Laura J Blair
Principal Investigator (NIH-funded) · BIOCHEMISTRY · USF
Affiliated program: Neuroscience PhD
This profile was assembled automatically from NIH RePORTER award records. Department and program affiliations are inferred and may be out of date — confirm on the university website.
Funding summary
- Active NIH grants
- 4
- Total NIH funding
- $2.1M
- Award records
- 4
Research topics
Matched from this investigator's NIH project titles and abstracts.
Active NIH awards
The hsp90 Cochaperone FKBP51 Regulates tau Structure and Function
5R01NS073899-13NINDS · FY 2025 · $679K
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.
The hsp90 Cochaperone FKBP51 Regulates tau Structure and Function
3R01NS073899-12S1NINDS · FY 2025 · $14K
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.
The hsp90 Cochaperone FKBP51 Regulates tau Structure and Function
5R01NS073899-12NINDS · FY 2024 · $712K
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.
The hsp90 Cochaperone FKBP51 Regulates tau Structure and Function
2R01NS073899-11NINDS · FY 2023 · $722K
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.