Cognitive Aging in Older Breast Cancer Survivors

Author:

Root James C.1,Li Yuelin1,Schofield Elizabeth1ORCID,Orlow Irene2ORCID,Ryan Elizabeth1,Traina Tiffany3,Patel Sunita K.4ORCID,Ahles Tim A.1

Affiliation:

1. Neurocognitive Research Lab, Department of Psychiatry and Behavioral Sciences, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA

2. Molecular Epidemiology Laboratory, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA

3. Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA

4. Departments of Population Science and Supportive Care Medicine, City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA

Abstract

Background: Cancer and cancer treatments may affect aging processes, altering the trajectory of cognitive aging, but the extant studies are limited in their intervals of assessment (two–five years). We studied the cognitive performance of a cohort of survivors and controls aged from 60 to 89 years utilizing cross-sectional cognitive performance data as an indicator of potential aging trajectories and contrasted these trends with longitudinal data collected over two years. Methods: Female breast cancer survivors who had been diagnosed and treated at age 60 or older and were 5- to 15-year survivors (N = 328) and non-cancer controls (N = 158) were assessed at enrollment and at 8, 16, and 24 months with standard neuropsychological tests and comprehensive geriatric assessment. Results: A cross-sectional baseline analysis found the expected inverse association of age with cognition in both groups, with survivors performing lower overall than controls in learning and memory (LM). Younger survivors, i.e., those under 75 years of age, exhibited lower performance in both LM and attention, and processing speed and executive function (APE), compared to controls, with no differences being observed between older survivors and controls, which tracked with deficit accumulation trends. Conclusion: Cognitive differences between the survivors and controls for the LM and APE domains were prominent in younger survivors, as was deficit accumulation, suggesting a mediating effect on cognition. Deficit accumulation may represent a modifiable risk factor in cancer survivorship that may be targeted for prevention and intervention.

Funder

National Cancer Institute

American Cancer Society

Internal MSK grants

Publisher

MDPI AG

Subject

Cancer Research,Oncology

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