Charissa Andreotti1, James C Root1, Tim A Ahles1, Bruce S McEwen2, Bruce E Compas3. 1. Department of Psychiatry and Behavioral Sciences, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 2. The Rockefeller University, New York, NY, USA. 3. Department of Psychology and Human Development, Vanderbilt University, Nashville, TN, USA.
Abstract
BACKGROUND: Cognitive decline and accompanying neurological changes associated with non-CNS cancer diagnosis and treatment have been increasingly identified in a subset of patients. Initially believed to be because of neurotoxic effects of chemotherapy exposure, observation of cognitive decline in patients not treated with chemotherapy, cancer-diagnosed individuals prior to treatment, and patients receiving alternative treatment modalities (surgery, endocrine therapy, and radiation) has led to the investigation of additional potential etiologies and moderating factors. Stressful experiences have long been posited as a contributor to these cognitive changes. Through reciprocal connectivity with peripheral systems, the brain maintains a dynamic circuitry to adapt to stress (allostasis). However, overuse of this system leads to dysregulation and contributes to pathophysiology (allostatic load). At this time, little research has been conducted to systematically examine the role of allostatic load in cancer-related cognitive dysfunction. METHODS AND RESULTS: Here, we integrate theories of stress biology, neuropsychology, and coping and propose a model through which individuals with a high level of allostatic load at diagnosis may be particularly vulnerable to the neurocognitive effects of cancer. CONCLUSIONS: Opportunities for future research to test and extend proposed mechanisms are discussed in addition to points of prevention and intervention based on individual variation in stress reactivity and coping skills.
BACKGROUND:Cognitive decline and accompanying neurological changes associated with non-CNS cancer diagnosis and treatment have been increasingly identified in a subset of patients. Initially believed to be because of neurotoxic effects of chemotherapy exposure, observation of cognitive decline in patients not treated with chemotherapy, cancer-diagnosed individuals prior to treatment, and patients receiving alternative treatment modalities (surgery, endocrine therapy, and radiation) has led to the investigation of additional potential etiologies and moderating factors. Stressful experiences have long been posited as a contributor to these cognitive changes. Through reciprocal connectivity with peripheral systems, the brain maintains a dynamic circuitry to adapt to stress (allostasis). However, overuse of this system leads to dysregulation and contributes to pathophysiology (allostatic load). At this time, little research has been conducted to systematically examine the role of allostatic load in cancer-related cognitive dysfunction. METHODS AND RESULTS: Here, we integrate theories of stress biology, neuropsychology, and coping and propose a model through which individuals with a high level of allostatic load at diagnosis may be particularly vulnerable to the neurocognitive effects of cancer. CONCLUSIONS: Opportunities for future research to test and extend proposed mechanisms are discussed in addition to points of prevention and intervention based on individual variation in stress reactivity and coping skills.
Authors: Jamie Arndt; Enny Das; Sanne B Schagen; Stephanie A Reid-Arndt; Linda D Cameron; Tim A Ahles Journal: Psychooncology Date: 2013-07-10 Impact factor: 3.894
Authors: Catherine M Bender; John D Merriman; Amanda L Gentry; Gretchen M Ahrendt; Sarah L Berga; Adam M Brufsky; Frances E Casillo; Meredith M Dailey; Kirk I Erickson; Frances M Kratofil; Priscilla F McAuliffe; Margaret Q Rosenzweig; Christopher M Ryan; Susan M Sereika Journal: Cancer Date: 2015-04-23 Impact factor: 6.860
Authors: John D Merriman; Susan M Sereika; Adam M Brufsky; Priscilla F McAuliffe; Kandace P McGuire; Jamie S Myers; Mary L Phillips; Christopher M Ryan; Amanda L Gentry; Lindsay D Jones; Catherine M Bender Journal: Psychooncology Date: 2015-10-20 Impact factor: 3.894
Authors: Grace C Haser; R Michael Tuttle; Henry K Su; Eran E Alon; Donald Bergman; Victor Bernet; Elise Brett; Rhoda Cobin; Eliza H Dewey; Gerard Doherty; Laura L Dos Reis; Jeffrey Harris; Joshua Klopper; Stephanie L Lee; Robert A Levine; Stephen J Lepore; Ilya Likhterov; Mark A Lupo; Josef Machac; Jeffrey I Mechanick; Saral Mehra; Mira Milas; Lisa A Orloff; Gregory Randolph; Tracey A Revenson; Katherine J Roberts; Douglas S Ross; Meghan E Rowe; Robert C Smallridge; David Terris; Ralph P Tufano; Mark L Urken Journal: Endocr Pract Date: 2016-01-22 Impact factor: 3.443
Authors: Kevin R Krull; Yin Ting Cheung; Wei Liu; Slim Fellah; Wilburn E Reddick; Tara M Brinkman; Cara Kimberg; Robert Ogg; Deokumar Srivastava; Ching-Hon Pui; Leslie L Robison; Melissa M Hudson Journal: J Clin Oncol Date: 2016-06-06 Impact factor: 44.544
Authors: Leandra Desjardins; Jennifer C Thigpen; Molly Kobritz; Alexandra H Bettis; Meredith A Gruhn; Megan Ichinose; Kristen Hoskinson; Claire Fraley; Allison Vreeland; Colleen McNally; Bruce E Compas Journal: Child Neuropsychol Date: 2017-10-02 Impact factor: 2.500