Relevant bibliographies by topics / Progressive supranuclear palsy

Academic literature on the topic 'Progressive supranuclear palsy'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Progressive supranuclear palsy"

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Bartošová, Tereza, and Jiří Klempíř. "Progressive supranuclear palsy." Česká a slovenská neurologie a neurochirurgie 83/116, no. 6 (December 31, 2020): 584–601. http://dx.doi.org/10.48095/cccsnn2020584.

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Rajput, Alex, and Ali H. Rajput. "Progressive Supranuclear Palsy." Drugs & Aging 18, no. 12 (2001): 913–25. http://dx.doi.org/10.2165/00002512-200118120-00003.

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Fedorova, N. V., E. V. Bril, T. K. Kulua, and A. D. Mikhaylova. "Progressive supranuclear palsy." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 121, no. 5 (2021): 111. http://dx.doi.org/10.17116/jnevro2021121051111.

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Golbe, Lawrence. "Progressive Supranuclear Palsy." Seminars in Neurology 34, no. 02 (June 25, 2014): 151–59. http://dx.doi.org/10.1055/s-0034-1381736.

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Karceski, S. "Progressive supranuclear palsy." Neurology 71, no. 22 (November 24, 2008): e70-e72. http://dx.doi.org/10.1212/01.wnl.0000338599.69090.fb.

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LEECH, EDWARD E. "Progressive Supranuclear Palsy." American Journal of Nursing 99, no. 6 (June 1999): 24BBBB. http://dx.doi.org/10.1097/00000446-199906000-00037.

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Pourfar, M. "Progressive Supranuclear Palsy." Science of Aging Knowledge Environment 2004, no. 30 (July 28, 2004): dn1. http://dx.doi.org/10.1126/sageke.2004.30.dn1.

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Litvan, Irene. "PROGRESSIVE SUPRANUCLEAR PALSY." Neurologist 4, no. 1 (January 1998): 13–20. http://dx.doi.org/10.1097/00127893-199801000-00003.

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Kernich, Catherine Ann. "PROGRESSIVE SUPRANUCLEAR PALSY." Neurologist 5, no. 4 (July 1999): 229. http://dx.doi.org/10.1097/00127893-199907000-00007.

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Jankovic, Joseph, and Haydee Rohaidy. "Progressive Supranuclear Palsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (August 1987): 547–54. http://dx.doi.org/10.1017/s0317167100038099.

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ABSTRACT:Progressive supranuclear palsy (PSP) was first recognized as a distinct morbid entity by Richardson, Steele and Olszewski a quarter century ago. Subsequent experience has confirmed and extended their original observations. PSP has become familiar as a chronic progressive disorder with extrapyramidal rigidity, bradykinesia, gait impairment, bulbar palsy, dementia and a characteristic supranuclear ophthalmoplegia. It is an important cause of parkinsonism. Its etiology remains obscure. Familial concentrations have not been observed.Some cases exhibit no oculomotor dysfunction. Dementia is usually mild. Recent neuropsychological studies have defined features consistent with frontal lobe cortical dysfunction. Seizures and paroxysmal EEG activity may occur.CT and MRI scans show midbrain atrophy early and later atrophy of the pontine and midbrain tegmentum and the frontal and temporal lobes. PET scans have shown frontal hypometabolism and loss of striatal D-2 dopamine receptors. Postmortem studies have documented involvment of both dopaminergic and cholinergic systems. Treatment remains palliative and unsatisfactory.
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Dissertations / Theses on the topic "Progressive supranuclear palsy"

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Warren, Naomi M. "The cholinergic neurochemistry of progressive supranuclear palsy." Thesis, University of Newcastle upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432505.

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Ghosh, B. "The neurobiology of cognition in progressive supranuclear palsy." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599367.

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Social cognition has not been studied in PSP, despite its clinical importance with regard to patients’ progressive decline in independence and communication. This thesis focuses on the extent and neural basis of social cognition in PSP. Cognitive function was assessed in multiple domains including social cognition, executive function and perception, at baseline and after one year. At baseline, subjects underwent structural magnetic resonance imaging and saccadometry. Patients were poor at both emotion recognition and theory of mind tasks in visual and auditory modalities, compared with matched controls. Social cognition correlated with global cognitive decline but was not attributable to perceptual disturbance and was independent if executive function. The latency of visually evoked saccades correlated with global and social cognitive performance. Regression analysis revealed latency as the best predictor of cognitive function, above disease duration and motor function. Voxel based morphometry of grey and white matter confirms that areas previously implicated in social cognition were atrophic in PSP. Moreover, this atrophy correlated with social cognition dysfunction, implying a functional association. In summary, social cognition is an integral part of the cognitive syndrome of PSP, and is associated with focal atrophy of regions associated with normal social cognition.
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Williams, D. "Clinical, pathological and biochemical diversity in progressive supranuclear palsy." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445185/.

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This thesis examines the clinical, pathological and biochemical diversity of progressive supranuclear palsy (PSP). The material and patients used for these studies involved 23 clinically diagnosed living patients and 127 pathologically confirmed cases of PSP, archived at the Queen Square Brain Bank (QSBB). Differences between 'classic' PSP and 'atypical' PSP were identified, and a number of clinical features that separate them from other bradykinetic rigid syndromes were explored. In addition to the clinical phenotype associated with PSP-tau pathology initially described by Richardson in 1963 (Richardson's syndrome, RS) two other distinct clinical syndromes were identified: PSP-Parkinsonism (PSP-P) and pure akinesia with gait freezing (PAGF). The following clinical features, in addition to the operational diagnostic criteria, were supportive of underlying PSP-tau pathology in patients presenting with Parkinsonism: an absence of drug induced dyskinesias, autonomic failure and visual hallucinations the presence of falls within 6 years of disease onset UPSIT scores above the 12th percentile for gender and age and abnormalities in auditory startle response and auditory blink reflex. PSP-tau pathology always involved the subthalamic nucleus (STN), globus pallidus (GP) and substantia nigra (SN), but involvement outside these structures was variable and could be sub-divided into at least three different patterns. Severe tau pathology in PSP-P and PAGF was restricted to the GP, STN and SN. Co-existent pathological diagnoses did not differ between RS, PSP-P and PAGF. The ratio of pathological 4-repeat:3-repeat tau in PSP was variable. In RS the mean ratio was higher than in PSP-P (2.84 vs. 1.63 (p<0.003). Mutations of MAPT did not account for the diversity of clinical features The proposed clinical and pathological sub-classification of PSP will be helpful in clinical practice. Pathological and biochemical correlates raise the possibility that PSP-P and PAGF may represent discrete nosological entities. Further research may ultimately lead to their absolute distinction from Richardson's syndrome and related tauopathies.
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Nath, Uma. "The epidemiology of progressive supranuclear palsy in the United Kingdom." Thesis, University of Newcastle upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247847.

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Schofield, Emma Medical Sciences Faculty of Medicine UNSW. "Characterisation of cortical pathology and clinicopathological correlates in progressive supranuclear palsy." Awarded by:University of New South Wales. School of Medical Sciences, 2006. http://handle.unsw.edu.au/1959.4/27326.

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This thesis characterises the cortical pattern of degeneration in progressive supranuclear palsy (PSP) and its consequences. Global atrophy was first examined using a recently developed staging scheme in pathologically-proven PSP cases compared with other tauopathies: gross atrophy was not observed in PSP. Quantification of regional volume loss throughout the brain was then used to determine the magnitude of more focal tissue atrophy in PSP, cortical dysfunction was investigated by measuring cerebral blood flow (CBF) changes, and several cortical cellular pathologies were analysed. Any changes observed were related to each other and clinical assessments of motor, cognitive and behavioural abnormalities. At mid-stage PSP, frontal and subcortical atrophy related to decreased CBF in the frontal cortex and cognitive decline. Parietocerebellar CBF increases were also identified (related to frontal CBF deficits) and related to motor and non-motor deficits. By end-stage PSP, focal atrophy had advanced from frontal and subcortical structures to include atrophy in the parietal lobe. Parietal lobe atrophy related to behavioural abnormalities. Histopathological analysis at end-stage revealed that the cortical atrophy and cell loss does not relate to tau deposition. The focal cortical cell loss related exclusively to motor deficits whilst the more widespread cortical tau deposition related to cognitive and behavioural impairments. Both the tau deposition and these non-motor impairments increased in severity over time. The results show that frontal atrophy and dysfunction occurs rapidly and early in PSP and relate to increasing cognitive deficits. Such deficits appear to cause compensatory CBF enhancement in parietocerebellar regions which then also undergo rapid and severe neurodegeneration. These later changes occur in concert with the more classic PSP symptoms, such as oculomotor features. Throughout the disease, the progressive increase in frontotemporal tau deposition contributes to cognitive and behavioural deficits which become most marked late in the disease. The findings strongly suggest that progressive clinical dysfunction in PSP is directly related to progressive cortical degeneration. Cortical degeneration appears to occur in two independent functional networks. Increased CBF in PSP may be a useful early indicator for future neurodegeneration, although the cellular mechanism leading to cell death requires further investigation.
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Takahashi, Makio. "Morphological and biochemical correlations of abnormal tau filaments in progressive supranuclear palsy." Kyoto University, 2003. http://hdl.handle.net/2433/148680.

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Crawford, Linda Marie. "Behavioural features in people with progressive supranuclear palsy : a longitudinal, prospective, comparison study." Thesis, University of East Anglia, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426863.

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Paviour, Dominic Curtis. "A prospective clinico-radiological study of progressive supranuclear palsy using serial MRI with registration." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445004/.

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The purpose of this thesis is to investigate: whether cross sectional MRI can help to discriminate progressive supranuclear palsy (PSP), multiple system atrophy (Parkinsonian subtype, MSA-P) and Parkinson's disease (PD) whether established methods of serial volumetric MRI analysis can be applied to measure in-vivo rates of brain atrophy in PSP and whether cross sectional MRI and MRI-derived atrophy rates have a clinical correlate. Volumetric and diffusion-weighted MRI (DWI) scans were performed in 24 patients with PSP, 11 with MSA-P, 12 with PD and 18 healthy controls. Detailed clinical and neuropsychological assessments were undertaken, and results at the time of initial assessment and follow-up compared. Whole brain and regional brain volumes were measured on positionally matched (registered) baseline and follow up MR images. The boundary shift integral (BSI), an image analysis technique for assessing volume differences from registered MR scans was applied to whole brain, and hypothesis-driven regions of interest in order to allow quantification of atrophy rates. PSP can be reliably discriminated from MSA-P with quantitative regional volume measurements of the superior cerebellar peduncle, midbrain, pons and cerebellum (p<0.001). DWI may help to identify regional pathological change in-vivo, discriminating MSA-P and PSP using apparent diffusion coefficients in the middle cerebellar peduncle (p0.001). The mean (SD) brain atrophy rate in PSP, 1.2 (1.0) %year_1 was greater than in healthy controls 0.4(0.5)%year"1 (p=0.04) but similar to MSA-P 1.0(l.l)%year'1. In PSP, the mean midbrain atrophy rate was most significantly different from controls (p<0.001). Ponto-cerebellar atrophy rates discriminated MSA-P and PSP (p<0.05). The distinct patterns and rates of atrophy in these diseases have a meaningful clinical correlate and power calculations confirm that in PSP, regional atrophy rates are quantifiable and feasible markers of disease progression that have utility in clinical trials as a marker for evaluating disease-modifying treatments in PSP.
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Baschieri, Francesca <1988&gt. "Circadian rhythms, sleep and autonomic function in progressive supranuclear palsy: characteristic features and reciprocal interactions." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2021. http://amsdottorato.unibo.it/9982/1/Baschieri_Francesca_tesi.pdf.

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Background: Progressive supranuclear palsy (PSP) is a rare neurodegenerative condition. The aims of this study were to evaluate the association between sleep, the circadian system and autonomic function in a cohort of PSP patients. Methods: Patients with PSP diagnosed according to consensus criteria were recruited prospectively and retrospectively and performed the following tests: body core temperature (BcT), sleep-wake cycle, systolic and diastolic blood pressure (SBP, DBP) continuous monitoring for 48 h under controlled environmental conditions; cardiovascular reflex tests (CRTs). The analysis of circadian rhythmicity was performed with the single cosinor method. For state-dependent analysis, the mean value of variables in each sleep stage was calculated as well as the difference to the value in wake. Results: PSP patients presented a reduced total duration of night sleep, with frequent and prolonged awakenings. During daytime, patients had very short naps, suggesting a state of profound sleep deprivation across the 24-h. REM sleep behaviour disorder was found in 15%, restless legs syndrome in 46%, periodic limb movements in 52% and obstructive sleep apnea in 54%. BcT presented the expected fall during night-time, however, compared to controls, mean values during day and night were higher. However BcT state-dependent modulation was maintained. Increased BcT could be attributed to an inability to properly reduce sympathetic activity favoured by the sleep deprivation. At CRTs, PSP presented mild cardiovascular adrenergic impairment and preserved cardiovagal function. 14% had non-neurogenic orthostatic hypotension. Only 2 PSP presented the expected BP dipping pattern, possibly as a consequence of sleep disruption. State-dependent analysis showed a partial loss of the state-dependent modulation for SBP. Discussion: This study showed that PSP presented abnormalities of sleep, circadian rhythms and cardiovascular autonomic function that are likely to be closely linked one to another.
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Rittman, Timothy. "Connectivity biomarkers in neurodegenerative tauopathies." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/248866.

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The primary tauopathies are a group of neurodegenerative diseases affecting movement and cognition. In this thesis I study Progressive Supranuclear Palsy (PSP) and the Corticobasal Syndrome (CBS), two parkinsonian disorders associated with accumulation of hyperphos- phorylated and abnormally folded tau protein. I contrast these two disorders with Parkinson’s disease (PD), which is associated with the accumulation of alpha-synuclein but has a genetic association with the MAPT gene encoding tau. Understanding the tauopathies to develop effective treatments will require a better grasp of the relationships between clinical syndromes and cognitive measures and how the anatomical and neurochemical networks that underlie clinical features might be altered by disease. I investigate simple clinical biomarkers, showing that a two-minute test of verbal fluency is a potential diagnostic biomarker to distinguish between PD and PSP and that the ACE-R and its subscores could play a role in monitoring cognition over time in PD, PSP and CBS. I assess the implementation of network analysis in Functional Mag- netic Resonance Imaging (fMRI) data, introduce Maybrain software for graphical network analysis and visualisation. I go on to show an overlap between graph theory network measures and I identify three main factors underlying graph network measures of: efficiency and distance, hub characteristics, network community measures. I apply these measures in PD, PSP and the CBS. All three diseases caused a loss of functional connectivity in com- parison to the control group that was concentrated in more highly connected brain regions and in longer distance connections. In ad- dition, widely localised cognitive function of verbal fluency co-varied with the connection strength in highly connected regions across PD, PSP and CBS. To take this further, I investigated specific functional covariance networks. All three disease groups showed reduced connectivity between the basal ganglia network and other networks, and between the anterior salience network and other networks. Localised areas of increased co- variance suggest a breakdown of network boundaries which correlated with motor severity in PSP and CBS, and duration of disease in CBS. I explore the link between gene expression of the tau gene MAPT and its effects on functional connectivity showing that the expression of MAPT correlated with connection strength in highly connected hub regions that were more susceptible to a loss of connection strength in PD and PSP. I conclude by discussing how tau protein aggregates and soluble tau oligomers may explain the changes in functional brain networks. The primary tauopathies are a group of neurodegenerative diseases affecting movement and cognition. In this thesis I study Progressive Supranuclear Palsy (PSP) and the Corticobasal Syndrome (CBS), two parkinsonian disorders associated with accumulation of hyperphos- phorylated and abnormally folded tau protein. I contrast these two disorders with Parkinson’s disease (PD), which is associated with the accumulation of alpha-synuclein but has a genetic association with the MAPT gene encoding tau. Understanding the tauopathies to develop effective treatments will require a better grasp of the relationships between clinical syndromes and cognitive measures and how the anatomical and neurochemical networks that underlie clinical features might be altered by disease. I investigate simple clinical biomarkers, showing that a two-minute test of verbal fluency is a potential diagnostic biomarker to distinguish between PD and PSP and that the ACE-R and its subscores could play a role in monitoring cognition over time in PD, PSP and CBS. I assess the implementation of network analysis in Functional Mag- netic Resonance Imaging (fMRI) data, introduce Maybrain software for graphical network analysis and visualisation. I go on to show an overlap between graph theory network measures and I identify three main factors underlying graph network measures of: efficiency and distance, hub characteristics, network community measures. I apply these measures in PD, PSP and the CBS. All three diseases caused a loss of functional connectivity in com- parison to the control group that was concentrated in more highly connected brain regions and in longer distance connections. In ad- dition, widely localised cognitive function of verbal fluency co-varied with the connection strength in highly connected regions across PD, PSP and CBS. To take this further, I investigated specific functional covariance networks. All three disease groups showed reduced connectivity between the basal ganglia network and other networks, and between the anterior salience network and other networks. Localised areas of increased co- variance suggest a breakdown of network boundaries which correlated with motor severity in PSP and CBS, and duration of disease in CBS. I explore the link between gene expression of the tau gene MAPT and its effects on functional connectivity showing that the expression of MAPT correlated with connection strength in highly connected hub regions that were more susceptible to a loss of connection strength in PD and PSP. I conclude by discussing how tau protein aggregates and soluble tau oligomers may explain the changes in functional brain networks.
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Books on the topic "Progressive supranuclear palsy"

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National Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison, ed. Parálisis supranuclear progresiva. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Neurological Disorders and Stroke, 2000.

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Adolfo, Brusa, and Peloso Paolo Francesco, eds. Introduction to Progressive Supranuclear Palsy: Steele-Richardson-Olszowski Syndrome. Rome: Libbey, 1993.

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Irene, Litvan, and Agid Yves, eds. Progressive supranuclear palsy: Clinical and research approaches. New York: Oxford University Press, 1992.

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Eduardo, Tolosa, Duvoisin Roger C. 1927-, and Cruz-Sánchez F. F, eds. Progressive supranuclear palsy: Diagnosis, pathology, and therapy. Wien: Springer-Verlag, 1994.

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Tolosa, E., R. Duvoisin, and F. F. Cruz-Sánchez, eds. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-6641-3.

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Parker, James N., and Philip M. Parker. The official patient's sourcebook on progressive supranuclear palsy. Edited by Icon Group International Inc. San Diego, Calif: Icon Health Publications, 2002.

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National Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison., ed. Parálisis supranuclear progresiva. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Neurological Disorders and Stroke, 2000.

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Clagett, Rita. Killing Mother: Progressive Supranuclear Palsy. Independently Published, 2011.

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Killing Mother: Progressive Supranuclear Palsy. Llumina Press, 2011.

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Progressive supranuclear palsy: Diagnosis, pathology, and therapy. Wien: Springer-Verlag, 1994.

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Book chapters on the topic "Progressive supranuclear palsy"

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Stamelou, Maria, and Wolfgang H. Oertel. "Progressive Supranuclear Palsy." In Movement Disorders Curricula, 193–202. Vienna: Springer Vienna, 2017. http://dx.doi.org/10.1007/978-3-7091-1628-9_18.

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Morris, Huw R. "Progressive Supranuclear Palsy." In Neurodegeneration, 72–82. Oxford, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118661895.ch8.

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Shen, Kevin, Sumayya J. Almarzouqi, and Andrew G. Lee. "Progressive Supranuclear Palsy." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_1302-1.

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Tröster, Alexander I. "Progressive Supranuclear Palsy." In Encyclopedia of Clinical Neuropsychology, 2840–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_522.

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Bhidayasiri, Roongroj, and Daniel Tarsy. "Progressive Supranuclear Palsy." In Current Clinical Neurology, 32–33. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60327-426-5_16.

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Tröster, Alexander I. "Progressive Supranuclear Palsy." In Encyclopedia of Clinical Neuropsychology, 1–4. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_522-3.

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Shen, Kevin, Sumayya J. Almarzouqi, and Andrew G. Lee. "Progressive Supranuclear Palsy." In Encyclopedia of Ophthalmology, 1448–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1302.

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Stacy, Mark. "Progressive Supranuclear Palsy." In Parkinson’s Disease and Movement Disorders, 229–34. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-410-8_16.

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Anderson, Robert M. "Progressive Supranuclear Palsy." In Critical Issues in Neuropsychology, 290–92. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2480-9_44.

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Litvan, Irene. "Progressive Supranuclear Palsy." In Atypical Parkinsonian Disorders, 287–308. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:287.

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Conference papers on the topic "Progressive supranuclear palsy"

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Souza, Leonardo de, Maxime Bertoux, Luciano Mariano, Elisa Resende, Antônio Lúcio Teixeira, Francisco Cardoso, Sarah Camargos, Vítor Tumas, and Paulo Caramelli. "MENTALIZING IN FRONTOTEMPORAL DEMENTIA AND PROGRESSIVE SUPRANUCLEAR PALSY." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda015.

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Background: Mentalizing and emotion recognition are impaired in behavioral variant frontotemporal dementia (bvFTD). It is not clear whether these abilities are disturbed in progressive supranuclear palsy (PSP). Objective: To investigate social cognition (SC) between bvFTD and PSP. The neural basis of SC in PSP and bvFTD groups were also investigated by neuroimaging. Methods: Data from the notification sheet were collected and patients were classified according to current clinical and pathological criteria. Results: Groups did not differ on age, schooling and sex. Compared to controls, bvFTD and PSP patients had reduced scores in all tests of SC. bvFTD and PSP did not differ on measures of SC. PSP and bvFTD had cerebral atrophy in critical regions for SC. The cortical correlates of emotion recognition overlapped in bvFTD and PSP, correlating with frontal medial cortex, insula and limbic structures. PSP and bvFTD patients also displayed similar patterns of brain correlations (anterior temporal lobes) for social norms. The neural correlates of mentalizing were associated with frontal and temporal poles bilaterally, in both bvFTD and PSP. Conclusion:PSP patients exhibit impairment in mentalizing. PSP and bvFTD share clinical, cognitive and neuroimaging features.
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Pirtošek, Zvezdan. "Dementia in progressive supranuclear palsy and corticobasal syndrome." In Rijeka Forum on Neurodegenerative Diseases (2 ; 2018 ; Rijeka). Hrvatska akademija znanosti i umjetnosti, 2019. http://dx.doi.org/10.21857/ydkx2crex9.

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Macedo, Arthur Cassa, Luciano Inácio, Mariano Elisa De Paula França Resende, Antônio Lúcio Teixeira Júnior, Sarah Teixeira Camargos, Francisco Eduardo Costa Cardoso, Paulo Caramelli, and Leonardo Cruz De Souza. "EPISODIC MEMORY IMPAIRMENT IN PROGRESSIVE SUPRANUCLEAR PALSY (PSP): A NEUROIMAGING INVESTIGATION." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda016.

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Background: Progressive supranuclear palsy (PSP) has been classically considered a “subcortical dementia” with a frontal pattern of cognitive decline, but episodic memory dysfunction also occurs in most patients. However, it remains uncertain whether this is due to executive dysfunction or to the involvement of key brain areas responsible for memory processes. Objective: We aim to identify the specific brain regions underlying episodic memory impairment in PSP. Methods: In this cross-sectional study, we included 21 patients with PSP and 20 healthy controls matched for age, sex, and schooling. Participants underwent the Brief Cognitive Battery (BCB, including the Figures Test for episodic memory) and had brain MRI. Both standard exploratory voxel‐based morphometry and region of interest analyses were performed with FSL software. Results: Compared to controls, PSP patients performed worse (p < 0.001) on the BCB (delayed recall). Adjusting for both age and Frontal Assessment Battery scores, neuroimaging analyses of the correlation between delayed recall (5 minutes) and grey matter volumes yielded significant clusters on medial temporal structures, including the hippocampus, entorhinal cortex, and parahippocampal gyrus (FWE, p < 0.05). Conclusion: Our results suggest that atrophy of medial temporal structures may play a role in episodic memory impairment in PSP, indicating that amnesia in PSP is not due to executive dysfunction.
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Hlavnička, Jan, Tereza Tykalová, Roman Čmejla, Jiří Klempíř, Evžen Růžička, and Jan Rusz. "Dysprosody Differentiate Between Parkinson’s Disease, Progressive Supranuclear Palsy, and Multiple System Atrophy." In Interspeech 2017. ISCA: ISCA, 2017. http://dx.doi.org/10.21437/interspeech.2017-762.

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Gerbis, Natasha, Ariadna Fontes-Villalba, Patrick Aouad, Suran Fernando, and John DE Parratt. "116 Paraneoplastic progressive-supranuclear palsy like brainstem syndrome associated with lung adenocarcinoma." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.116.

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Mariano, Luciano, Leonardo de Souza, Paulo Caramelli, Antonio Teixeira Júnior, Henrique Guimarães, Elisa Resende, Leandro Gambogi, Vítor Tumas, Francisco Cardoso, and Sarah Camargos. "APATHY IN FRONTOTEMPORAL DEMENTIA AND PROGRESSIVE SUPRANUCLEAR PALSY: AN EXPLORATORY NEUROIMAGING INVESTIGATION." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda018.

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Abstract:
Background: Apathy is a multidimensional syndrome that impairs motivation and mechanisms of behavioural regulation. As apathy is almost ubiquitous in neurodegenerative disorders, understanding the neural basis is required to expand knowledge and ameliorate our instruments. Objective: Verify the feasibility, safety, and adherence of a remote physical and cognitive exercise protocol for elders; and to compare two different protocols and its effects on strength, cognitive functions and well-being. Methods: Use of the PICO strategy, conducted on September 17, on PubMed using “Alzheimer disease” and “diabetes mellitus” as descriptors, identifying 14 articles, selecting 4 after screening. Inclusion criteria: clinical and randomized controlled trials with diabetic and Alzheimer patients, published on the last 5 years. Exclusion criteria: articles focused on medications. Results: Overall adherence to the proposed sessions was 82,36% (sd16,8) in IG and 76,5% (sd24,04) in CG. There were no serious adverse events or drop-outs during the study. There was an improvement in strength and verbal fluency for IG and GDS for both groups (p ≤ 0,05). Conclusion: Both protocols seem a feasible program, reaching an acceptable level of adherence and safety. The technology used can represent a sustainable path for large scale use to promote aging active in developing countries.
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Brendel, M., H. Barthel, T. van Eimeren, K. Marek, L. Beyer, M. Song, J. Sauerbeck, et al. "18 F-PI2620 Tau-PET in Progressive Supranuclear Palsy – A Multi-Center Evaluation." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708120.

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Hoddell, Kate, Laura Dewhirst, and Derek Willis. "136 Care of patients with progressive supranuclear palsy in the hospice setting: an audit." In The APM’s Annual Supportive and Palliative Care Conference, In association with the Palliative Care Congress, “Towards evidence based compassionate care”, Bournemouth International Centre, 15–16 March 2018. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/bmjspcare-2018-aspabstracts.163.

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Aghakhanyan, G., M. Rullmann, J. J. Rumpf, M. L. Schroeter, C. Scherlach, M. Patt, M. Brendel, et al. "Tau network topology in progressive supranuclear palsy variants as elucidated by [18F]PI-2620 PET." In 60. Jahrestagung der Deutschen Gesellschaft für Nuklearmedizin. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1746010.

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Talai, Sahand, Kai Boelmans, Jan Sedlacik, and Nils D. Forkert. "Automatic classification of patients with idiopathic Parkinson's disease and progressive supranuclear palsy using diffusion MRI datasets." In SPIE Medical Imaging, edited by Samuel G. Armato and Nicholas A. Petrick. SPIE, 2017. http://dx.doi.org/10.1117/12.2254418.

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