Spatial patterns of the tau pathology in progressive supranuclear palsy

Armstrong, Richard A.; Cairns, Nigel J.

doi:10.1007/s10072-012-1006-0

Cited by 28 publications

(19 citation statements)

References 44 publications

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“…Our findings, which are in keeping with those of neuropathological studies, indicate that neuronal and glial cell pathology are not spatially correlated [41]. Supporting previous observations, the results of the present study also indicate that GM and WM damage may develop concurrently, though independently, probably as a consequence of the varying distribution of the neurodegenerative processes, i.e., neurofibrillary tangles, oligodendroglial inclusions, and tufted astrocytes.…”

Section: Discussionsupporting

confidence: 92%

Neuroimaging evidence of gray and white matter damage and clinical correlates in progressive supranuclear palsy

et al. 2015

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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). Volumetric and DTI analyses were computed using SPM and FSL tools. 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. The neurodegenerative changes that occur in PSP involve both GM and WM structures and develop concurrently though independently. WM damage in PSP correlates with clinical scores of disease severity and cognitive impairment, thus providing further insight into the pathophysiology of the disease.

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Section: Discussionsupporting

confidence: 92%

Neuroimaging evidence of gray and white matter damage and clinical correlates in progressive supranuclear palsy

et al. 2015

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“…The localization of tau-containing astrocytes does not always match that of tau-containing neurons in tauopathies [14,19,28,76,[88][89][90][91][92]. Curiously, tufted astrocytes and astrocytic plaques are often located near the blood vessels [93], and perivascular distribution is overwhelming in a rare familial behavioral variant frontotemporal dementia associated with astrocyte-predominant tauopathy [87].…”

Section: Introductionmentioning

confidence: 99%

Astrogliopathy in Tauopathies

Ferrer

2018

Neuroglia

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Astrocytes are involved in many diseases of the central nervous system, not only as reactive cells to neuronal damage but also as primary actors in the pathological process. Astrogliopathy is a term used to designate the involvement of astrocytes as key elements in the pathogenesis and pathology of diseases and injuries of the central nervous system. Astrocytopathy is utilized to name non-reactive astrogliosis covering hypertrophy, atrophy and astroglial degeneration with loss of function in astrocytes and pathological remodeling, as well as senescent changes. Astrogliopathy and astrocytopathy are hallmarks of tauopathies-neurodegenerative diseases with abnormal hyper-phosphorylated tau aggregates in neurons and glial cells. The involvement of astrocytes covers different disease-specific types such as tufted astrocytes, astrocytic plaques, thorn-shaped astrocytes, granular/fuzzy astrocytes, ramified astrocytes and astrocytes with globular inclusions, as well as others which are unnamed but not uncommon in familial frontotemporal degeneration linked to mutations in the tau gene. Knowledge of molecular differences among tau-containing astrocytes is only beginning, and their distinct functional implications remain rather poorly understood. However, tau-containing astrocytes in certain conditions have deleterious effects on neuronal function and nervous system integrity. Moreover, recent studies have shown that tau-containing astrocytes obtained from human brain tauopathies have a capacity for abnormal tau seeding and spreading in wild type mice. Inclusive conceptions include a complex scenario involving neurons, glial cells and local environmental factors that potentiate each other and promote disease progression in tauopathies.

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“…2, 3, 6, 8, 15, 20, 22, 25 Straight filament NFTs, astrocytic plaques, and coiled bodies often accumulate in CBD in a clustered formation. 3, 16, 26 Asymmetrical frontal and parietal lobe atrophy is seen in CBD cases. 23, 27 Atrophy can also be seen in the thalamus, subthalamic nucleus, pallidum, dentate nucleus, and brainstem nuclei.…”

Section: Tau In Parkinsonismmentioning

confidence: 99%

“…The regional distribution of lesions is not clustered and generally presents as random dispersions. 16, 17 The majority of NFT tau pathology is situated in subcortical regions, primarily in the basal ganglia, with involvement specifically in the striatum, caudate, putamen, subthalamic nucleus, substantia nigra, and also dentate nucleus of the cerebellum. 16, 18, 19 …”

Section: Tau In Parkinsonismmentioning

confidence: 99%

Imaging tau pathology in Parkinsonisms

Coakeley

Strafella

2017

npj Parkinson's Disease

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The recent development of positron emission tomography radiotracers targeting pathological tau in vivo has led to numerous human trials. While investigations have primarily focused on the most common tauopathy, Alzheimer’s disease, it is imperative that testing also be performed in parkinsonian tauopathies, such as progressive supranuclear palsy, corticobasal degeneration, and frontotemporal dementia and parkinsonism linked to chromosome 17. Tau aggregates differ in isoforms and conformations across disorders, and as a result one radiotracer may not be appropriate for all tauopathies. In this review, we evaluate the preclinical and clinical reports of current tau radiotracers in parkinsonian disorders. These radiotracers include [18F]FDDNP, [11C]PBB3, [18F]THK-5317, [18F]THK-5351, and [18F]AV-1451 ([18F]T807). There are concerns of off-target binding with [18F]FDDNP and [11C]PBB3, which may increase the signal to noise ratio and thereby decrease the efficacy of these radiotracers. Testing in [18F]THK-5317, [18F]THK-5351, and [18F]AV-1451 has been performed in progressive supranuclear palsy, while [18F]THK-5317 and [18F]AV-1451 have also been tested in corticobasal degeneration patients. [18F]THK-5317 and [18F]THK-5351 have demonstrated binding in brain regions known to be afflicted with pathological tau; however, due to small sample sizes these studies should be replicated before concluding their appropriateness in parkinsonian tauopathies. [18F]AV-1451 has demonstrated mixed results in progressive supranuclear palsy patients and post-mortem analysis shows minimal to no binding to non-Alzheimer’s disease tauopathies brain slices.

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Spatial patterns of the tau pathology in progressive supranuclear palsy

Cited by 28 publications

References 44 publications

Neuroimaging evidence of gray and white matter damage and clinical correlates in progressive supranuclear palsy

Neuroimaging evidence of gray and white matter damage and clinical correlates in progressive supranuclear palsy

Astrogliopathy in Tauopathies

Imaging tau pathology in Parkinsonisms

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