# The hsp90 Cochaperone FKBP51 Regulates tau Structure and Function

> **NIH NIH R01** · UNIVERSITY OF SOUTH FLORIDA · 2024 · $711,953

## Abstract

Project Summary/Abstract
Neuropsychiatric symptoms (NPS), like depression, are common early in Alzheimer’s disease (AD) and correlate
with a faster decline in patients. NPS and cognitive deficits in AD have been linked with the accumulation of tau
protein. Two independent studies associated an allelic variant in the 51kDa FK506-binding protein (FKBP51)
with increased risk for depression in AD. FKBP51 also regulates tau accumulation and toxicity to nerve cells. We
will use transgenic mouse models to determine if either removing or inhibiting FKBP51 in mice will be protective
against tau accumulation. We will also study whether mice that have this risk variant in combination with tau
accumulation are more vulnerable to NPS. The critical knowledge gained through this work will add to our
understanding of the role of FKBP51 in regulating tau pathogenesis especially during disease progression. This
work will have a positive impact in AD research as we will further validate FKBP51 as a target and characterize
the molecular landscape associated with vulnerability to NPS in tauopathies.

## Key facts

- **NIH application ID:** 10792603
- **Project number:** 5R01NS073899-12
- **Recipient organization:** UNIVERSITY OF SOUTH FLORIDA
- **Principal Investigator:** Laura J Blair
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $711,953
- **Award type:** 5
- **Project period:** 2011-04-01 → 2028-02-29

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10792603

## Citation

> US National Institutes of Health, RePORTER application 10792603, The hsp90 Cochaperone FKBP51 Regulates tau Structure and Function (5R01NS073899-12). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10792603. Licensed CC0.

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