Abstract

Transcellular propagation of tau aggregates may underlie the progression of pathology in Alzheimer's disease (AD) and other tauopathies. Braak staging (B1, B2, B3) is based on phospho-tau accumulation within connected brain regions: entorhinal cortex (B1); hippocampus/limbic system (B2); and frontal and parietal lobes (B3). We previously developed a specific and sensitive assay that uses flow cytometry to quantify tissue seeding activity based on fluorescence resonance energy transfer (FRET) in cells that stably express tau reporter proteins. In a tauopathy mouse model, we have detected seeding activity far in advance of histopathological changes. It remains unknown whether individuals with AD also develop seeding activity prior to accumulation of phospho-tau. We measured tau seeding activity across four brain regions (hippocampus, frontal lobe, parietal lobe, and cerebellum) in 104 fresh-frozen human AD brain samples from all Braak stages. We observed widespread seeding activity, notably in regions predicted to be free of phospho-tau deposition, and in detergent-insoluble fractions that lacked tau detectable by ELISA. Seeding activity correlated positively with Braak stage and negatively with MMSE. Our results are consistent with early transcellular propagation of tau seeds that triggers subsequent development of neuropathology. The FRET-based seeding assay may also complement standard neuropathological classification of tauopathies.

Document Type

Article

Publication Date

1-2017

Notes/Citation Information

Published in Acta Neuropathologica, v. 133, issue 1, p. 91-100.

© Springer-Verlag Berlin Heidelberg 2016

The copyright holder has granted the permission for posting the article here.

This is a post-peer-review, pre-copyedit version of an article published in Acta Neuropathologica. The final authenticated version is available online at: https://doi.org/10.1007/s00401-016-1644-z.

Digital Object Identifier (DOI)

https://doi.org/10.1007/s00401-016-1644-z

Funding Information

Studies were supported by the Tau Consortium (to M.I.D), Coins for Alzheimer’s Research Trust (to N.J.C), and NIH grants awarded to M.I.D. (R01AG048678), J.L.F. (1F32NS087805), C.L.W. (AG12300), N.J.C. (P50 AG005681 and P01 AG003991) and P.T.N. (AG028383).

Related Content

The online version of this article (doi: 10.1007/s00401-016-1644-z) contains supplementary material, which is available to authorized users.

401_2016_1644_MOESM1_ESM.pdf (55101 kB)
Supplemental Figure 1.

401_2016_1644_MOESM2_ESM.pdf (263 kB)
Supplemental Figure 2.

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