The age of individuals has consequences not only for their fitness and behaviour but also for the functioning of the groups they form. Because social behaviour often changes with age, population age structure is expected to shape the social organization, the social environments individuals experience and the operation of social processes within populations. Although research has explored changes in individual social behaviour with age, particularly in controlled settings, there is limited understanding of how age structure governs sociality in wild populations. Here, we synthesize previous research into age-related effects on social processes in natural populations, and discuss the links between age structure, sociality and ecology, specifically focusing on how population age structure might influence social structure and functioning. We highlight the potential for using empirical data from natural populations in combination with social network approaches to uncover pathways linking individual social ageing, population age structure and societal functioning. We discuss the broader implications of these insights for understanding the social impacts of anthropogenic effects on animal population demography and for building a deeper understanding of societal ageing in general.This article is part of the discussion meeting issue 'Understanding age and society using natural populations'.
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http://dx.doi.org/10.1098/rstb.2022.0464 | DOI Listing |
Alzheimers Dement
December 2024
EQT Life Sciences Partners, Amsterdam, 1071 DV Amsterdam, Netherlands.
Background: Alzheimer's disease (AD) trials report a high screening failure rate (potentially eligible trial candidates who do not meet inclusion/exclusion criteria during screening) due to multiple factors including stringent eligibility criteria. Here, we report the main reasons for screening failure in the 12-week screening phase of the ongoing evoke (NCT04777396) and evoke+ (NCT04777409) trials of semaglutide in early AD.
Method: Key inclusion criteria were age 55-85 years; mild cognitive impairment due to AD (Clinical Dementia Rating [CDR] global score of 0.
Background: Alzheimer's disease (AD) is the most prevalent cause of dementia accounting for an estimated 60% to 80% of cases. Despite advances in the research field, developing truly effective therapies for AD symptoms remains a major challenge. Sweet almond contain nutrients that have the potential of combating age-related brain dysfunction, by improving learning, memory and neurocognitive performance.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: The Neurovascular Unit is a multicellular structure of the CNS known to become dysfunctional in Alzheimer's Disease (AD) and cerebral amyloid angiopathy. Amyloidosis disrupts the function of cerebrovascular endothelial cells (cECs) via extrinsic and intrinsic apoptosis, and induction of blood brain barrier (BBB) permeability. Findings in our lab demonstrated that pan-Carbonic Anhydrase inhibitors (CAi's) prevent mitochondria-mediated apoptotic mechanisms in cECs.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: Amid recent approvals, early Alzheimer's disease (AD) remains an active area of treatment development, but research on the utility of recruitment incentives in early AD trials remains limited. We examined how trial design features impact enrollment decisions among Mild Cognitive Impairment (MCI) patients and their family members.
Method: We performed a conjoint analysis experiment to compare early AD patients' preferences for trial features.
Alzheimers Dement
December 2024
Tohoku University, Sendai, Miyagi, Japan.
Background: Loneliness has been linked to cognitive decline and an elevated risk of Alzheimer's disease (AD). Previous studies measured loneliness at a single point time, which may not accurately capture the longitudinal changes of different loneliness types (e.g.
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