Caring for the caregiver: Why policy must shift from addressing needs to enabling caregivers to flourish.

Policies supporting caregivers ("caregiver policies") are limited in the extent to which they meet the needs of those who care for others. Where policies do exist, they focus on relieving the burdens associated with caring or the needs of the person they care for, rather than consider the holistic needs of the caregiver that would enable them to flourish. We argue that the established approach to caregiver policies reflects a policy failure, requiring a reassessment of current practice related to caregiver support. Often, caregiver policies target the care recipient rather than the caregiver's needs. Through a consultative exercise, we identified five areas of need that existing caregiver policies touch upon. Yet current approaches remain piecemeal and inadequate in a global context. Caregiver policies should not just relieve burden to the extent that caregivers can continue in the role, but they should support caregivers to flourish, and future work may benefit from drawing on related frameworks from positive psychology, such as the PERMA™ model; this is important for both policymakers and researchers.

Navigating the Perfect Storm of Ageism, Mentalism, and Ableism: A Prevention Model.

Many of society's systemic implicit biases against older persons predate COVID-19. A perfect storm of these biases now rages against older persons much more explicitly and visibly during the COVID-19 pandemic. They comprise of blends of discrimination based on age ("ageism"), multiplied by the prejudice against persons with mental symptoms (mentalism), and by notions against persons with disabilities (ableism). The collective result of this tragedy has caused a devastating impact on older persons' lives and flagrant violation of their human rights. We explore the evidence to better understand the drivers of these biases and ways to mitigate their impact. We also review strategies to alleviate the effects of ageism, mentalism, and ableism using a prevention model.

Ageism and COVID-19: what does our society's response say about us?

The goal of this commentary is to highlight the ageism that has emerged during the COVID-19 pandemic. Over 20 international researchers in the field of ageing have contributed to this document. This commentary discusses how older people are misrepresented and undervalued in the current public discourse surrounding the pandemic. It points to issues in documenting the deaths of older adults, the lack of preparation for such a crisis in long-term care homes, how some 'protective' policies can be considered patronising and how the initial perception of the public was that the virus was really an older adult problem. This commentary also calls attention to important intergenerational solidarity that has occurred during this crisis to ensure support and social-inclusion of older adults, even at a distance. Our hope is that with this commentary we can contribute to the discourse on older adults during this pandemic and diminish the ageist attitudes that have circulated.

E3 ligase RFWD3 is a novel modulator of stalled fork stability in BRCA2-deficient cells.

BRCA1/2 help maintain genomic integrity by stabilizing stalled forks. Here, we identify the E3 ligase RFWD3 as an essential modulator of stalled fork stability in BRCA2-deficient cells and show that codepletion of RFWD3 rescues fork degradation, collapse, and cell sensitivity upon replication stress. Stalled forks in BRCA2-deficient cells accumulate phosphorylated and ubiquitinated replication protein A (ubq-pRPA), the latter of which is mediated by RFWD3. Generation of this intermediate requires SMARCAL1, suggesting that it depends on stalled fork reversal. We show that in BRCA2-deficient cells, rescuing fork degradation might not be sufficient to ensure fork repair. Depleting MRE11 in BRCA2-deficient cells does block fork degradation, but it does not prevent fork collapse and cell sensitivity in the presence of replication stress. No such ubq-pRPA intermediate is formed in BRCA1-deficient cells, and our results suggest that BRCA1 may function upstream of BRCA2 in the stalled fork repair pathway. Collectively, our data uncover a novel mechanism by which RFWD3 destabilizes forks in BRCA2-deficient cells.