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The effects of normal aging on amyloid‐β deposition in nondemented adults with Down syndrome as imaged by carbon 11–labeled Pittsburgh compound B
Author(s) -
Lao Patrick J.,
Betthauser Tobey J.,
Hillmer Ansel T.,
Price Julie C.,
Klunk William E.,
Mihaila Iulia,
Higgins Andrew T.,
Bulova Peter D.,
Hartley Sigan L.,
Hardison Regina,
Tumuluru Rameshwari V.,
Murali Dhanabalan,
Mathis Chester A.,
Cohen Annie D.,
Barnhart Todd E.,
Devenny Darlynne A.,
Mailick Marsha R.,
Johnson Sterling C.,
Handen Benjamin L.,
Christian Bradley T.
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.05.013
Subject(s) - pittsburgh compound b , precuneus , neuropathology , cortex (anatomy) , alzheimer's disease , amyloid (mycology) , psychology , pathogenesis , medicine , pathology , neuroscience , disease , cognition
In Down syndrome (DS), the overproduction of amyloid precursor protein is hypothesized to predispose young adults to early expression of Alzheimer‐like neuropathology. Methods PET imaging with carbon 11–labeled Pittsburgh compound B examined the pattern of amyloid‐β deposition in 68 nondemented adults with DS (30–53 years) to determine the relationship between deposition and normal aging. Standard uptake value ratio (SUVR) images were created with cerebellar gray matter as the reference region. Results Multiple linear regression revealed slight but highly significant (corrected P < .05) positive correlations between SUVR and age. The striatum showed the strongest correlation, followed by precuneus, parietal cortex, anterior cingulate, frontal cortex, and temporal cortex. Conclusion There is an age‐related amyloid‐β deposition in the DS population, but as a pattern of elevated cortical retention becomes apparent, the correlation of SUVR with age ceases to be significant. Factors unrelated to aging may drive an increase in deposition during early Alzheimer's disease pathogenesis.