Plasma rich in growth factors (PRGF-Endoret) reduces neuropathologic hallmarks and improves cognitive functions in an Alzheimer's disease mouse model

Neurobiol Aging. 2014 Jul;35(7):1582-95. doi: 10.1016/j.neurobiolaging.2014.01.009. Epub 2014 Jan 17.

Abstract

Impaired growth factor function is thought to drive many of the alterations observed in Alzheimer's disease (AD) patients. Endogenous regenerative technology, PRGF (plasma rich in growth factor)-Endoret, is designed for the delivery of a complex pool of patient's own active morphogens that may stimulate tissue regeneration. We obtained and characterized PRGF-Endoret preparations from human blood. We used, as experimental approach in vivo, APP/PS1 mice, characterized by age-dependent brain amyloid-β (Aβ) accumulation. Intranasal administration of PRGF-Endoret to APP/PS1 mice resulted in an important decrease in brain Aβ deposition and tau phosphorylation. PRGF-Endoret-treated APP/PS1 mice also showed decreased astrocyte reactivity, and prevented protein synaptic loss. In vitro approaches demonstrated that PRGF-Endoret treatment modulated astrocyte activation, reducing inflammatory responses, and promoted Aβ degradation. Furthermore, PRGF-Endoret stimulated global improvements in anxiety, learning, and memory behaviors. Our findings show that PRGF-Endoret exerts multifunctional and complementary effects that result in the reversal of the broad range of cognitive deficits in AD, suggesting that PRGF-Endoret may hold promise as an innovative therapy in AD.

Keywords: Alzheimer's disease; Astrocytes; Aβ degradation; Cognition; Cognitive impairment; Intranasal administration; PRGF-Endoret; Transgenic mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Intranasal
  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / psychology
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Anxiety
  • Astrocytes / drug effects
  • Brain / metabolism
  • Cells, Cultured
  • Cognition / drug effects*
  • Disease Models, Animal*
  • Humans
  • Intercellular Signaling Peptides and Proteins / administration & dosage*
  • Intercellular Signaling Peptides and Proteins / pharmacology
  • Intercellular Signaling Peptides and Proteins / physiology
  • Learning / drug effects
  • Male
  • Memory / drug effects
  • Mice
  • Mice, Transgenic*
  • Phosphorylation / drug effects
  • Plasma
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Intercellular Signaling Peptides and Proteins
  • tau Proteins