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• W3199567892 abstract "Objective: Evaluate whether single nucleotide polymorphisms (SNPs) previously associated with longevity are protective against neurofibrillary tangle tau (NFT) pathology in primary age-related tauopathy (PART) or Alzheimer’s disease (AD). Background: GWAS have identified longevity-associated SNPs, but these loci have not been evaluated relative to age-related pathological accumulation including NFTs and amyloid-beta (Aβ). PART is characterized neuropathologically by NFTs in the absence of Aβ pathology. Previous work demonstrated that PART has reduced frequency of AD-susceptibility alleles relative to AD, suggesting genetic evidence for Aβ “resistance.” We hypothesized that longevity-associated genetic loci may further confer increased resistance in PART. Design/Methods: We evaluated 765 aging individuals from the Religious Orders Study or Memory and Aging Project (ROSMAP) characterized post-mortem as PART (Braak=I–IV, CERAD=0) or AD (Braak=III–VI, CERAD=2–3). We extracted 29 SNPs previously associated with longevity (age ≥ 90 or event-free survival) from the Affymetrix panel. We performed linear regression to relate SNP x Group interactions, adjusting for sex and age. In a validation study with 155 ADNI cases we related significant SNPs to floretaucipir in the superior temporal cortex (STC; consistent with Braak V–VI) in cases defined as amyloid-negative or amyloid-positive (florbetapir>1.11) using a similar regression model. Results: The ROSMAP cohort revealed a significant interaction for proxy SNP rs8102566 (ATCAY; d’ 0.95) x Group associated with dose-dependent reduced Braak NFT severity in PART relative to AD (β=−0.36, p=0.008). In ADNI we observed a similar association for rs10412199 (ATCAY) x Group interaction associated with reduced dose-dependent STC floretaucipir uptake (β=−0.12, p=0.022) in amyloid-negative cases. Conclusions: We observed convergent neuropathological and PET evidence for a locus in ATCAY, previously implicated in neuronal development, associating with reduced NFT severity in PART, but not AD. These findings enrich evidence that NFTs in PART may be guided by distinct mechanisms from AD NFTs and that common genetic variation may contribute to “resistance” in PART. Disclosure: Dr. Jefferson-George has nothing to disclose. Dr. Wolk has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Merck, Jannsen, Eli Lilly and GE. Dr. Lee has nothing to disclose. Dr. Das has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Rancho Biosciences. Dr. Wisse has nothing to disclose. Dr. De Jager has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen and Roche. Dr. De Jager has received research support from Biogen and Roche. Dr. Schneider has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Avid. Dr. Bennett has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with AbbVie, Takeda. Dr. McMillan has nothing to disclose." @default.
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• W3199567892 date "2019-04-09" @default.
• W3199567892 modified "2023-10-17" @default.
• W3199567892 title "Convergent Evidence for a Longevity Genetic Locus Associated with Tau Load in PART (S34.007)" @default.
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