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Developmental Changes in τ Phosphorylation: Fetal τ Is Transiently Phosphorylated in a Manner Similar to Paired Helical Filament‐τ Characteristic of Alzheimer's Disease
Abstract
Rat and human fetal brain τ were probed with a panel of monoclonal antibodies (tau‐1, AT8, 8D8, RT97, SMI31, SMI34) that distinguish between paired helical filament (PHF)‐τ of Alzheimer's disease and normal adult brain τ. These antibodies discriminate between normal and PHF‐τ because their epitopes are phosphorylated in PHF‐τ. Although only one molecular isoform of τ was shown to be expressed in fetal brain, two fetal τ species could be distinguished on sodium dodecyl sulfate‐polyacrylamide gel electrophoresis and the slower migrating species was recognized by all of the PHF‐τ‐specific antibodies. Moreover, this immunoreactivity was shown to be phosphorylation dependent. Our observations suggest that the abnormal phosphorylation of τ in Alzheimer's disease may be the result of reactivation of pathways governing the phosphorylation of τ in the developing brain.
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“Earlier work showed that fetal tau was highly phosphorylated during development, but the precise mechanisms and functions of this process are still unknown32,80–82.”
From Multi-omic phenotyping of MAPT V337M neurons reveals early changes in axonogenesis and tau phosphorylation (2026) · cites this paper as [80]
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Classification and basic pathology of Alzheimer disease
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Self-citationIncrease in Tau Pathology in P290S Mapt Knock-In Mice Crossed with App NL-G-F Mice
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Metadata
- Authors
- Brion, J., Smith, C., Couck, A., Gallo, J., & Anderton, B. H.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1993-12
- Volume
- 61
- Issue
- 6
- Pages
- 2071-2080
- ISSN
- 0022-3042
- 1471-4159
- Cited by
- 182
- References
- 4
- Language
- en
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