anterior cerebral regions, and another with mnesic and visuospatial alterations, with damage in posterior cerebral regions. The Montreal Cognitive Assessment (MoCA) is one of the recommended screening tools, and one of the most used, to assess cognitive impairment in PD. However, its ability to specifically identify these two profiles of cognitive impairment has not been studied. The aim of this study was, therefore, to analyze the capacity of the MoCA to detect cognitive impairment, and also to identify anterior and posterior profiles defined by the dual syndrome hypothesis. For this purpose, 59 patients with idiopathic PD were studied with the MoCA and a neuropsychological battery of tests covering all cognitive domains. Results of logistic regression analysis with ROC (Receiver Operating Characteristic) curves showed that MoCA detected cognitive impairment and identified patients with a profile of anterior/attentional and executive deficit, with acceptable sensibility and specificity. However, it did not identify patients with a posterior/mnesic-visuospatial impairment. We discuss the reasons for the lack of sensitivity of MoCA in this profile, and other possible implications of these results with regards the usefulness of this tool to assess cognitive impairment in PD.

Alpha-Synuclein and Cognitive Decline in Parkinson Disease.

Parkinson disease (PD) is the second most common neurodegenerative disorder in elderly people. It is characterized by the aggregation of misfolded alpha-synuclein throughout the nervous system. Aside from cardinal motor symptoms, cognitive impairment is one of the most disabling non-motor symptoms that occurs during the progression of the disease. The accumulation and spreading of alpha-synuclein pathology from the brainstem to limbic and neocortical structures is correlated with emerging cognitive decline in PD. This review summarizes the genetic and pathophysiologic relationship between alpha-synuclein and cognitive impairment in PD, together with potential areas of biomarker advancement.

Region-Specific Neurovascular Decoupling Associated With Cognitive Decline in Parkinson's Disease.

Background: Cognitive deficits are prominent non-motor symptoms in Parkinson’s disease (PD) and have been shown to involve the neurovascular unit (NVU). However, there is a lack of sufficient neuroimaging research on the associated modulating mechanisms. The objective of this study was to identify the contribution of neurovascular decoupling to the pathogenesis of cognitive decline in PD.Methods: Regional homogeneity (ReHo), a measure of neuronal activity, and cerebral blood flow (CBF), a measure of vascular responses, were obtained from patients with PD with mild cognitive impairment (MCI) and normal cognition (NC) as well as matched healthy controls (HCs). Imaging metrics of neurovascular coupling (global and regional CBF-ReHo correlation coefficients and CBF-ReHo ratios) were compared among the groups.Results: Neurovascular coupling was impaired in patients with PD-MCI with a decreased global CBF-ReHo correlation coefficient relative to HC subjects (P < 0.05). Regional dysregulation was specific to the PD-MCI group and localized to the right middle frontal gyrus, right middle cingulate cortex, right middle occipital gyrus, right inferior parietal gyrus, right supramarginal gyrus, and right angular gyrus (P < 0.05). Compared with HC subjects, patients with PD-MCI showed higher CBF-ReHo ratios in the bilateral lingual gyri (LG), bilateral putamen, and left postcentral gyrus and lower CBF-ReHo ratios in the right superior temporal gyrus, bilateral middle temporal gyri, bilateral parahippocampal gyri, and right inferior frontal gyrus. Relative to the HC and PD-NC groups, the PD-MCI group showed an increased CBF-ReHo ratio in the left LG, which was correlated with poor visual–spatial performance (r = −0.36 and P = 0.014).Conclusion: The involvement of neurovascular decoupling in cognitive impairment in PD is regionally specific and most prominent in the visual–spatial cortices, which could potentially provide a complementary understanding of the pathophysiological mechanisms underlying cognitive deficits in PD.

Effect of physical therapy on posture and quality of life in subject with parkinson\\\\\\\'s disease

It is a chronic progressive degenerative disorder of extra pyramidal system caused by loss of dopaminergic neurons in the substantia nigra and characterized by tremors, rigidity, bradykinesia, and disturbance of gait and posture.The neuropsychiatric symptoms of PD may include depression, psychosis, apathy, impulse control disorders that are linked with the poor quality of life due to the progression of disease. Despite, cognitive impairment in PD is of great significance in terms of therapeutic approaches in order to deal with motor deficits of disorder. Multiple studies have revealed that exercise has been proven to be effective for the maintenance of health and well-being in Parkinson’s. More importantly it is shown to play a significant role in addressing secondary prevention based on strength, flexibility, functional independence as well as gait and balance respectively.To evaluate the effect of physical therapy on posture and quality of life in subject with Parkinson’s diseaseSource of Data: Radha multispecielist Hospital, Shreeji Hospital, Parul Shevashram,Venus.Sampaling Method: Convenience,samplingSample Size: 30 subject were included (15 in) each groupsSelection f Sample: convenientStudy Design: experimentalStudy Duration: 30 min/day/7 weekPost intervention assessment will be done by body posture questionnaire and SF-36, for posture and quality of life assessment in 30 subjects meeting inclusion and exclusion criteria dividing in to two group by convenience.Group AGroup B(1)Patient with 50 to 75 years of age (2)Participants patient diagnosed with Parkinson’s diseases (3) Both gender are included (4) The participants were at stage 3 of Parkinson’s disease, according the Hoehn and Yahr scale. (1) The examined patients did not have other coexisting neurodegenerative. (2)Mentally challenged (3) Orthopedic deformity. (1) Short form health survey. (20) Body posture questionnaire.This study included 30 patient 18 male and 12 female giving a sex ratio. Mean age of participant was 62 year. There were 15 patients in control group and 15 patients in experimental group. All patients completed treatment and evaluated at baseline and at the end of study. Mean value of sf-36 was 50.59 and 52.59 for experimental and control group respectively. These means later increase to 74.90 and 59.00 respectively with p value 0.001. Mean value of body posture questionnaire was 47.27 and50.07 for experimental and control group respectively. These mean later increase to72.47 and 59 respectively with p value 0.001 Statistically significant change was present for posture and quality of life with p&amp;#60;0.001 for both group.The obtained results revealed that the influence of applied program had a positive influence on posture and quality of life in people with Parkinson’s disease.When functional movement is applied on a regular basis, improvement of quality of life and everyday life activities can be noticed.

Comparison of Mini-Mental State Examination and Montreal Cognitive Assessment Ratings Across Levels of Parkinson's Disease Severity.

Cognitive impairment (CI) is common in Parkinson's disease (PD) and an important cause of disability. Screening facilitates early detection of CI and has implications for management. Preclinical disability is when patients have functional limitations but maintain independence through compensatory measures. The objective of this study was to investigate the relationship between scores on the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) with levels of PD severity and disability. PD patients (n = 2,234) in a large observational study were stratified by disease severity, based on Total Unified Parkinson's Disease Rating Scale (Total UPDRS) and Hoehn and Yahr (HY) stage. Using MMSE (n = 1,184) or MoCA (n = 1,050) and basic (ADL) and instrumental activities of daily living (IADL) scales for disability, linear regression analysis examined associations between cognitive status and disability. Cognition and disability were highly correlated, with the strongest correlation between IADL and MoCA. Only 16.0% of mean MMSE scores were below threshold for CI (28) and only in advanced PD (Total UPDRS 60+, HY≥3). MoCA scores fell below CI threshold (26) in 66.2% of the sample and earlier in disease (Total UPDRS 30+, HY≥2), corresponding with impairments in ADLs. In a large clinical dataset, a small fraction of MMSE scores fell below cutoff for CI, reinforcing that MMSE is an insensitive screening tool in PD. MoCA scores indicated CI earlier in disease and coincided with disability. This study shows that MoCA, but not MMSE is sensitive to the emergence of early cognitive impairment in PD and correlates with the concomitant onset of disability.

Brain age and Alzheimer's-like atrophy are domain-specific predictors of cognitive impairment in Parkinson's disease

Recently, it was shown that patients with Parkinson's disease (PD) who exhibit an “Alzheimer's disease (AD)-like” pattern of brain atrophy are at greater risk for future cognitive decline. This study aimed to investigate whether this association is domain-specific and whether atrophy associated with brain aging also relates to cognitive impairment in PD. SPARE-AD, an MRI index capturing AD-like atrophy, and atrophy-based estimates of brain age were computed from longitudinal structural imaging data of 178 PD patients and 84 healthy subjects from the LANDSCAPE cohort. All patients underwent an extensive neuropsychological test battery. Patients diagnosed with mild cognitive impairment or dementia were found to have higher SPARE-AD scores as compared to patients with normal cognition and healthy controls. All patient groups showed increased brain age. SPARE-AD predicted impairment in memory, language and executive functions, whereas advanced brain age was associated with deficits in attention and working memory. Data suggest that SPARE-AD and brain age are differentially related to domain-specific cognitive decline in PD. The underlying pathomechanisms remain to be determined.