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Basic Science and Pathogenesis.

Mitchell Marta Ariza1,2, Dominique Leitner1, Evgeny Kanshin1

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Down syndrome (DS) and Alzheimer's disease (AD) share early protein deposition. This study characterizes understudied proteins in DS and AD plaques, revealing roles in cellular functions and potential new biomarkers.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Down syndrome (DS) is the leading genetic cause of Alzheimer's disease (AD), marked by early amyloid-β (Aβ) and phosphorylated tau (pTau) accumulation.
  • Previous proteomics identified differentially abundant proteins in DS, early-onset AD (EOAD), and late-onset AD (LOAD) plaques, linked to endo/lysosomal pathways, immunity, and myelin.
  • Several of these proteins are understudied in AD and DS, with some novel to human AD proteomics.

Purpose of the Study:

  • To characterize understudied proteins in Aβ plaques from DS, EOAD, and LOAD using immunohistochemistry.
  • To elucidate the roles of these proteins in AD neuropathology.
  • To identify potential biomarkers and therapeutic targets for DS and AD.

Main Methods:

  • Immunohistochemistry (IHC) was performed on temporal and frontal cortex tissues from DS, EOAD, LOAD, and age-matched control cases.
  • Proteins were selected based on their presence in Aβ plaques, limited prior characterization, and potential relevance to AD pathology.
  • The study focused on proteins identified in a prior proteomics analysis of Aβ plaques.

Main Results:

  • The study provides the first immunohistological evidence for these less-studied proteins in DS and AD brain tissues.
  • These proteins are associated with endo/lysosomal functions, synaptic activity, and myelin maintenance.
  • Their roles are linked to lysosomal storage diseases, protein aggregation, and myelin sheath stability.

Conclusions:

  • The findings highlight key functional aspects of the amyloid plaque proteome in DS compared to EOAD and LOAD.
  • Understanding these under-explored proteins enhances knowledge of AD neuropathology beyond traditional Aβ and Tau.
  • Results may facilitate future mechanistic studies, biomarker discovery, and therapeutic strategies for DS and AD.