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Longitudinal study showed that PSP-RS exhibited no further changes in cortical thinning, which remained relatively focal, while midbrain atrophy and WM damage significantly progressed. Corpus callosum and frontal WM tract changes correlated with the progression of both disease severity and behavioural dysfunction.
This study demonstrated the feasibility of carrying out longitudinal diffusion tensor MRI in patients with PSP-RS and its sensitivity to identifying the progression of pathology. No commercial use is permitted unless otherwise expressly granted. Richard; Williamson, David; Jones, P.
Objective We tested whether in vivo neuroinflammation relates to the distinctive distributions of pathology in Alzheimer disease AD and progressive supranuclear palsy PSP. Methods Sixteen patients with symptomatic AD including amnestic mild cognitive impairment with amyloid-positive PET scan , 16 patients with PSP—Richardson syndrome, and 13 age-, sex-, and education-matched healthy controls were included in this case-control study.
Results [11C]PK binding in the medial temporal lobe and occipital, temporal, and parietal cortices was increased in patients with AD, relative both to patients with PSP and to controls. Conclusions Together, our results suggest that neuroinflammation has an important pathogenic role in the 2 very different human neurodegenerative disorders of AD and PSP.
The increase and distribution of microglial activation suggest that immunotherapeutic strategies may be useful in slowing the progression of both diseases. Background Two recent randomized, placebo-controlled trials of putative disease-modifying agents davunetide, tideglusib in progressive supranuclear palsy PSP failed to show efficacy, but generated data relevant for future trials. Methods We provide sample size calculations based on data collected in PSP patients assigned to placebo in these trials.
A placebo effect was calculated. A placebo effect was not detected in these scales. Conclusions We propose the 1-year PSP-Rating Scale score change as the single primary readout in clinical neuroprotective or disease-modifying trials.
To date, pharmacological treatment options for progressive supranuclear palsy PSP , a neurodegenerative tauopathy, are limited. The MAO-B inhibitor rasagiline has shown neuroprotective effects in preclinical models of neurodegeneration. To evaluate the safety, tolerability and therapeutic effect of rasagiline on symptom progression in PSP. Of the 44 patients randomized, 26 completed the trial per protocol. Rasagiline was well tolerated, with a slight increase of known side effects hallucinations, ventricular extrasystoles.
Symptom progression averaged at No difference was seen in SEADL, depression, cognitive function, frontal executive function and posturographic measurements. Post hoc analyses of PSP-RS subdomains indicate a potential beneficial effect in the "limb motor" subdomain, whereas performance appeared lower in the "mentation" and "history" subdomains in the treatment group. While rasagiline is well tolerated in PSP, a beneficial effect on overall symptom progression was not detected. Post hoc analyses suggest the implementation of more specific endpoints in future studies.
Disruption of spatial organization and interjoint coordination in Parkinson's disease, progressive supranuclear palsy, and multiple system atrophy.
Patients with basal ganglia diseases may exhibit ideomotor apraxia. To define the nature of the impairment of the action production system, we studied a repetitive gesture of slicing bread by three-dimensional computergraphic analysis in eight nondemented patients with Parkinson's disease in the "on" state, five with progressive supranuclear palsy and four with multiple system atrophy.
Two patients with Parkinson's disease and two with progressive supranuclear palsy showed ideomotor apraxia for transitive movements on standard testing.
A Selspott II system was used for kinematic analysis of wrist trajectories and angular motions of the shoulder and elbow joints. Spatial disruption of wrist trajectories was more severe in patients with ideomotor apraxia. We posit that the basal ganglia are part of the parallel parieto-frontal circuits devoted to sensorimotor integration for object-oriented behavior.
The severity and characteristics of spatial abnormalities of a transitive movement would therefore depend on the location and distribution of the pathologic process within these circuits. Automatic classification of patients with idiopathic Parkinson's disease and progressive supranuclear palsy using diffusion MRI datasets. Parkinsonian syndromes encompass a spectrum of neurodegenerative diseases, which can be classified into various subtypes.
The differentiation of these subtypes is typically conducted based on clinical criteria. The aim of this study is to present an image-based classification method of patients with Parkinson's disease PD and patients with progressive supranuclear palsy PSP , an atypical variant of PD. Therefore, apparent diffusion coefficient ADC parameter maps were calculated based on diffusion-tensor magnetic resonance imaging MRI datasets.
Mean ADC values were determined in 82 brain regions using an atlas-based approach. The extracted mean ADC values for each patient were then used as features for classification using a linear kernel support vector machine classifier. To increase the classification accuracy, a feature selection was performed, which resulted in the top 17 attributes to be used as the final input features.
In conclusion, the classification of PD and PSP patients based on ADC features obtained from diffusion MRI datasets is a promising new approach for the differentiation of Parkinsonian syndromes in the broader context of decision support systems. Retinal degeneration in progressive supranuclear palsy measured by optical coherence tomography and scanning laser polarimetry.
This cross-sectional study compared the retinal morphology between patients with progressive supranuclear palsy PSP and healthy controls. The macular volume and the thickness of the majority of macular sectors were reduced compared to controls.
PSP seems to be associated with reduced thickness and volume of the macula and reduction of the RNFL, independent of disease duration or severity. Speech disorders reflect differing pathophysiology in Parkinson's disease, progressive supranuclear palsy and multiple system atrophy.
Although speech disorder is frequently an early and prominent clinical feature of Parkinson's disease PD as well as atypical parkinsonian syndromes APS such as progressive supranuclear palsy PSP and multiple system atrophy MSA , there is a lack of objective and quantitative evidence to verify whether any specific speech characteristics allow differentiation between PD, PSP and MSA.
The accurate differential diagnosis of dysarthria subtypes was based on the quantitative acoustic analysis of 16 speech dimensions. Whilst PD speakers manifested pure hypokinetic dysarthria, ataxic components were more affected in MSA whilst PSP subjects demonstrated severe deficits in hypokinetic and spastic elements of dysarthria.
Dysarthria in PSP was dominated by increased dysfluency, decreased slow rate, inappropriate silences, deficits in vowel articulation and harsh voice quality whereas MSA by pitch fluctuations, excess intensity variations, prolonged phonemes, vocal tremor and strained-strangled voice quality. Thus, motor speech examination may provide useful information in the evaluation of these diseases with similar manifestations. Effects of robot assisted gait training in progressive supranuclear palsy PSP: Progressive supranuclear palsy PSP is a rare neurodegenerative disease clinically characterized by prominent axial extrapyramidal motor symptoms with frequent falls.
Over the last years the introduction of robotic technologies to recover lower limb function has been greatly employed in the rehabilitative practice.
This observational trial is aimed at investigating the changes in the main spatiotemporal following end-effector robot training in people with PSP.
Five cognitively intact participants with PSP and gait disorders. Patients were submitted to a rehabilitative program of robot-assisted walking sessions for 45 min, 5 times a week for 4 weeks.
The spatiotemporal parameters at the beginning T0 and at the end of treatment T1 were recorded by a gait analysis laboratory. Robot training was feasible, acceptable and safe and all participants completed the prescribed training sessions.
All patients showed an improvement in the gait spatiotemporal index Mean velocity, Cadence, Step length, and Step width T0 vs. Robot training is a feasible and safe form of rehabilitation for cognitively intact people with PSP.
The lack of side effects and the positive results in the gait parameter index in all patients support the recommendation to extend the trials of this treatment. Further investigation regarding the effectiveness of robot training in time is necessary. Clinicopathological studies over the last decade have broadened the clinical spectrum of progressive supranuclear palsy PSP to include several distinct clinical syndromes. These differences correspond with variations in pathological profiles reported in the literature.
Blink reflex recovery cycle to differentiate Progressive Supranuclear Palsy from Cortico-basal syndrome. Progressive Supranuclear Palsy PSP and Cortico-basal syndrome CBS may share similar clinical findings and peculiar tests to distinguish between the two disorders could be useful. Supervised machine learning has been proposed as a revolutionary approach for identifying sensitive medical image biomarkers or combination of them allowing for automatic diagnosis of individual subjects.
The aim of this work was to assess the feasibility of a supervised machine learning algorithm for the assisted diagnosis of patients with clinically diagnosed Parkinson's disease PD and Progressive Supranuclear Palsy PSP. Morphological T1-weighted Magnetic Resonance Images MRIs of PD patients 28 , PSP patients 28 and healthy control subjects 28 were used by a supervised machine learning algorithm based on the combination of Principal Components Analysis as feature extraction technique and on Support Vector Machines as classification algorithm.
Voxels influencing classification between PD and PSP patients involved midbrain, pons, corpus callosum and thalamus, four critical regions known to be strongly involved in the pathophysiological mechanisms of PSP. Classification accuracy of individual PSP patients was consistent with previous manual morphological metrics and with other supervised machine learning application to MRI data, whereas accuracy in the detection of individual PD patients was significantly higher with our classification method.
The algorithm provides excellent discrimination of PD patients from PSP patients at an individual level, thus encouraging the application of computer-based diagnosis in clinical practice. Clinical, cognitive, and behavioural correlates of white matter damage in progressive supranuclear palsy.
White matter WM tract alterations were assessed in patients with progressive supranuclear palsy PSP relative to healthy controls and patients with idiopathic Parkinson's disease PD to explore the relationship of WM tract damage with clinical disease severity, performance on cognitive tests, and apathy.
In PSP, the contribution of WM tract damage to global disease severity and cognitive and behavioural disturbances was assessed using Random Forest analysis. Relative to controls, PSP patients showed diffusion tensor DT MRI abnormalities of the corpus callosum, superior cerebellar peduncle SCP , cingulum and uncinate fasciculus bilaterally, and right inferior longitudinal fasciculus. DT MRI metrics of the corpus callosum, right superior longitudinal and inferior longitudinal fasciculus, and left uncinate were the best predictors of executive dysfunction.
In PSP, apathy severity was related to the damage to the corpus callosum, right superior longitudinal, and uncinate fasciculi. Neuroimaging evidence of gray and white matter damage and clinical correlates in progressive supranuclear palsy. To evaluate gray matter GM and white matter WM abnormalities and their clinical correlates in patients with progressive supranuclear palsy PSP.
Sixteen PSP patients and sixteen age-matched healthy subjects underwent a clinical evaluation and multimodal magnetic resonance imaging, including three-dimensional T1-weighted imaging and diffusion tensor imaging DTI.
PSP patients showed GM volume decrease, involving the frontal cortex, putamen, pallidum, thalamus and accumbens nucleus, cerebellum, and brainstem. Additionally, they had widespread changes in WM bundles, mainly affecting cerebellar peduncles, thalamic radiations, corticospinal tracts, corpus callosum, and longitudinal fasciculi. GM volumes did not correlate with WM abnormalities. DTI indices of WM damage, but not GM volumes, correlated with clinical scores of disease severity and cognitive impairment.
WM damage in PSP correlates with clinical scores of disease severity and cognitive impairment, thus providing further insight into the pathophysiology of the disease. Identification of common variants influencing risk of the tauopathy Progressive Supranuclear Palsy. Progressive supranuclear palsy PSP is a movement disorder with prominent tau neuropathology.
Environmental causes of tauopathies include repetitive head trauma associated with some sports. We found significant novel signals P Abnormal cortical synaptic plasticity in primary motor area in progressive supranuclear palsy. No study has yet investigated whether cortical plasticity in primary motor area M1 is abnormal in patients with progressive supranuclear palsy PSP. We studied M1 plasticity in 15 PSP patients and 15 age-matched healthy subjects. Ten patients underwent iTBS again 1 year later.
H reflex size remained unchanged after iTBS. The enhanced LTP-like cortical synaptic plasticity parallels disease progression. Neuropsychiatric and cognitive profile of early Richardson's syndrome, Progressive Supranuclear Palsy-parkinsonism and Parkinson's disease. This makes the precocious diagnosis more challenging. We aimed at defining qualitative and quantitative differences of neuropsychiatric and neuropsychological profiles between PSP-P, PSP-RS and PD patients recruited within 24 months after the onset of symptoms, in order to clarify if the identification of peculiar cognitive and psychiatric symptoms is of help for early PSP diagnosis.
All patients were submitted to clinical, neurological, neuropsychiatric diagnostic evaluation and to a comprehensive neuropsychiatric and neuropsychological battery. Predictors of PSP-P and PSP-RS diagnosis were identified by multivariate logistic regressions including neuropsychiatric and neuropsychological features that differed significantly among groups. The three groups differed significantly at the Apathy Rating Scale score and at several neuropsychological domains.
The multivariate logistic regressions indicated that the diagnosis of PSP-RS was predicted by phonological verbal fluency deficit whereas the presence of apathy significantly predicted the PSP-P diagnosis. Environmental and occupational risk factors for progressive supranuclear palsy: The cause of progressive supranuclear palsy PSP is largely unknown. Based on evidence for impaired mitochondrial activity in PSP, we hypothesized that the disease may be related to exposure to environmental toxins, some of which are mitochondrial inhibitors.
This multicenter case-control study included incident PSP cases of cases and age-, sex-, and race-matched controls primarily from the same geographical areas. All subjects were administered standardized interviews to obtain data on demographics, residential history, and lifetime occupational history. An industrial hygienist and a toxicologist unaware of case status assessed occupational histories to estimate past exposure to metals, pesticides, organic solvents, and other chemicals.
Cases and controls were similar on demographic factors. In unadjusted analyses, PSP was associated with lower education, lower income, more smoking pack-years, more years of drinking well water, more years living on a farm, more years living 1 mile from an agricultural region, more transportation jobs, and more jobs with exposure to metals in general. However, in adjusted models, only more years of drinking well water was significantly associated with PSP. There was an inverse association with having a college degree.
We did not find evidence for a specific causative chemical exposure; higher number of years of drinking well water is a risk factor for PSP. This result remained significant after adjusting for income, smoking, education and occupational exposures. This is the first case-control study to demonstrate PSP is associated with environmental factors. Cognitive impairment in progressive supranuclear palsy-Richardson's syndrome is related to white matter damage.
Beside motor symptoms, patients with progressive supranuclear palsy syndrome PSPs commonly present cognitive and behavioral disorders. In this study we aimed to assess the structural brain correlates of cognitive impairment in PSPs. We enrolled 23 patients with probable PSP Richardson's syndrome and 15 matched healthy controls. Patients underwent an extensive clinical and neuropsychological evaluation. Cortical thickness measures and diffusion tensor metrics of white matter tracts were obtained.
Random forest analysis was used to identify the strongest MRI predictors of cognitive impairment in PSPs at an individual patient level. PSPs patients were in a moderate stage of the disease showing mild cognitive deficits with prominent executive dysfunction.
PSPs patients also showed a distributed white matter damage involving the main tracts including the superior cerebellar peduncle, corpus callosum, corticospinal tract, and extramotor tracts, such as the inferior fronto-occipital, superior longitudinal and uncinate fasciculi, and cingulum, bilaterally.
PSPs patients show both focal cortical thinning in dorsolateral anterior regions and a distributed white matter damage involving the main motor and extramotor tracts. White matter measures are highly associated with cognitive deficits. Progressive supranuclear palsy PSP is a disease of later life that is currently regarded as a form of neurodegenerative tauopathy.
Disturbance of gaze is a cardinal clinical feature of PSP that often helps clinicians to establish the diagnosis. Since the neurobiology of gaze control is now well understood, it is possible to use eye movements as investigational tools to understand aspects of the pathogenesis of PSP. In this review, we summarize each disorder of gaze control that occurs in PSP, drawing on our studies of 50 patients, and on reports from other laboratories that have measured the disturbances of eye movements.
When these gaze disorders are approached by considering each functional class of eye movements and its neurobiological basis, a distinct pattern of eye movement deficits emerges that provides insight into the pathogenesis of PSP. Although some aspects of all forms of eye movements are affected in PSP, the predominant defects concern vertical saccades slow and hypometric, both up and down , impaired vergence, and inability to modulate the linear vestibulo-ocular reflex appropriately for viewing distance.
These vertical and vergence eye movements habitually work in concert to enable visuomotor skills that are important during locomotion with the hands free. Taken with the prominent early feature of falls, these findings suggest that PSP tauopathy impairs a recently evolved neural system concerned with bipedal locomotion in an erect posture and frequent gaze shifts between the distant environment and proximate hands.
This approach provides a conceptual framework that can be used to address the nosological challenge posed by overlapping clinical and neuropathological features of neurodegenerative tauopathies. Tau burden and the functional connectome in Alzheimer's disease and progressive supranuclear palsy.
Alzheimer's disease and progressive supranuclear palsy PSP represent neurodegenerative tauopathies with predominantly cortical versus subcortical disease burden. In Alzheimer's disease, neuropathology and atrophy preferentially affect 'hub' brain regions that are densely connected. It was unclear whether hubs are differentially affected by neurodegeneration because they are more likely to receive pathological proteins that propagate trans-neuronally, in a prion-like manner, or whether they are selectively vulnerable due to a lack of local trophic factors, higher metabolic demands, or differential gene expression.
We assessed the relationship between tau burden and brain functional connectivity, by combining in vivo PET imaging using the ligand AV, and graph theoretic measures of resting state functional MRI in 17 patients with Alzheimer's disease, 17 patients with PSP, and 12 controls.
Strongly connected nodes displayed more tau pathology in Alzheimer's disease, independently of intrinsic connectivity network, validating the predictions of theories of trans-neuronal spread but not supporting a role for metabolic demands or deficient trophic support in tau accumulation.
This was not a compensatory phenomenon, as the functional consequence of increasing tau burden in Alzheimer's disease was a progressive weakening of the connectivity of these same nodes, reducing weighted degree and local efficiency and resulting in weaker 'small-world' properties. Conversely, in PSP, unlike in Alzheimer's disease, those nodes that accrued pathological tau were those that displayed graph metric properties associated with increased metabolic demand and a lack of trophic support rather than strong functional connectivity.
Together, these findings go some way towards explaining why Alzheimer's disease affects large scale connectivity networks throughout cortex while neuropathology in PSP is concentrated in a small number of subcortical structures.
Further, we demonstrate that in. Frontal dynamic aphasia in progressive supranuclear palsy: Distinguishing between generation and fluent sequencing of novel thoughts. Frontal dynamic aphasia is characterised by a profound reduction in spontaneous speech despite well-preserved naming, repetition and comprehension. Since Luria , designated this term, two main forms of dynamic aphasia have been identified: Both forms of dynamic aphasia have been interpreted as arising due to disturbances in early prelinguistic conceptual preparation mechanisms that are critical for language production.
We investigate language-specific and domain-general accounts of dynamic aphasia and address two issues: Thus, we report patient WAL who presented with frontal dynamic aphasia in the context of progressive supranuclear palsy PSP.
WAL was given a series of experimental tests that showed that his dynamic aphasia was not underpinned by a language-specific deficit in selection or in microplanning. By contrast, WAL presented with a domain-general deficit in fluent sequencing of novel thoughts. The latter replicated the pattern documented in a previous PSP patient Robinson, et al. Thus, WAL is the first unequivocal case to show a distinction between novel thought generation and subsequent fluent sequencing.
Moreover, WAL's generation deficit encompassed verbal and non-verbal responses, showing a similar but more profoundly reduced pattern. A new MRI rating scale for progressive supranuclear palsy and multiple system atrophy: Aim To evaluate a standardised MRI acquisition protocol and a new image rating scale for disease severity in patients with progressive supranuclear palsy PSP and multiple systems atrophy MSA in a large multicentre study.
The 32 item ordinal scale evaluated abnormalities within the basal ganglia and posterior fossa, blind to diagnosis. Internal consistency and reliability were checked.
Discriminant and predictive validity of extracted factors and total scores were tested for disease severity as per clinical diagnosis. PCA revealed four meaningful clusters of covarying parameters factor F F1: The total score significantly discriminated for disease severity or diagnosis; factorial scores differentially discriminated for disease severity according to diagnosis PSP: Implications for mechanisms of motion vision.
Smooth ocular tracking of a moving visual stimulus comprises a range of responses that encompass the ocular following response OFR , a pre-attentive, short-latency mechanism, and smooth pursuit, which directs the retinal fovea at the moving stimulus.
In order to determine how interdependent these two forms of ocular tracking are, we studied vertical OFR in progressive supranuclear palsy PSP , a parkinsonian disorder in which vertical smooth pursuit is known to be impaired. We measured eye movements of 9 patients with PSP and 12 healthy control subjects. Subjects viewed vertically moving sine-wave gratings that had a temporal frequency of We measured OFR amplitude as change in eye position in the 70 — ms, open-loop interval following stimulus onset.
Vertical smooth pursuit was studied as subjects attempted to track a 0. When OFR amplitude was re-measured, taking into account the increased latency in PSP patients, there was still no difference from control subjects. We confirmed that smooth pursuit was consistently impaired in PSP; group mean tracking gain at 0. We propose that OFR is spared because it is generated by low-level motion processing that is dependent on posterior cerebral cortex, which is less affected in PSP.
Conversely, smooth pursuit depends more on projections from frontal cortex to the pontine nuclei, both of which are involved in PSP. To assess disease severity and progression , we constructed and validated a new clinical rating scale as an ancillary study. Methods and Findings Patients were assessed at entry and 6-montly for up to 3 years.
The total score was significantly and linearly related to survival p progression of PSP. The slope of change was constant with increasing disease severity demonstrating good linearity of the scale throughout disease stages. Although MSA and PSP differed quantitatively on the total score at entry and on rate of progression , the relative contribution of clinical dimensions to overall. Autologous mesenchymal stem cell therapy for progressive supranuclear palsy: Background Progressive Supranuclear Palsy PSP is a sporadic and progressive neurodegenerative disease which belongs to the family of tauopathies and involves both cortical and subcortical structures.
No effective therapy is to date available. BM MSC can be efficiently delivered to the affected brain regions of PSP patients where they can exert their beneficial effects through different mechanisms including the secretion of neurotrophic factors. Here we propose a randomized, placebo-controlled, double-blind phase I clinical trial in patients affected by PSP with MSC delivered via intra-arterial injection.
Discussion To our knowledge, this is the first clinical trial to be applied in a no-option parkinsonism that aims to test the safety and to exploit the properties of autologous mesenchymal stem cells in reducing disease progression. Progressive supranuclear palsy PSP and multiple system atrophy MSA are progressive disabling neurological conditions usually fatal within 10 years of onset.
Little is known about the economic costs of these conditions. This paper reports service use and costs from France, Germany and the UK and identifies patient characteristics that are associated with cost.
Service use during the previous six months was measured at entry to the study and costs calculated. Mean six-month costs were calculated for patients. Data on patient sociodemographic and clinical characteristics were recorded and used in regression models to identify predictors of service costs and unpaid care costs i.
Formal and unpaid costs were significantly higher the more severe the illness, as indicated by the Parkinson's Plus Symptom scale. There was a significant inverse relationship between service and unpaid care costs. Deep brain stimulation of the pedunculopontine nucleus for treatment of gait and balance disorder in progressive supranuclear palsy: Effects of frequency modulations and clinical outcome.
The pedunculopontine nucleus has been suggested as a potential deep brain stimulation target for axial symptoms such as gait and balance impairment in idiopathic Parkinson's disease as well as atypical Parkinsonian disorders. Seven consecutive patients with progressive supranuclear palsy received bilateral pedunculopontine nucleus deep brain stimulation. Inclusion criteria comprised of the clinical diagnosis of progressive supranuclear palsy, a levodopa-resistant gait and balance disorder, age progressive supranuclear palsy generates frequency-dependent effects with improvement of cyclic gait parameters at low frequency and amelioration of hypokinesia at high frequency stimulation.
However, these effects do not translate into a clinically important improvement. Published by Elsevier Ltd. Validation of mobile eye-tracking as novel and efficient means for differentiating progressive supranuclear palsy from Parkinson's disease. Objective measurement devices can help to reliably detect subtle eye movement disturbances to improve sensitivity and specificity of the clinical diagnosis.
The present study aims at transferring findings from restricted stationary video-oculography VOG to a wearable head-mounted device, which can be readily applied in clinical practice. We investigated the eye movements in 10 possible or probable PSP patients, 11 Parkinson's disease PD patients, and 10 age-matched healthy controls HCs using a mobile, gaze-driven video camera setup EyeSeeCam.
Ocular movements were analyzed during a standardized fixation protocol and in an unrestricted real-life scenario while walking along a corridor. Differences were particularly evident for saccades in the vertical plane, and stronger for saccades than for other eye movements.
Differences were more pronounced during the standardized protocol than in the real-life scenario. Combined analysis of saccade velocity and saccade amplitude during the fixation protocol with the EyeSeeCam provides a simple, rapid Progressive supranuclear palsy: In this study, we investigated the occurrence and severity of the neuronal and glial cytoskeletal pathology in these six brainstem nuclei from 17 individuals with clinically diagnosed and neuropathologically confirmed progressive supranuclear palsy PSP.
The association between the severity of the pathology and the duration of the disease was investigated by means of correlation analysis. In the six nuclear greys studied, glial cells undergo alterations of their cytoskeleton on an irregular basis, whereby diseased oligodendrocytes predominantly presented as coiled bodies and affected astrocytes as thorn-shaped astrocytes.
In all six nuclei, the severity of the neuronal or glial cytoskeletal pathology showed no correlation with the duration of PSP. In view of their functional role, the neuronal pathology in the nuclei studied offers a possible explanation for the autonomic dysfunctions that eventually develop in the course of PSP.
Alternative promoter usage is an important mechanism for transcriptome diversity and the regulation of gene expression. The existence of an alternative promoter for MAPT gene was considered for a long time to explain differential tissue specificity and differential response to transcription and growth factors between mRNA transcripts. The alternative promoter usage could explain partly the different tau proteins expression patterns observed in tauopathies.
Here, we report on our discovery of a functional alternative promoter for MAPT, located upstream of the gene's second exon exon 1. By analyzing genome databases and brain tissue from control individuals and patients with Alzheimer's disease or progressive supranuclear palsy, we identified novel shorter transcripts derived from this alternative promoter.
We suggest that these new MAPT isoforms can be translated into normal or amino-terminal-truncated tau proteins. We further suggest that activation of MAPT's alternative promoter under pathological conditions leads to the production of truncated proteins, changes in protein localization and function, and thus neurodegeneration. Pittsburgh Compound B and AV positron emission tomography assessment of molecular pathologies of Alzheimer's disease in progressive supranuclear palsy. Little is known about Alzheimer's disease molecular proteins, beta-amyloid and paired helical filament PHF tau, in progressive supranuclear palsy PSP.
Recent techniques have been developed to allow for investigations of these proteins in PSP. We determined the frequency of beta-amyloid deposition in PSP, and whether beta-amyloid deposition in PSP is associated with PHF-tau deposition pattern, or clinical features.
Apolipoprotein APOE genotyping was also performed. Statistical testing for correlations and associations between variables of interest were also performed. We found little evidence for beta-amyloid related differences in clinical metrics, proportion of APOE e4 carriers, pattern of AV uptake, or pattern of atrophy. Beta-amyloid deposition occurs in a relatively high proportion of PSP subjects.
Unlike in Alzheimer's disease, however, there is little evidence that beta-amyloid, and PHF-tau, play a significant role in neurodegeneration in PSP. A double-labeling immunohistochemical study of tau exon 10 in Alzheimer's disease, progressive supranuclear palsy and Pick's disease. Neurofibrillary tangles NFT , one of the histopathological hallmarks of Alzheimer's disease AD and progressive supranuclear palsy PSP , and Pick bodies in Pick's disease PiD are composed of microtubule-associated protein tau, which is the product of alternative splicing of a gene on chromosome Alternative expression of exon 10 leads to formation of three- or four-repeat tau isoforms.
To study the differential expression of exon 10, we performed double-labeling immunohistochemistry of the hippocampal formation in nine AD, four PSP and three PiD cases. Cryostat sections were processed with and without formic acid FA treatment, and double-stained with anti-tau Alz or PHF-1 or anti-amyloid P component antibodies and one of two specific anti-exon 10 antibodies E The effect of proteinase-K treatment was also evaluated.
The results suggest the following. First, in AD, E immunoreactivity is present in most intracellular NFT, but not in most dystrophic neurites and neuropil threads, suggesting differential expression of tau isoforms in specific cellular domains. The results suggest that expression of exon 10 in tau is specific for cellular domains in a disease-specific manner. The binaural masking level difference: Under binaural listening conditions, the detection of target signals within background masking noise is substantially improved when the interaural phase of the target differs from that of the masker.
Neural correlates of this binaural masking level difference BMLD have been observed in the inferior colliculus and temporal cortex, but it is not known whether degeneration of the inferior colliculus would result in a reduction of the BMLD in humans. PSP is associated with severe atrophy of the upper brain stem, including the inferior colliculus, confirmed by voxel-based morphometry of structural MRI.
Stimuli comprised in-phase sinusoidal tones presented to both ears at three levels high, medium, and low masked by in-phase noise, which rendered the low-level tone inaudible. Critically, the BMLD was measured using a low-level tone presented in opposite phase across ears, making it audible against the noise. The cortical waveforms from bilateral auditory sources revealed significantly larger N1m peaks for the out-of-phase low-level tone compared with the in-phase low-level tone, for both groups, indicating preservation of early cortical correlates of the BMLD in PSP.
In PSP a significant delay was observed in the onset of the N1m deflection and the amplitude of the P2m was reduced, but these differences were not restricted to the BMLD condition. The results demonstrate that although PSP causes subtle auditory deficits, binaural processing can survive the presence of significant damage to the upper brain stem. Since the advent of computed tomography and magnetic resonance imaging scans, neurological disorders have less often been falsely labeled as conversion disorder CD.
However, misdiagnosis of a neurological disorder as CD still occurs, especially in cases with insidious onset. A year-old woman consulted two different neurologists in because of falling spells since and was diagnosed with CD. However, despite treatment for CD, the patient's physical symptoms deteriorated over a year. After repeated physical and psychiatric examinations, neurocognitive assessment, and consultation with a third neurologist because of suspicion of neurological disease, the patient was diagnosed with PSPS.
A diagnosis of CD should not be considered definitive if no improvement occurs in terms of physical, mental, and cognitive symptoms despite appropriate therapy. Intrinsic functional connectivity alterations in progressive supranuclear palsy: Differential effects in frontal cortex, motor, and midbrain networks. The topography of functional network changes in progressive supranuclear palsy can be mapped by intrinsic functional connectivity MRI.
The objective of this study was to study functional connectivity and its clinical and behavioral correlates in dedicated networks comprising the cognition-related default mode and the motor and midbrain functional networks in patients with PSP.
Whole-brain-based "resting-state" functional MRI and high-resolution T1-weighted magnetic resonance imaging data together with neuropsychological and video-oculographic data from 34 PSP patients 22 with Richardson subtype and 12 with parkinsonian subtype and 35 matched healthy controls were subjected to network-based functional connectivity and voxel-based morphometry analysis.
After correction for global patterns of brain atrophy, the group comparison between PSP patients and controls revealed significantly decreased functional connectivity P The pattern of verbal, visuospatial and procedural learning in Richardson variant of progressive supranuclear palsy in comparison to Parkinson's disease. Progressive supranuclear palsy PSP is regarded either within spectrum of atypical parkinsonian syndromes or frontotemporal lobar degeneration.
We compared the verbal, visuospatial and procedural learning profiles in patients with PSP and Parkinson's disease PD. Furthermore, the relationship between executive factors initiation and inhibition and learning outcomes was analyzed.
Motor sequencing task did not differentiate between patients. Visuospatial learning impairment in PSP-RS is possibly linked to impulsivity and failure to inhibit automatic responses. A voxel based comparative analysis using magnetization transfer imaging and T1-weighted magnetic resonance imaging in progressive supranuclear palsy. In progressive supranuclear palsy PSP tissue damage occurs in specific cortical and subcortical regions. Voxel based analysis using T1-weighted images depict quantitative gray matter GM atrophy changes.
Magnetization transfer MT imaging depicts qualitative changes in the brain parenchyma. Voxel based analysis of T1-weighted MRI was performed to investigate brain atrophy while MT was used to study qualitative abnormalities in the brain tissue. Magnetization transfer ratio images and magnetization-prepared rapid acquisition of gradient echo revealed extensive bilateral volume and qualitative changes in the orbitofrontal, prefrontal cortex and limbic lobe and sub cortical GM.
The prefrontal structures involved were the rectal gyrus, medial, inferior frontal gyrus IFG and middle frontal gyrus MFG. The anterior cingulate, cingulate gyrus and lingual gyrus of limbic lobe and subcortical structures such as caudate, thalamus, insula and claustrum were also involved. Cerebellar involvement mainly of anterior lobe was also noted. The findings suggest that voxel based MT imaging permits a whole brain unbiased investigation of central nervous system structural integrity in PSP.
Combined measurement of plasma cystatin C and low-density lipoprotein cholesterol: A valuable tool for evaluating progressive supranuclear palsy. Progressive supranuclear palsy PSP was previously thought as a cause of atypical Parkinsonism. Although Cystatin C Cys C and low-density cholesterol lipoprotein-C LDL-C are known to play critical roles in Parkinsonism, it is unknown whether they can be used as markers to distinguish PSP patients from healthy subjects and to determine disease severity.
Regional expression of the MAPT gene is associated with loss of hubs in brain networks and cognitive impairment in Parkinson disease and progressive supranuclear palsy. Abnormalities of tau protein are central to the pathogenesis of progressive supranuclear palsy, whereas haplotype variation of the tau gene MAPT influences the risk of Parkinson disease and Parkinson's disease dementia.
We assessed whether regional MAPT expression might be associated with selective vulnerability of global brain networks to neurodegenerative pathology. Regional connectivity varied according to the normal expression of MAPT. The regional expression of MAPT correlated with the proportionate loss of regional connectivity in Parkinson's disease. Executive cognition was impaired in proportion to the loss of hub connectivity. These effects were not seen with SNCA, suggesting that alpha-synuclein pathology is not mediated through global network properties.
The results establish a link between regional MAPT expression and selective vulnerability of functional brain networks to neurodegeneration. Published by Elsevier Inc. There are several theories about PSP's cause. A central hypothesis in many This theory stems from a clue found on the Pacific The autoradiography was well correlated with the immunohistochemical staining in adjacent tissue slides.
The [ 18F]FDDNP DVR signal appears to be primarily due to the large amount of bound hyperphosphorylated tau p-tau and the amyloid beta negligibly contributes to the total signal. The binding of [18F]FDDNP to the human neuroanatomy was investigated in two cohorts of distinct tauopathies and compared to the binding in two tau-negative cohorts against control patients.
We carried out differential diagnosis of brain blood flow images using single-photon emission computed tomography SPECT for patients with Parkinson's disease PD or progressive supranuclear paralysis PSP using statistical parametric mapping SPM and to whom we had applied anatomical standardization.
A total of 27 patients were studied using SPM: The decline of brain bloodstream in the PSP group was more notable in the midbrain, near the domain where the humming bird sign was observable, than in the PD group.
The observable differences in brain bloodstream decline in the midbrain of PSP and PD patients suggest the potential usefulness of this technique's clinical application to distinction diagnosis. Because it is often difficult to precisely diagnose and distinguish progressive supranuclear palsy PSP from corticobasal degeneration CBD , multiple system atrophy-parkinsonism MSA-P and Parkinson's disease PD at the onset of the disease, we compared the patients and clarified the features of these diseases.
The clinical characteristics of PSP were supranuclear gaze disturbance, optokinetic nystagmus OKN impairment and falls at the first visit. Diseases presenting extrapyramidal symptoms are accompanied by nigral cell loss. In the present study we investigated the neuromelanin-positive SNc volume in patients with the other parkinsonian disorders including multiple system atrophy MSA , progressive supranuclear palsy PSP and corticobasal degeneration CBD and compared the results with those with PD, spinocerebellar ataxia SCA and controls.
The border of the neuromelanin-positive region of the SNc was traced manually on these images with a pentablet pointing device and the SNc volume was calculated. The mean volumes for the left and right SN were used for statistical analyses. Symmetric corticobasal degeneration S- CBD. Corticobasal degeneration CBD is a neurodegenerative disease characterized pathologically by neuronal loss, gliosis and tau deposition in neocortex, basal ganglia and brainstem.
Typical clinical presentation is known as corticobasal syndrome CBS and involves the core features of progressive asymmetric rigidity and apraxia, accompanied by other signs of cortical and extrapyramidal dysfunction. Asymmetry is also emphasized on neuroimaging.
Clinical records were reviewed and quantitative volumetric analysis of symmetric atrophy on head MRI using atlas based parcellation was performed. Subjects were classified as S- CBD if no differences had been observed between right- and left-sided cortical or extrapyramidal signs or symptoms. Five cases 2 female met criteria for S- CBD. None had limb dystonia, myoclonus, apraxia or alien limb phenomena. CBD can have a symmetric presentation, clinically and radiologically, in which typical features of CBS, such as limb apraxia, myoclonus, dystonia and alien limb phenomenon, may be absent.
Copyright c Elsevier Ltd. Ultrastructural characterization of the tau-immunoreactive tubules in the oligodendroglial perikarya and their inner loop processes in progressive supranuclear palsy. Coiled bodies and interfascicular threads are conspicuous white matter abnormalities of brains of patients with progressive supranuclear palsy PSP.
Both structures are argyrophilic and immunoreactive for the microtubule-binding protein tau. This report concerns the ultrastructural localization of interfascicular threads and their relationship to coiled bodies in five PSP patients.
We showed for the first time that abnormal tubules with a to nm diameter and fuzzy outer contours were the common structures of coiled bodies in the oligodendroglial perikarya and of interfascicular threads.
Moreover, the tubules were immunolabeled by anti-tau antibodies. The abnormal tau-positive tubules of interfascicular threads were located in the inner loop of the myelin sheath. Our study further indicated that the thread-like structures in the white matter comprised, at least in part, oligodendroglial processes, and that they were also present in gray matter. We consider that the formation of coiled bodies in the perikarya and of interfascicular threads represents a common cytoskeletal abnormality of the oligodendroglia of PSP patients.
Moreover, even though the white matter alterations of PSP resemble those of corticobasal degeneration, there are certain ultrastructural differences in the abnormal oligodendroglial tubules of the two diseases.
Microtubule-associated Tau proteins are major actors in neurological disorders, the so-called tauopathies. In some of them, and specifically in Alzheimer's disease AD , hyperphosphorylated forms of Tau aggregate into neurofibrillary tangles.
Following and understanding the complexity of Tau's molecular profile with its multiple isoforms and post-translational modifications represent an important issue, and a major analytical challenge. Immunodetection methods are, in fact, limited by the number, specificity, sensitivity, and capturing property of the available antibodies.
Mass spectrometry MS has recently allowed protein quantification in complex biological fluids using isotope-labeled recombinant standard for absolute quantification PSAQ. To study Tau proteins, which are found at very low concentrations within the cerebrospinal fluid CSF , we relied on an innovative two-step pre-fractionation strategy, which was not dependent on immuno-enrichment. We then developed a sensitive multiplex peptide detection capability using targeted high-resolution MS to quantify Tau-specific peptides covering its entire sequence.
This approach was used on a clinical cohort of patients with AD, progressive supranuclear palsy PSP , and dementia with Lewy body DLB and with control non-neurodegenerative disorders. Taken together these results provide important information on Tau biology for future therapeutic interventions, and improved molecular diagnosis of tauopathies.
Voxelwise and region-of-interest group comparisons were performed in template space, with receiver operating characteristic curve analyses to assess single-subject discrimination. Qualitative comparisons with postmortem tau are reported in 1 patient who died 9 months after 18 F-flortaucipir. The purpose of this study was to evaluate whether the pattern of striatal dopamine transporter DAT availability could differentiate between progressive supranuclear palsy PSP and frontotemporal dementia FTD in the first few years of the disease.
The discriminatory power of variables including DAT activity and clinical parameters was investigated by receiver operating characteristics ROC analyses. Additionally, we analyzed the correlation between striatal subregional DAT availability and cognitive profiles.
The PSP and FTD groups had generally similar subregional patterns of DAT activity in terms of the anteroposterior and ventrodorsal gradients and asymmetry, except for a different preferential involvement in the caudate.
The ROC analysis showed that the DAT activity of the whole striatum had an excellent discriminatory power relative to Parkinsonism or neurocognitive profiles. Correlation analysis showed that verbal memory was significantly correlated with DAT availability in the whole striatum and the putaminal subregion only in patients with PSP. The surgical technique has evolved since then and several studies have concluded that Laparoscopic common bile duct exploration LCBDE procedures are superior to sequential endolaparoscopic treatment in terms of both clinical and economical outcomes, Cuschieri et al.
Here we present our series from January to March In a retrospective study from January to March , we performed laparoscopic cholecystectomies, out of which patients underwent intraoperative cholangiogram and patients eventually had CBD exploration.
Choledochoduodenosotomy was done in 2 patients. Patients were followed regularly at six monthly intervals with a range of six months to three years of follow-up. There were no major complications like bile leak or pancreatitis. There were no cases of retained stones or intraabdominal infection. Primary closure of choledochotomy in select patients is a.
Surveys of PSP patients have hinted at a predilection A questionnaire survey on Guadeloupe revealed that people with PSP-like Alzheimer's disease AD is a debilitating neurodegenerative disease that is affecting an increasing number of people.
Current AD treatments do not stop or reverse the disease progression , highlighting the need for new, more effective therapeutics. Cannabidiol CBD is a non-psychoactive phytocannabinoid that has demonstrated neuroprotective, anti-inflammatory and antioxidant properties in vitro. Thus, it is investigated as a potential multifunctional treatment option for AD.
Here, we summarize the current status quo of in vivo effects of CBD in established pharmacological and transgenic animal models for AD. The studies demonstrate the ability of CBD to reduce reactive gliosis and the neuroinflammatory response as well as to promote neurogenesis. Importantly, CBD also reverses and prevents the development of cognitive deficits in AD rodent models. Further investigations should address the long-term potential of CBD and evaluate mechanisms involved in the therapeutic effects described.
The CBD with the credible contents as a powerful and time-saving tool provide more comprehensive and accurate information for further CRC biomarker research. All of these web operations were implemented under the Windows system.
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