The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
Keith A Josephs - One of the best experts on this subject based on the ideXlab platform.
-
Utility of the Movement Disorders Society Criteria for Progressive Supranuclear Palsy in Clinical Practice.
Movement Disorders Clinical Practice, 2019Co-Authors: Hugo Botha, Jennifer L. Whitwell, Keith A JosephsAbstract:Objectives: When the 2017 Movement Disorders Society Criteria for Progressive Supranuclear Palsy is applied, patients may appear to have multiple phenotypes. The maximum allocation extinction rules were developed to provide a consistent method for applying the criteria and reaching a single diagnostic label. In this study, we apply both to a neuropathologic cohort of Progressive Supranuclear Palsy and other parkinsonian conditions. Methods: An autopsy cohort of 54 patients with Progressive Supranuclear Palsy and 56 patients with other neuropathologic diseases was selected. Clinical data were retrospectively abstracted, and the diagnostic criteria for Progressive Supranuclear Palsy were applied. All possible phenotypes applicable were listed and maximum allocation extinction rules were applied to assess reduction in the number of phenotypes ascribed per patient. Results: In the Progressive Supranuclear Palsy group, 52 patients met the criteria for multiple phenotypes, with an average of 7 phenotypes per patient. In the nonProgressive Supranuclear Palsy group, all 56 patients had features of more than one phenotype, up to 3 per patient. After application of maximum allocation extinction rules, the majority of the patients in both groups had a single predominant phenotype. Freezing of gait, Supranuclear gaze Palsy, and frontal behavioral syndrome were more common in the Progressive Supranuclear Palsy group. Conclusions: The diagnostic criteria for Progressive Supranuclear Palsy identify many clinical features, thereby leading to assignment of multiple phenotypes per patient. We demonstrate that the maximum allocation extinction rules can effectively lead to a single consensus phenotype, maintaining a uniform diagnostic label for clinical and research applications.
-
Cognitive impairment in Progressive Supranuclear Palsy is associated with tau burden.
Movement Disorders, 2017Co-Authors: Shunsuke Koga, Keith A Josephs, Ryan J. Uitti, Monica Sanchez-contreras, Adam Parks, Koji Kasanuki, Matthew C. Baker, J. Eric Ahlskog, Neill R. Graff-radford, Jay A. Van GerpenAbstract:Background Cognitive impairment is one of the core features of Progressive Supranuclear Palsy. This study aimed to clarify the profile of cognitive impairment and its underlying pathology in Progressive Supranuclear Palsy. Methods We retrospectively reviewed medical records to evaluate the pattern and severity of cognitive impairment in 121 autopsy-confirmed Progressive Supranuclear Palsy patients. A subset of 37 patients underwent neuropsychological evaluation as part of their clinical workup. The burden of Progressive Supranuclear Palsy-related tau pathology (neurofibrillary tangles/pretangles, coiled bodies, tufted astrocytes, and threads) was semiquantitatively scored in 20 vulnerable brain regions. Concurrent pathologies potentially associated with cognitive impairment, such as Alzheimer's-type pathology, were also assessed. To evaluate possible genetic risk factors for cognitive impairment, genetic analysis for APOE and MAPT was performed. Results Ninety patients (74%) had documented cognitive impairment based on neurologic evaluation. In a subgroup with neuropsychological testing (n = 37), executive functioning was the most severely impaired cognitive domain. A global cognitive impairment index (Spearman's rho, −0.49; P = 0.005) and executive functioning were negatively correlated with total tau burden (Spearman's rho, −0.51; P = 0.003), but not correlated with the Alzheimer's-type pathology. APOE ɛ4 carriers had more severe amyloid pathology, but total tau burden and a global cognitive impairment index did not differ from APOE ɛ4 noncarriers. Conclusion Cognitive impairment in Progressive Supranuclear Palsy, most notably executive dysfunction, is associated with severity of Progressive Supranuclear Palsy-related tau pathology. © 2017 International Parkinson and Movement Disorder Society
-
18f av 1451 tau positron emission tomography in Progressive Supranuclear Palsy
Movement Disorders, 2017Co-Authors: Jennifer L. Whitwell, Clifford R. Jack, Val J Lowe, Nirubol Tosakulwong, Stephen D Weigand, Matthew L Senjem, Christopher G Schwarz, Anthony J Spychalla, Ronald C Petersen, Keith A JosephsAbstract:Background The [18 F]AV-1451 positron emission tomography ligand allows the in vivo assessment of tau proteins in the brain. It shows strong binding in Alzheimer's dementia, but little is known about how it performs in Progressive Supranuclear Palsy, a primary 4R tauopathy. Objectives The objectives of this study were to determine whether [18 F]AV-1451 uptake can be observed in Progressive Supranuclear Palsy and to characterize the regional distribution when compared with controls and Alzheimer's dementia. Methods [18 F]AV-1451 positron emission tomography was performed in 10 patients with probable Progressive Supranuclear Palsy. These patients were age- and gender-matched to 50 controls and 10 Alzheimer's dementia patients who had undergone identical [18 F]AV-1451 imaging. Regional comparisons of [18 F]AV-1451 uptake were performed across the whole brain using region-of-interest and voxel-level analyses, and correlations between regional [18 F]AV-1451 and the Progressive Supranuclear Palsy rating scale were assessed. Results An elevated [18 F]AV-1451 signal was observed in Progressive Supranuclear Palsy when compared with controls in the pallidum, midbrain, dentate nucleus of the cerebellum, thalamus, caudate nucleus, and frontal regions. Signal in the cerebellar dentate and pallidum were also greater in Progressive Supranuclear Palsy when compared with Alzheimer's dementia. Conversely, the [18 F]AV-1451 signal across the cortex was higher in Alzheimer's dementia when compared with Progressive Supranuclear Palsy. The [18 F]AV-1451 signal in a number of regions correlated with the Progressive Supranuclear Palsy rating scale. Conclusions Progressive Supranuclear Palsy is associated with an elevated [18 F]AV-1451 signal in a characteristic and distinct regional pattern that correlates with disease severity and differs from the patterns observed in Alzheimer's dementia. © 2016 International Parkinson and Movement Disorder Society.
-
[18F]AV-1451 tau positron emission tomography in Progressive Supranuclear Palsy
Movement Disorders, 2016Co-Authors: Jennifer L. Whitwell, Clifford R. Jack, Val J Lowe, Nirubol Tosakulwong, Stephen D Weigand, Matthew L Senjem, Christopher G Schwarz, Anthony J Spychalla, Ronald C Petersen, Keith A JosephsAbstract:BACKGROUND: The [18 F]AV-1451 positron emission tomography ligand allows the in vivo assessment of tau proteins in the brain. It shows strong binding in Alzheimer's dementia, but little is known about how it performs in Progressive Supranuclear Palsy, a primary 4R tauopathy. OBJECTIVES: The objectives of this study were to determine whether [18 F]AV-1451 uptake can be observed in Progressive Supranuclear Palsy and to characterize the regional distribution when compared with controls and Alzheimer's dementia. METHODS: [18 F]AV-1451 positron emission tomography was performed in 10 patients with probable Progressive Supranuclear Palsy. These patients were age- and gender-matched to 50 controls and 10 Alzheimer's dementia patients who had undergone identical [18 F]AV-1451 imaging. Regional comparisons of [18 F]AV-1451 uptake were performed across the whole brain using region-of-interest and voxel-level analyses, and correlations between regional [18 F]AV-1451 and the Progressive Supranuclear Palsy rating scale were assessed. RESULTS: An elevated [18 F]AV-1451 signal was observed in Progressive Supranuclear Palsy when compared with controls in the pallidum, midbrain, dentate nucleus of the cerebellum, thalamus, caudate nucleus, and frontal regions. Signal in the cerebellar dentate and pallidum were also greater in Progressive Supranuclear Palsy when compared with Alzheimer's dementia. Conversely, the [18 F]AV-1451 signal across the cortex was higher in Alzheimer's dementia when compared with Progressive Supranuclear Palsy. The [18 F]AV-1451 signal in a number of regions correlated with the Progressive Supranuclear Palsy rating scale. CONCLUSIONS: Progressive Supranuclear Palsy is associated with an elevated [18 F]AV-1451 signal in a characteristic and distinct regional pattern that correlates with disease severity and differs from the patterns observed in Alzheimer's dementia. © 2016 International Parkinson and Movement Disorder Society.
-
Highly specific radiographic marker predates clinical diagnosis in Progressive Supranuclear Palsy.
Parkinsonism & Related Disorders, 2016Co-Authors: Emily Owens, Keith A Josephs, J. E. Ahlskog, Karl N. Krecke, Robert D. Fealey, Anhar Hassan, Bryan T. Klassen, Joseph Y. Matsumoto, James H. BowerAbstract:Abstract Introduction The diagnosis of Progressive Supranuclear Palsy is often challenging early in the course of the disease, when clinical signs of the condition may be less apparent and patients do not clearly meet diagnostic criteria. In this study, we examine a potential radiographic marker in Progressive Supranuclear Palsy, and assess the timing of its presence in relation to diagnosis. Methods A retrospective review of patients fulfilling clinical research criteria for multiple system atrophy, Parkinson's disease, and Progressive Supranuclear Palsy (total n = 75) was performed. Midbrain and pontine diameters, and the midbrain to pons ratio were calculated by a neuroradiologist blinded to the clinical diagnosis. The timing of the presence of a midbrain to pons ratio of less than or equal to 0.52 was assessed in the Progressive Supranuclear Palsy group in reference to the time of diagnosis. Results The midbrain to pons ratio was significantly reduced in the Progressive Supranuclear Palsy cohort (p Conclusions The midbrain to pons ratio is an easily applied and highly specific tool in the diagnosis of Progressive Supranuclear Palsy, and is frequently present before the diagnosis is made.
Y Agid - One of the best experts on this subject based on the ideXlab platform.
-
rem sleep behavior disorder and rem sleep without atonia in patients with Progressive Supranuclear Palsy
Sleep, 2005Co-Authors: Isabelle Arnulf, Marie Vidailhet, M Merinoandreu, Frederic Bloch, Eric Konofal, Valerie Cochen, J P Derenne, Y AgidAbstract:STUDY OBJECTIVE: To compare sleep characteristics, rapid eye movement (REM) sleep without atonia, and REM sleep behavior disorder (RBD) in patients with Progressive Supranuclear Palsy (tauopathy), patients with Parkinson's disease (a synucleinopathy), and control subjects. DESIGN: Sleep interview, overnight polysomnography, and Multiple Sleep Latency Tests. PATIENTS: Forty-five age- and sex-matched patients with probable Progressive Supranuclear Palsy, (n=15, aged 68 +/- 8 years, 7 men), patients with Parkinson disease (n=15), and control subjects (n=15). SETTINGS: Tertiary-care academic hospital. INTERVENTION: N/A. RESULTS: Compared to the 2 other groups, patients with Progressive Supranuclear Palsy had a longer duration of wakefulness after sleep onset and twice as much sleep fragmentation and percentage of stage 1 sleep but had similar apnea-hypopnea indexes, periodic leg movements indexes, and mean daytime sleep latencies. REM sleep percentage was as low in patients with Progressive Supranuclear Palsy (8% +/- 6% of total sleep time) as in patients with Parkinson disease (10% +/- 4%), versus 20% +/- 6% in controls (analysis of variance, P < .0001). Interestingly, patients with Progressive Supranuclear Palsy had percentages of REM sleep without atonia (chin muscle activity: 33% +/- 36% of REM sleep) similar to those of patients with Parkinson disease (28% +/- 35%) and dramatically higher than those of controls (0.5% +/- 1%, analysis of variance, P = .008). Four (27%) patients with Progressive Supranuclear Palsy had more than 50% REM sleep without atonia (as did a similar number of patients with Parkinson disease), and 2 of them (13%, vs 20% of patients with Parkinson disease) had clinical RBD. The four patients with Progressive Supranuclear Palsy with excessive daytime sleepiness slept longer at night than the 11 patients with Progressive Supranuclear Palsy who were alert (442 +/- 14 minutes vs 312 +/- 74 minutes, student t tests, P = .004), suggesting a primary nonnarcoleptic hypersomnia. CONCLUSION: REM sleep without atonia and RBD were as frequent in patients with Progressive Supranuclear Palsy as in patients with Parkinson disease. It suggests that the downstream cause of parkinsonism, rather than its primary neuropathology (synucleinopathy vs tauopathy), is a key factor for REM sleep behavior disorder.
Jennifer L. Whitwell - One of the best experts on this subject based on the ideXlab platform.
-
Utility of the Movement Disorders Society Criteria for Progressive Supranuclear Palsy in Clinical Practice.
Movement Disorders Clinical Practice, 2019Co-Authors: Hugo Botha, Jennifer L. Whitwell, Keith A JosephsAbstract:Objectives: When the 2017 Movement Disorders Society Criteria for Progressive Supranuclear Palsy is applied, patients may appear to have multiple phenotypes. The maximum allocation extinction rules were developed to provide a consistent method for applying the criteria and reaching a single diagnostic label. In this study, we apply both to a neuropathologic cohort of Progressive Supranuclear Palsy and other parkinsonian conditions. Methods: An autopsy cohort of 54 patients with Progressive Supranuclear Palsy and 56 patients with other neuropathologic diseases was selected. Clinical data were retrospectively abstracted, and the diagnostic criteria for Progressive Supranuclear Palsy were applied. All possible phenotypes applicable were listed and maximum allocation extinction rules were applied to assess reduction in the number of phenotypes ascribed per patient. Results: In the Progressive Supranuclear Palsy group, 52 patients met the criteria for multiple phenotypes, with an average of 7 phenotypes per patient. In the nonProgressive Supranuclear Palsy group, all 56 patients had features of more than one phenotype, up to 3 per patient. After application of maximum allocation extinction rules, the majority of the patients in both groups had a single predominant phenotype. Freezing of gait, Supranuclear gaze Palsy, and frontal behavioral syndrome were more common in the Progressive Supranuclear Palsy group. Conclusions: The diagnostic criteria for Progressive Supranuclear Palsy identify many clinical features, thereby leading to assignment of multiple phenotypes per patient. We demonstrate that the maximum allocation extinction rules can effectively lead to a single consensus phenotype, maintaining a uniform diagnostic label for clinical and research applications.
-
18f av 1451 tau positron emission tomography in Progressive Supranuclear Palsy
Movement Disorders, 2017Co-Authors: Jennifer L. Whitwell, Clifford R. Jack, Val J Lowe, Nirubol Tosakulwong, Stephen D Weigand, Matthew L Senjem, Christopher G Schwarz, Anthony J Spychalla, Ronald C Petersen, Keith A JosephsAbstract:Background The [18 F]AV-1451 positron emission tomography ligand allows the in vivo assessment of tau proteins in the brain. It shows strong binding in Alzheimer's dementia, but little is known about how it performs in Progressive Supranuclear Palsy, a primary 4R tauopathy. Objectives The objectives of this study were to determine whether [18 F]AV-1451 uptake can be observed in Progressive Supranuclear Palsy and to characterize the regional distribution when compared with controls and Alzheimer's dementia. Methods [18 F]AV-1451 positron emission tomography was performed in 10 patients with probable Progressive Supranuclear Palsy. These patients were age- and gender-matched to 50 controls and 10 Alzheimer's dementia patients who had undergone identical [18 F]AV-1451 imaging. Regional comparisons of [18 F]AV-1451 uptake were performed across the whole brain using region-of-interest and voxel-level analyses, and correlations between regional [18 F]AV-1451 and the Progressive Supranuclear Palsy rating scale were assessed. Results An elevated [18 F]AV-1451 signal was observed in Progressive Supranuclear Palsy when compared with controls in the pallidum, midbrain, dentate nucleus of the cerebellum, thalamus, caudate nucleus, and frontal regions. Signal in the cerebellar dentate and pallidum were also greater in Progressive Supranuclear Palsy when compared with Alzheimer's dementia. Conversely, the [18 F]AV-1451 signal across the cortex was higher in Alzheimer's dementia when compared with Progressive Supranuclear Palsy. The [18 F]AV-1451 signal in a number of regions correlated with the Progressive Supranuclear Palsy rating scale. Conclusions Progressive Supranuclear Palsy is associated with an elevated [18 F]AV-1451 signal in a characteristic and distinct regional pattern that correlates with disease severity and differs from the patterns observed in Alzheimer's dementia. © 2016 International Parkinson and Movement Disorder Society.
-
[18F]AV-1451 tau positron emission tomography in Progressive Supranuclear Palsy
Movement Disorders, 2016Co-Authors: Jennifer L. Whitwell, Clifford R. Jack, Val J Lowe, Nirubol Tosakulwong, Stephen D Weigand, Matthew L Senjem, Christopher G Schwarz, Anthony J Spychalla, Ronald C Petersen, Keith A JosephsAbstract:BACKGROUND: The [18 F]AV-1451 positron emission tomography ligand allows the in vivo assessment of tau proteins in the brain. It shows strong binding in Alzheimer's dementia, but little is known about how it performs in Progressive Supranuclear Palsy, a primary 4R tauopathy. OBJECTIVES: The objectives of this study were to determine whether [18 F]AV-1451 uptake can be observed in Progressive Supranuclear Palsy and to characterize the regional distribution when compared with controls and Alzheimer's dementia. METHODS: [18 F]AV-1451 positron emission tomography was performed in 10 patients with probable Progressive Supranuclear Palsy. These patients were age- and gender-matched to 50 controls and 10 Alzheimer's dementia patients who had undergone identical [18 F]AV-1451 imaging. Regional comparisons of [18 F]AV-1451 uptake were performed across the whole brain using region-of-interest and voxel-level analyses, and correlations between regional [18 F]AV-1451 and the Progressive Supranuclear Palsy rating scale were assessed. RESULTS: An elevated [18 F]AV-1451 signal was observed in Progressive Supranuclear Palsy when compared with controls in the pallidum, midbrain, dentate nucleus of the cerebellum, thalamus, caudate nucleus, and frontal regions. Signal in the cerebellar dentate and pallidum were also greater in Progressive Supranuclear Palsy when compared with Alzheimer's dementia. Conversely, the [18 F]AV-1451 signal across the cortex was higher in Alzheimer's dementia when compared with Progressive Supranuclear Palsy. The [18 F]AV-1451 signal in a number of regions correlated with the Progressive Supranuclear Palsy rating scale. CONCLUSIONS: Progressive Supranuclear Palsy is associated with an elevated [18 F]AV-1451 signal in a characteristic and distinct regional pattern that correlates with disease severity and differs from the patterns observed in Alzheimer's dementia. © 2016 International Parkinson and Movement Disorder Society.
-
Modeling trajectories of regional volume loss in Progressive Supranuclear Palsy.
Movement Disorders, 2013Co-Authors: Keith A Josephs, Jeffrey L. Gunter, Clifford R. Jack, Matthew L Senjem, Jayawant N. Mandrekar, Jennifer L. WhitwellAbstract:Progressive Supranuclear Palsy is a neurodegenerative disease with Progressive brain atrophy over time. It is unknown which specific brain regions decline over time, whether regional volume loss occurs in a linear fashion, and whether regional atrophy correlates with clinical decline over time in Progressive Supranuclear Palsy. Twenty-eight subjects meeting probable Progressive Supranuclear Palsy criteria were prospectively recruited and completed 96 MRI scans over 2 years. Mixed-effect models were utilized to determine which regions had significant atrophy over time and whether decline was linear or nonlinear. We assessed 13 regions across the brain, as well as whole-brain and ventricular volume. Regional trajectories were also correlated with change in clinical measures of executive function and gait and ocular motor impairment. A linear decline was observed in all frontal and temporal regions, the superior parietal lobe, the thalamus, the caudate nuclei, and the midbrain, as well as in the whole brain. Ventricular expansion was also linear. Nonlinear decline was observed for the caudal middle frontal lobe and globus pallidus. Rates of change in the superior frontal lobe, thalamus, and midbrain were beyond those expected in normal aging. Decline in frontal lobe volume and the midbrain area correlated best to decline in clinical measures. In Progressive Supranuclear Palsy, atrophy is occurring in multiple brain regions, particularly in those that have previously been implicated in the disease. Decline is mainly linear but can be nonlinear for some regions. The frontal lobe and midbrain seem to be playing the most significant roles in the Progressive worsening of clinical signs in Progressive Supranuclear Palsy. © 2013 Movement Disorder Society
-
Neuroimaging comparison of primary Progressive apraxia of speech and Progressive Supranuclear Palsy
European Journal of Neurology, 2012Co-Authors: Jennifer L. Whitwell, Jeffrey L. Gunter, Clifford R. Jack, Matthew L Senjem, Joseph R. Duffy, Edythe A. Strand, Mary M. Machulda, Kejal Kantarci, Scott D.z. Eggers, Keith A JosephsAbstract:Background—Primary Progressive apraxia of speech, a motor speech disorder of planning and programming is a tauopathy that has overlapping histological features with Progressive Supranuclear Palsy. We aimed to compare, for the first time, atrophy patterns, as well as white matter tract degeneration, between these two syndromes. Methods—Sixteen primary Progressive apraxia of speech subjects were age and gender-matched to 16 Progressive Supranuclear Palsy subjects and 20 controls. All subjects were prospectively recruited, underwent neurological and speech evaluations, and 3.0 Tesla magnetic resonance imaging. Grey and white matter atrophy was assessed using voxel-based morphometry and atlasbased parcellation, and white matter tract degeneration was assessed using diffusion tensor imaging. Results—All Progressive Supranuclear Palsy subjects had typical occulomotor/gait impairments but none had speech apraxia. Both syndromes showed grey matter loss in supplementary motor area, white matter loss in posterior frontal lobes and degeneration of the body of the corpus callosum. While lateral grey matter loss was focal, involving superior premotor cortex, in primary Progressive apraxia of speech, loss was less focal extending into prefrontal cortex in Progressive Supranuclear Palsy. Caudate volume loss and tract degeneration of superior cerebellar peduncles was also observed in Progressive Supranuclear Palsy. Interestingly, area of the midbrain was reduced in both syndromes compared to controls, although this was greater in Progressive Supranuclear Palsy.
Nigel Leigh - One of the best experts on this subject based on the ideXlab platform.
-
cognitive impairment in patients with multiple system atrophy and Progressive Supranuclear Palsy
Brain, 2010Co-Authors: Richard G Brown, Yves Agid, Lucette Lacomblez, Bernard Landwehrmeyer, Ingo Uttner, Bruno Dubois, Albert C Ludolph, Gilbert Bensimon, Christine Payan, Nigel LeighAbstract:This article reports the severity and profile of neuropsychological impairment on a prevalent cohort of patients with a clinical diagnosis of either multiple system atrophy (n = 372) or Progressive Supranuclear Palsy (n = 311) from the Neuroprotection and Natural History in Parkinson Plus Syndromes cohort. The Dementia Rating Scale and Frontal Assessment Battery were used to assess global cognition and executive dysfunction. For the Dementia Rating Scale impairment was observed in similar to 57% of the Progressive Supranuclear Palsy group and 20% of the multiple system atrophy group. In the former, impairment in a single cognitive domain was observed in 40%, with the same number showing impairment in multiple domains, while in the latter the figures were 28.6 and 13.5%, respectively. On the Frontal Assessment Battery, impairment was observed in 62.0% of patients with Progressive Supranuclear Palsy and 31.8% of those with multiple system atrophy. Although the Progressive Supranuclear Palsy group performed worse overall, the cognitive profiles of the two groups on the Dementia Rating Scale subscales were identical, with the main impairment of the Initiation and Perseveration subscale. The impaired patients in the two groups were largely indistinguishable, qualitatively and quantitatively. Impairment was associated with greater age and clinical disability in both groups and was evident even in the early stages (22% in multiple system atrophy and 50% in Progressive Supranuclear Palsy). Where a pathological diagnosis was available, the original clinical diagnosis was confirmed in the majority of cases, including those with significant cognitive impairment. The rate of impairment in those with a confirmed pathological diagnosis was comparable to that of the sample as a whole. These results demonstrate, in the largest prospectively recruited cohort of patients with Progressive Supranuclear Palsy and multiple system atrophy studied to date, the existence of a cognitive profile similar to that previously reported in idiopathic Parkinson's disease. The results indicate a high level of cognitive impairment associated with Progressive Supranuclear Palsy, but also point to comparable dysfunction in a substantial proportion of the patients with multiple system atrophy. Significant cognitive impairment appears consistent with a diagnosis of multiple system atrophy, even early in the disease, with important implications for diagnosis, research and management.
Sarah Coakeley - One of the best experts on this subject based on the ideXlab platform.
-
positron emission tomography imaging of tau pathology in Progressive Supranuclear Palsy
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Sarah Coakeley, Yuko Koshimori, Pablo Rusjan, Madeleine Harris, Christine Ghadery, Anthony E Lang, Alan A WilsonAbstract:Progressive Supranuclear Palsy is a rare form of atypical Parkinsonism that differs neuropathologically from other parkinsonian disorders. While many parkinsonian disorders such as Parkinson’s disease, Lewy body dementia, and multiple system atrophy are classified as synucleinopathies, Progressive Supranuclear Palsy is coined a tauopathy due to the aggregation of pathological tau in the brain. [18F]AV-1451 (also known as [18F]-T807) is a positron emission tomography radiotracer that binds to paired helical filaments of tau in Alzheimer’s disease. We investigated whether [18F]AV-1451 could be used as biomarker for the diagnosis and disease progression monitoring in Progressive Supranuclear Palsy. Six Progressive Supranuclear Palsy, six Parkinson’s disease, and 10 age-matched healthy controls were recruited. An anatomical MRI and a 90-min PET scan, using [18F]AV-1451, were acquired from all participants. The standardized uptake value ratio from 60 to 90 min post-injection was calculated in each region of in...
