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[P2–165]: INVESTIGATING THE ROLE OF UBIQUILIN2 IN AGE‐RELATED NEURODEGENERATION
Author(s) -
Paulson Henry L.,
Sharkey Lisa M.,
Safren Nate,
Pithadia Amit,
Fischer Svetlana,
Zeng Li,
Dulchavsky Mark E.,
Patel Ronak,
Lantis Gabrielle,
Barmada Sami,
Ivanova Magdalena
Publication year - 2017
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.2017.06.816
Subject(s) - neurodegeneration , frontotemporal dementia , biology , neuroscience , genetically modified mouse , microbiology and biotechnology , autophagy , protein aggregation , dementia , transgene , pathology , disease , medicine , genetics , gene , apoptosis
at baseline. In the following year assessment subjects were classified as decliners or not according to their worsening nominal performance in GCS or FAQ. Results: Cortisol levels were found to be higher in both cognitively impaired groups (p1⁄40.0002), and sTNFR1 levels were higher only in dementia group (p1⁄40.0007). In logistic regression analysis adjusted for multiple covariates sTNFR1 levels were associated with prevalent dementia (OR1⁄41.0044; CI:1.002-1.007); instead, cortisol levels were associated (OR:1.084; CI:1.024-1.147) with prevalent cognitive impairment (CIND + dementia), but not with dementia itself, and in a clinical covariate adjusted-model, cortisol levels did not hold statistical association with CIND status. In both groups with cognitive impairment cortisol levels did not correlate with performance in cognitive measures. No biomarker was found to be associated with GCS and FAQ decline according to the employed logistic regression models. CIND status at baseline was the main predictor of functional decline in one year follow-up (OR1⁄43.17; CI:1.191.45). Conclusions:The absence of a graded pattern for cortisol and sTNFR1 serum levels across the three groups categorized according their functional and cognitive status, a lack of correlation between serum levels andmeasures of cognitive performance, and the absence of associations with the investigated longitudinal outcomes suggest that these biomarkers do not play a lead role in the mechanisms underlying age-associated cognitive and functional impairment.