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Basic Science and Pathogenesis.

Jack Badman1, Bjorn Bakker1, Rajnish Kumar2

  • 1Karolinska Institutet, Solna, Sweden.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Deleting the signal peptidyl peptidase 2b (SPPL2b) gene reduced amyloid-beta pathology and synaptic loss in an Alzheimer's disease (AD) mouse model. This study identified potential SPPL2b inhibitors for AD therapy.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Signal peptidyl peptidase 2b (SPPL2b) is an intramembrane peptidase implicated in Alzheimer's disease (AD) pathophysiology.
  • SPPL2b cleaves transmembrane proteins such as APP, influencing amyloid-beta (Aβ) production.
  • Previous studies indicated SPPL2b inhibition reduces Aβ42 and Aβ40 production.

Purpose of the Study:

  • To explore the therapeutic potential of SPPL2b inhibition in AD.
  • To investigate the effects of SPPL2b gene deletion in an AD mouse model.
  • To identify potential SPPL2b inhibitory compounds through in silico screening.

Main Methods:

  • Generated a novel AD mouse model by crossing AppNL-G-F mice with SPPL2b-deficient mice.
  • Analyzed brain samples using western blotting, immunofluorescence, and Golgi staining.
  • Screened the Vitas-M commercial library to identify potential SPPL2b inhibitors.

Main Results:

  • SPPL2b knockout significantly reduced Aβ plaque deposition and gliosis in AD mice.
  • SPPL2b deletion protected against synaptic loss and decreased phospho-tau intensity.
  • Identified 100 potential SPPL2b inhibitory compounds.

Conclusions:

  • SPPL2b plays a critical role in AD Aβ pathology development.
  • SPPL2b is a promising therapeutic target for AD prevention and mitigation.
  • Identified compounds are undergoing evaluation for in vitro and in vivo efficacy.