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Concomitant Neuronal Tau Deposition and FKBP52 Decrease Is an Early Feature of Different Human and Experimental

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FKBP52 protein decreases in neurons in tauopathies like Alzheimer's disease (AD), suggesting a role in tau clearance. Restoring FKBP52 levels may offer a new therapeutic strategy for these neurodegenerative conditions.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Pathological tau proteins form neurofibrillary tangles in tauopathies such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal lobar degeneration (FTLD-Tau).
  • FKBP52 (FK506-binding protein 52) immunophilin interacts with tau and decreases in AD brain neurons, correlating with tau deposition.
  • FKBP52 co-localizes with autophagy-lysosomal markers and early pathological tau in AD neurons, indicating a potential role in autophagic tau clearance.

Purpose of the Study:

  • To investigate differences in neuronal FKBP52 expression and localization in AD, PSP, familial FTLD-Tau, and the hTau-P301S mouse model compared to controls.
  • To determine if FKBP52 levels and localization are altered in the early stages of tauopathy.

Main Methods:

  • Immunohistofluorescence analyses and quantification of FKBP52 in postmortem human brain samples from tauopathy patients.
  • Analysis of spinal cord samples from hTau-P301S mice.

Main Results:

  • A decrease in FKBP52 and its co-localization with early pathological tau forms within the neuronal autophagy-lysosomal pathway were observed in various tauopathies and in hTau-P301S mice.
  • FKBP52 reduction occurs early in the pathological process, evident in neurons with tau deposits in Braak IV AD brains and in asymptomatic young hTau-P301S mice.

Conclusions:

  • The findings suggest FKBP52 plays a role in cellular signaling and tau clearance.
  • Preventing FKBP52 decrease or restoring its expression at early pathological stages could be a novel therapeutic approach for tauopathies, including AD, FTLD-Tau, and PSP.