Introduction: We sought to examine the association between pre-existing caregiving strain levels and care recipient health outcomes following a new cancer diagnosis.
Materials And Methods: We used the National Health and Aging Trends Study (NHATS) linked with the National Study of Caregiving (NSOC) and Medicare claims to identify older adults receiving family caregiving within one year before an index cancer diagnosis. Caregiving strain was determined using NSOC items of self-reported emotional, physical, and financial difficulties measured before the cancer diagnosis.
Young adult (YA) LGBTQ+ cancer survivors face inequities and unmet needs that impact their well-being. However, the impact of age and cancer among LGBTQ+ individuals have not been adequately assessed. The North Carolina LGBTQ+ Health Needs Assessment survey, conducted at local Pride events, aimed to collect data to describe the well-being of LGBTQ+ people in NC.
View Article and Find Full Text PDFBackground: lesbian, gay, bisexual, transgender, queer, or another non-heterosexual or cisgender identity (LGBTQ+) cancer survivors experience high financial hardship. However, structural drivers of inequities do not impact all LGBTQ+ individuals equally. Using All of Us data, we conducted an intersectional analysis of behavioral financial hardship among LGBTQ+ cancer survivors.
View Article and Find Full Text PDFThe GC hexanucleotide repeat expansion in C9ORF72 is the major genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) (C9-ALS/FTD). Despite considerable efforts, the development of mouse models of C9-ALS/FTD useful for therapeutic development has proven challenging due to the intricate interplay of genetic and molecular factors underlying this neurodegenerative disorder, in addition to species differences. This study presents a robust investigation of the cellular pathophysiology and behavioral outcomes in a previously described AAV mouse model of C9-ALS expressing 66 GC hexanucleotide repeats.
View Article and Find Full Text PDFThe GC hexanucleotide repeat expansion in the major genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) (C9-ALS/FTD). Despite considerable efforts, the development of mouse models of C9-ALS/FTD useful for therapeutic development has proven challenging due to the intricate interplay of genetic and molecular factors underlying this neurodegenerative disorder, in addition to species differences. This study presents a robust investigation of the cellular pathophysiology and behavioral outcomes in a previously described AAV mouse model of C9-ALS expressing 66 GC hexanucleotide repeats.
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