BAG-1M is up-regulated in hippocampus of Alzheimer's disease patients and associates with tau and APP proteins

Evan Elliott, Offir Laufer, Irith Ginzburg

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

The accumulation of tau and amyloid beta proteins is the major molecular pathology of Alzheimer's disease (AD). The mechanisms leading to the accumulation of these proteins are not completely clear. Hsc-70/Hsp-70, a chaperone protein, has been shown to bind both these proteins and regulate their degradation. We have previously shown that the co-chaperone protein BAG-1 can inhibit the degradation of tau by forming a complex with Hsc-70 and tau. In this current work, we show that there is an increase in the BAG-1M isoform in the hippocampus of AD patients. In addition, BAG-1 binds to both tau and amyloid precursor protein physically, and is found highly expressed in the same neurons that contain intracellular tau or amyloid in hippocampal sections from AD patients. Over-expression of BAG-1M in cell culture also induced an increase in both tau and amyloid precursor protein levels. In conclusion, we report a specific increase of BAG-1M in human AD patients, which is both physically and functionally associated to the two major molecular markers of AD.

Original languageEnglish
Pages (from-to)1168-1178
Number of pages11
JournalJournal of Neurochemistry
Volume109
Issue number4
DOIs
StatePublished - May 2009
Externally publishedYes

Keywords

  • APP
  • Alzheimer's disease
  • BAG-1
  • Chaperones
  • Tau

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