Chronic depressive symptomatology and CSF amyloid beta and tau levels in mild cognitive impairment |
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| Authors: | Mitzi M Gonzales Philip S Insel Craig Nelson Duygu Tosun Michael Schöll Niklas Mattsson Simona Sacuiu David Bickford Michael W Weiner R Scott Mackin the Alzheimer's Disease Neuroimaging Initiative |
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| Institution: | 1. Department of Neurology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA;2. Center for Imaging of Neurodegenerative Diseases, Veterans Administration Medical Center, San Francisco, CA, USA;3. Department of Psychiatry, University of California, San Francisco, CA, USA;4. Department of Radiology, University of California, San Francisco, CA, USA;5. Wallenberg Centre for Molecular and Translational Medicine and the Department of Psychiatry and Neurochemistry, University of Gothenburg, Gothenburg, Sweden;6. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden;7. Department of Neurology, Skane University Hospital, Lund, Sweden;8. Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden;9. Department of Medicine, University of California, San Francisco, CA, USA |
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| Abstract: | Objectives To investigate the association between chronic subsyndromal symptoms of depression (SSD), cerebrospinal fluid (CSF) biomarkers, and neuropsychological performance in individuals with mild cognitive impairment (MCI). Methods Participants included 238 older adults diagnosed with MCI from the Alzheimer's Disease Neuroimaging Initiative repository with cognitive and CSF amyloid beta (Aβ1–42), total tau (t‐tau), and phosphorylated tau (p‐tau) data. The Neuropsychiatric Inventory identified individuals with chronic endorsement (SSD group N = 80) or no endorsement (non‐SSD group N = 158) of depressive symptoms across timepoints. CSF biomarker and cognitive performance were evaluated with linear regression models adjusting for age, education, gender, APOE genotype, global cognitive status, and SSD group. Results As compared to the non‐SSD group, the SSD group displayed lower CSF Aβ1–42 levels (β = ?24.293, S.E. = 6.345, P < 0.001). No group differences were observed for CSF t‐tau (P = 0.497) or p‐tau levels (P = 0.392). Lower CSF Aβ1–42 levels were associated with poorer performance on learning (β = 0.041, S.E. = 0.018, P = 0.021) and memory (β = ?0.012, S.E. = 0.005, P = 0.031) measures, whereas higher CSF t‐tau levels were associated with poorer performance on measures of global cognition (β = 0.022, S.E = 0.008, P = 0.007) and language (β = ?0.010, S.E = 0.004, P = 0.019). SSD was independently associated with diminished global cognition, learning and memory, language, and executive function performance over and above the effects of CSF biomarkers (all P < 0.05). Conclusions MCI participants with SSD displayed diminished CSF Aβ1–42 levels but did not differ from non‐SSD controls in CSF tau levels. Additionally, CSF biomarkers and SSD independently accounted for variance in cognitive performance, suggesting that these factors may uniquely confer cognitive risk in MCI. |
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| Keywords: | amyloid beta CSF biomarkers depression mild cognitive impairment tau |
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