AI Article Synopsis

  • Down syndrome (DS) results from an extra chromosome 21 and significantly raises the risk for early-onset Alzheimer's disease (AD), known as DS-associated AD (DSAD), with dementia typically beginning around age 55.
  • Individuals with DS usually start showing amyloid build-up in their brains in their late thirties to early forties, which is linked to Alzheimer's development.
  • Recent research has been exploring the use of monoclonal antibodies (mAbs) that target amyloid-β plaques as a possible treatment for DSAD, discussing both the potential benefits and the challenges faced in this area.

Article Abstract

Down syndrome (DS) is a genetic disorder caused by an extra copy of chromosome 21 (trisomy 21 or T21) and is associated with an increased risk of early-onset Alzheimer's disease (AD), also known as DS-associated AD (DSAD). Individuals with DS typically develop amyloid neuropathology in their late-thirties to early-forties and the mean age of onset of clinical dementia is approximately 55 years. Recent advances in AD clinical research have focused on monoclonal antibodies (mAbs) targeting amyloid-β (Aβ) plaques as a potential therapeutic approach. Therefore, there has been guarded enthusiasm about using anti-amyloid mAbs in the prevention/treatment of DSAD. This narrative review and perspective explores the current understanding of amyloid pathology in AD and DSAD, the rationale for using anti-amyloid mAbs in the treatment of DSAD, and the challenges and opportunities for research toward the application of this therapeutic strategy to older adults with DS.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11591668PMC
http://dx.doi.org/10.3390/brainsci14111084DOI Listing

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