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Exploring the PLD1-tau interaction in Frontotemporal Dementia.

Chandramouli Natarajan1,2, Shaneilahi M Budhwani1,2, Sravan Gopalkrishna Shetty Sreenivasamurthy1

  • 1Mitchell Center for Neurodegenerative Diseases, Department of Neurology, University of Texas Medical Branch, Galveston, Texas, USA, 77555.

Biorxiv : the Preprint Server for Biology
|February 23, 2026
PubMed
Summary
This summary is machine-generated.

Phospholipase D1 (PLD1) contributes to synaptic deficits and tau pathology in frontotemporal dementia (FTD). Targeting PLD1 may offer a therapeutic strategy for FTD and related tauopathies.

Keywords:
Brodmann Area 38 (BA38, temporal cortex)Fluorescence-assisted single synaptosome long-term potentiation (FASS-LTP)Frontotemporal dementia (FTD)Human clinical postmortem samplesPhospholipase D1 (PLD1)Proteomics

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Area of Science:

  • Neuroscience
  • Biochemistry

Background:

  • Frontotemporal dementia (FTD) is a leading cause of young-onset dementia, characterized by cognitive decline and frontotemporal atrophy.
  • Tauopathy is present in nearly 40% of FTD cases, but the molecular mechanisms driving tau aggregation and synaptic dysfunction are not fully understood.

Purpose of the Study:

  • To investigate the role of Phospholipase D1 (PLD1) in FTD-associated tau pathology and synaptic deficits.
  • To explore PLD1's contribution to synaptic dysfunction in FTD, considering its implication in Alzheimer's disease and amyotrophic lateral sclerosis.

Main Methods:

  • Analysis of postmortem temporal and frontal cortices from FTD patients and controls.
  • Utilized fluorescence-assisted single synaptosome long-term potentiation (FASS-LTP), immunofluorescence, proximity ligation assays (PLA), and PLD1-interactome proteomics.
  • Examined PLD1 expression, co-localization with tau species and synaptic markers, and proteomic alterations in different cellular compartments.

Main Results:

  • FTD brains showed reduced glutamatergic potentiation and elevated PLD1 expression in specific cortical regions.
  • PLD1 co-localized significantly with pathological tau species (total, hyperphosphorylated, and acetylated tau oligomers) and synaptic markers.
  • Proteomic analysis revealed compartment-specific alterations, including impaired synaptic proteostasis and increased astroglial involvement, with protein redistribution from synapses to cytosol.

Conclusions:

  • PLD1 is a critical mediator of synaptic dysfunction and tau pathology in FTD.
  • PLD1 acts through astroglial activation and disrupts synaptic proteostasis, contributing to neurodegeneration.
  • PLD1 attenuation presents a potential therapeutic target for FTD and related tauopathies to restore synaptic integrity.