AI Article Synopsis
- - The accumulation of amyloid β (Aβ) peptide, which is linked to Down syndrome (DS), leads to early onset dementia similar to Alzheimer's disease (AD), and existing treatments for AD are ineffective in DS.
- - New drug therapies, like Lecanemab, are monoclonal antibodies aimed at removing Aβ plaques, which could potentially benefit individuals with both AD and DS.
- - The text highlights the similarities between DS and AD, discusses challenges in targeting Aβ precursor proteins, and advocates for further exploration of antibody treatments for managing AD in patients with DS.
Article Abstract
Accumulation of the amyloid β (Aβ) peptide, derived from Aβ precursor protein (APP), is a trait of Down syndrome (DS), as is early development of dementia that resembles Alzheimer's disease (AD). Treatments for this AD in DS simply do not. New drug therapies for AD, e.g., Lecanemab, are monoclonal antibodies designed to clear amyloid plaques composed of Aβ. The increasingly real ability to target and dispose of Aβ favors the use of these drugs in individuals with AD in DS, and, perhaps as earlier intervention for cognitive impairment. We present pertinent similarities between DS and AD in adult DS subjects, discuss challenges to target APP metabolites, and suggest that recently developed antibody treatments against Aβ may be worth investigating to treat AD in DS.
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| http://dx.doi.org/10.1016/j.arr.2024.102281 | DOI Listing |
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