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.
Keywords: Aging; Amyloid; DYRK1; Down; Trisomy 21.
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