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Basic Science and Pathogenesis.

Stefan H Sillau1, Md Mahiuddin Ahmed2, Christina M Coughlan3

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Summary
This summary is machine-generated.

Individuals with Down syndrome (DS) show accelerated brain aging with increased neuronal damage and inflammation markers from childhood. This suggests potential therapeutic targets like GM-CSF for DS and typical aging.

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Area of Science:

  • Neuroscience
  • Gerontology
  • Genetics

Background:

  • Increasing age is a primary risk factor for Alzheimer's disease (AD) and cognitive decline.
  • Individuals with Down syndrome (DS) have a near 100% risk of developing AD neuropathology and dementia.
  • Previous research showed granulocyte-macrophage colony-stimulating factor (GM-CSF) improved cognition and reduced neuronal apoptosis in animal models and AD patients.

Purpose of the Study:

  • To investigate age-related changes in biomarkers of neuronal damage and inflammation in individuals with DS.
  • To compare these changes to those observed in normosomic individuals.
  • To assess neuronal apoptosis and gliosis in a mouse model of DS.

Main Methods:

  • Plasma concentrations of UCH-L1, NfL, and GFAP were measured in 316 individuals with DS (ages 2-60) using Quanterix SIMOA.
  • These levels were compared to data from age-matched, healthy, normosomic controls.
  • Neuronal apoptosis was assessed via Caspase-3 staining in the Dp16 mouse model of DS.

Main Results:

  • Individuals with DS exhibit significantly elevated plasma levels of neuronal damage markers (UCH-L1, NfL) and inflammation (GFAP) starting in childhood.
  • The rate of exponential increase of these markers with age is substantially faster in DS compared to normosomic individuals.
  • Preliminary findings indicate increased neuronal apoptosis and gliosis in the brains of Dp16 mice.

Conclusions:

  • Accelerated brain aging in DS, evidenced by increased neuronal damage and inflammation, is likely driven by heightened APP expression and neurotoxic Ab production, compounded by astrogliosis.
  • Clinical trials investigating GM-CSF (sargramostim) are warranted to evaluate its potential to mitigate neuronal damage and inflammation and enhance cognition in young adults with DS and in normally aging individuals.