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01.08.2005 | Regular Paper

Caspase-cleaved tau accumulation in neurodegenerative diseases associated with tau and α-synuclein pathology

verfasst von: Jodie Newman, Robert A. Rissman, Floyd Sarsoza, Ronald C. Kim, Malcolm Dick, David A. Bennett, Carl W. Cotman, Troy T. Rohn, Elizabeth Head

Erschienen in: Acta Neuropathologica | Ausgabe 2/2005

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Abstract

Alzheimer’s disease (AD), Pick’s disease (PiD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and dementia with Lewy bodies (DLB) are diseases associated with the accumulation of tau or α-synuclein. In AD, β-amyloid (Aβ)-associated caspase activation and cleavage of tau at Asp⁴²¹ (ΔTau) may be an early step in neurofibrillary tangle (NFT) formation. To examine whether ΔTau accumulates in other diseases not characterized by extracellular Aβ accumulation, we examined PiD, PSP, and CBD cases in comparison to those without extensive tau accumulation including frontotemporal lobar degeneration without Pick bodies (FTLD) and control cases. Additionally, we studied ΔTau accumulation in DLB cases associated with intracellular α-synuclein. ΔTau was observed in all disease cases except non-PiD FTLD and controls. These results demonstrate that the accumulation of ΔTau may represent a common pathway associated with abnormal accumulation of intracellular tau or α-synuclein and may be relatively less dependent on the extracellular accumulation of Aβ in non-AD dementias.

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Titel: Caspase-cleaved tau accumulation in neurodegenerative diseases associated with tau and α-synuclein pathology
verfasst von: Jodie Newman
Robert A. Rissman
Floyd Sarsoza
Ronald C. Kim
Malcolm Dick
David A. Bennett
Carl W. Cotman
Troy T. Rohn
Elizabeth Head
Publikationsdatum: 01.08.2005
Verlag: Springer-Verlag
Erschienen in: Acta Neuropathologica / Ausgabe 2/2005
Print ISSN: 0001-6322
Elektronische ISSN: 1432-0533
DOI: https://doi.org/10.1007/s00401-005-1027-3

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