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Biological membranes show uneven distribution of different types of lipids in the inner and outer layers, resulting in transverse asymmetric membranes. The treatment of the erythrocyte membrane with the enzyme phospholipase confirmed the asymmetric nature of the lipid bilayer. The enzyme hydrolyzes lipids into fatty acids and hydrophilic groups. The phospholipase acts only on the outer layer of the membrane, while the inner layer remains intact. The phospholipase treatment resulted in 80%...
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Sphingosine-1-phosphate Decreases Erythrocyte Dysfunction Induced by β-Amyloid.

Francesco Misiti1, Pierluigi Diotaiuti1, Giovanni Enrico Lombardo2

  • 1Human Sciences, Social and Health Department, University of Cassino and Lazio Meridionale, V. S. Angelo, Loc. Folcara, 03043 Cassino, Italy.

International Journal of Molecular Sciences
|May 25, 2024
PubMed
Summary

Sphingosine-1-phosphate (S1P) protects red blood cells from amyloid beta (Aβ) damage in Alzheimer's disease. S1P restores ATP release and oxygen delivery, offering new therapeutic potential for AD.

Keywords:
Alzheimer’s diseasebeta-amyloidcaspase-3erythrocytesphingosine-1-phosphate

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Hematology

Background:

  • Amyloid beta (Aβ) peptides are key in Alzheimer's disease (AD) pathogenesis.
  • Soluble Aβ oligomers impair red blood cell (RBC) function and oxygen delivery.
  • Bioactive lipids are explored for protection against Aβ toxicity.

Purpose of the Study:

  • Investigate sphingosine-1-phosphate (S1P) role in ATP release in Aβ-treated RBCs.
  • Elucidate S1P's protective mechanism against Aβ-induced RBC dysfunction.
  • Explore S1P as a potential therapeutic agent for AD.

Main Methods:

  • Spectrophotometric and immunoassay techniques used.
  • Quantified ATP, 2,3 DPG, and cAMP levels in RBCs.
  • Assessed caspase-3 activity in treated RBCs.

Main Results:

  • Aβ inhibited ATP release from RBCs.
  • S1P treatment rescued the inhibition of ATP release.
  • S1P restored 2,3 DPG and cAMP levels and involved caspase-3.
  • S1P mitigated Aβ-induced RBC functional impairments.

Conclusions:

  • S1P protects RBCs against Aβ toxicity via specific molecular pathways.
  • S1P normalizes ATP release and intracellular signaling in affected RBCs.
  • Findings suggest S1P as a novel therapeutic strategy for Alzheimer's disease.