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Basic Science and Pathogenesis.

Skarleth Cardenas Romero1, Mei-Yu Lai2, Matthew J Rosene3

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|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Enhancing lysosomal depalmitoylation with a Palmitoyl protein thioesterase-1 (PPT1) mimetic reduced amyloid-beta (Aβ) generation in Alzheimer's Disease (AD) models. This approach shows promise for delaying AD pathology by restoring lysosomal function.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Amyloidogenic protein palmitoylation is linked to Alzheimer's Disease (AD) Aβ plaque formation.
  • Palmitoyl protein thioesterase-1 (PPT1) deficiency exacerbates Aβ plaque accumulation in 5xFAD mice.
  • The role of lysosomal depalmitoylation in AD pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the effect of enhancing lysosomal depalmitoylation on Aβ generation and accumulation in AD.
  • To evaluate a PPT1-mimetic compound for its therapeutic potential in AD models.

Main Methods:

  • Utilized induced pluripotent stem cell (iPSC)-derived neurons (iNs) with an AD-associated APP mutation.
  • Treated iNs and 5xFAD mice with a PPT1-mimetic (NtBuHa).
  • Assessed Aβ levels, APP expression, and lysosomal markers; performed RNA-seq and proteomics on mouse brain tissue.

Main Results:

  • NtBuHa treatment significantly reduced Aβ-40 levels and showed a trend toward decreased Aβ-42 in iNs.
  • APP and Rab7 expression decreased in NtBuHa-treated iNs.
  • AAV9-PPT1 administration improved survival in 5xFAD mice, and gene expression analysis indicated restoration of lysosomal degradation pathways.

Conclusions:

  • PPT1 activity plays a crucial role in delaying AD pathology.
  • Enhancing lysosomal depalmitoylation modulates gene and protein expression related to amyloidogenic pathways.
  • Activating autophagy/lysosomal processes via PPT1 offers a potential therapeutic strategy for AD.