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Frequency of mixed neuropathologies in individuals with down syndrome with and without Alzheimer's dementia.

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Updated: May 12, 2025

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The cholinotrophic system in Down syndrome.

Elliott J Mufson1, Sylvia E Perez2

  • 1Department of Translational Neuroscience, St. Joseph's Hospital and Medical Center, Barrow Neurological Institute, Phoenix, AZ, United States; Department of Neurology, St. Joseph's Hospital and Medical Center, Barrow Neurological Institute, Phoenix, AZ, United States.

Handbook of Clinical Neurology
|May 8, 2025
PubMed
Summary
This summary is machine-generated.

Cholinergic neurons degenerate in Down syndrome (DS), with neurotrophic factors and tau pathology contributing to this decline. Biomarkers for dementia and therapeutic targets for the cholinergic system are identified.

Keywords:
Alzheimer diseaseBiomarkersCholinergicDevelopmentDown syndromeDrug targetsGenesNeurotrophic receptorPostnatalPrenatal

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Down syndrome (DS) involves degeneration of cholinergic basal forebrain (CBF) projection neurons and striatal cholinergic interneurons.
  • The neuropathobiology of these distinct cholinergic phenotypes in DS is not fully understood.
  • This review examines alterations in cholinergic, neurotrophic, and cell death factors, alongside tau and amyloid pathology in DS.

Purpose of the Study:

  • To review and summarize the neuropathological alterations affecting cholinergic neurons in Down syndrome.
  • To identify potential biomarkers for distinguishing between demented and non-demented individuals with DS.
  • To explore therapeutic targets for mitigating cholinergic neurodegeneration in DS.

Main Methods:

  • Review of existing literature on cholinergic system alterations in Down syndrome.
  • Analysis of neurotrophic factors, cell death pathways, tau pathology, and amyloidopathy in DS.
  • Investigation of potential biomarkers and therapeutic strategies.

Main Results:

  • The developing cholinergic system in trisomy is stable, but neurotrophic receptors are compromised in DS.
  • Both CBF and striatal cholinergic neurons show severe degeneration in adult and aged individuals with DS.
  • Cholinergic striatal neurons appear dystrophic in adults with DS, and both cell types exhibit tau pathology in elders.
  • Alterations in proNGF, NGF metabolites, and neuronal genes may serve as biomarkers for dementia in DS.

Conclusions:

  • Cholinergic neurodegeneration is a significant feature of Down syndrome, exacerbated by compromised neurotrophic support and tau pathology.
  • Biomarkers in plasma and CSF, including proNGF and specific neuronal genes, show promise for distinguishing dementia status in DS.
  • Targeting cholinergic pathways, neurotrophic factors (like NGF and its receptors), and specific gene pathways offers potential therapeutic avenues to slow neurodegeneration in DS, with implications for Alzheimer's disease (AD).