Efficacy monitoring using amyloid and tau PET imaging in Down syndrome populations

Abstract Background The triplication of the chromosome containing the gene for APP production conveys a very high risk for people with Down syndrome to develop Alzheimer’s disease by their fifth decade of life. Method The Alzheimer’s Biomarker Consortium ‐ Down Syndrome study has tracked the trajectory of PET‐measured amyloid and tau burden in the brains of individuals with Down Syndrome (>25 yrs of age) to carefully characterize their relationship with AD‐related cognitive decline. Result Compared to sporadic AD in the neurotypical population, there is a carefully characterized accelerated time course between the emergence of these neuropathologies and the presentation of MCI and clinical dementia in the Down syndrome population. Conclusion Clinical drug trials for the treatment and prevention of AD in Down syndrome are now being launched that use these biomarker data to inform and optimize study design. This presentation will discuss the time course of amyloid and tau within the context of treatment strategies for the removal or prevention of accumulation of AD neuropathology in Down syndrome.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2024-12-01
DOI
https://doi.org/10.1002/alz.094705
Primary Topic
Diabetes Management and Research
Type
article
Field-Weighted Citation Impact
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article

Efficacy monitoring using amyloid and tau PET imaging in Down syndrome populations

Bradley Christian, Matthew Zammit
Alzheimer s & Dementia
Diabetes Management and Research
article

Efficacy monitoring using amyloid and tau PET imaging in Down syndrome populations

Bradley Christian, Matthew Zammit
article en

Abstract

Abstract Background The triplication of the chromosome containing the gene for APP production conveys a very high risk for people with Down syndrome to develop Alzheimer’s disease by their fifth decade of life. Method The Alzheimer’s Biomarker Consortium ‐ Down Syndrome study has tracked the trajectory of PET‐measured amyloid and tau burden in the brains of individuals with Down Syndrome (>25 yrs of age) to carefully characterize their relationship with AD‐related cognitive decline. Result Compared to sporadic AD in the neurotypical population, there is a carefully characterized accelerated time course between the emergence of these neuropathologies and the presentation of MCI and clinical dementia in the Down syndrome population. Conclusion Clinical drug trials for the treatment and prevention of AD in Down syndrome are now being launched that use these biomarker data to inform and optimize study design. This presentation will discuss the time course of amyloid and tau within the context of treatment strategies for the removal or prevention of accumulation of AD neuropathology in Down syndrome.

Alzheimer s & DementiaVol. 20(S8)
University of Wisconsin–Madison (US)
Good health and well-being
Openalex Percentile: Top 62%
Diabetes Management and Research
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