Understanding Old Age and Victimisation: A Critical Exploration

Purpose – The purpose of paper is to shine light on the under-theorised relationship between old age and victmisation. In classical criminological studies, the relationship between “age”, victimisation and crime has been dominated by analysis of younger people's experiences. This paper aims to address this knowledge deficit by exploring older people's experiences by linking it to the social construction of vulnerability.

Design/methodology/approach – The paper explores both historical and contemporary narratives relating to the diverse experiences of older people as victims in the UK. In particular, from 1945 to the present, statistical context and theoretical advancement illuminates that older people as a social group have a deep “fear of crime” to their relative victimisation.

Findings – A careful survey of the criminological literature highlights a paucity of research relating to older people's views and experiences of crime and victimisation. The conceptual issue of vulnerability in different contexts is important in understanding ageing and victimisation in UK. The paper's findings illustrate that their experiences have remained marginalised in the debates around social policy, and how the criminal justice system responds to these changes remains yet to be seen.

Research limitations/implications – Any research attempt at theorising “age” should take into consideration not just younger people, but also the diverse experiences of older people. Policy makers may care to ponder that benchmarks be written that takes into full consideration of older people's experiences as vulnerability.

Practical implications – For criminal justice scholars and practitioners, there is a need to listen to the narratives of older people that should help shape and frame debate about their lived experiences. There should be an examination of existing formal and informal practices regarding elders, as the first step in developing an explicit and integrated set of policies and programmes to address the special needs of this group.

Originality/value – This is an original paper in highlighting how important old age is in construction of “victims” in modern society. By theorising age, victimisation and crime it is hoped to dispel and challenge some of the myths surrounding later life, crime and the older victim.

The role of ECE1 variants in cognitive ability in old age and Alzheimer's disease risk

The ß-amyloid peptide may play a central role in Alzheimer's disease (AD) pathogenesis. We have evaluated variants in seven Aß-degrading genes (ACE, ECE1, ECE2, IDE, MME, PLAU, and TF) for association with AD risk in the Genetic and Environmental Risk in Alzheimer's Disease Consortium 1 (GERAD1) cohort, and with three cognitive phenotypes in the Lothian Birth Cohort 1936 (LBC1936), using 128 and 121 SNPs, respectively. In GERAD1, we identified a significant association between a four-SNP intragenic ECE1 haplotype and risk of AD in individuals that carried at least one APOE e4 allele (P = 0.00035, odds ratio = 1.61). In LBC1936, we identified a significant association between a different two-SNP ECE1 intragenic haplotype and non-verbal reasoning in individuals lacking the APOE e4 allele (P = 0.00036, ß = -0.19). Both results showed a trend towards significance after permutation (0.05 <P <0.10). A follow-up cognitive genetic study evaluated the association of ECE1 SNPs in three additional cohorts of non-demented older people. Meta-analysis of the four cohorts identified the significant association (Z <0.05) of SNPs in the ECE-1b promoter with non-verbal reasoning scores, particularly in individuals lacking the APOE e4 allele. Our genetic findings are not wholly consistent. Nonetheless, the AD associated intronic haplotype is linked to the 338A variant of known ECE1b promoter variant, 338C>A (rs213045). We observed significantly less expression from the 338A variant in two human neuroblastoma cell lines and speculate that this promoter may be subject to tissue-specific regulation.

Hypercyclic and mixing operator semigroups

We describe a class of topological vector spaces admitting a mixing uniformly continuous operator group $\{T_t\}_{t\in\C^n}$ with holomorphic dependence on the parameter $t$. This result covers those existing in the literature. We also
describe a class of topological vector spaces admitting no supercyclic strongly continuous operator semigroups $\{T_t\}_{t\geq 0}$.

Age- and Light-Dependent Development of Localised Retinal Atrophy in CCL2(-/-)CX3CR1(GFP/GFP) Mice

Previous studies have shown that CCL2/CX3CR1 deficient mice on C57BL/6N background (with rd8 mutation) have an early onset (6 weeks) of spontaneous retinal degeneration. In this study, we generated CCL2(-/-)CX3CR1(GFP/GFP) mice on the C57BL/6J background. Retinal degeneration was not detected in CCL2(-/-)CX3CR1(GFP/GFP) mice younger than 6 months. Patches of whitish/yellowish fundus lesions were observed in 17~60% of 12-month, and 30~100% of 18-month CCL2(-/-)CX3CR1(GFP/GFP) mice. Fluorescein angiography revealed no choroidal neovascularisation in these mice. Patches of retinal pigment epithelium (RPE) and photoreceptor damage were detected in 30% and 50% of 12- and 18-month CCL2(-/-)CX3CR1(GFP/GFP) mice respectively, but not in wild-type mice. All CCL2(-/-)CX3CR1(GFP/GFP) mice exposed to extra-light (~800lux, 6 h/day, 6 months) developed patches of retinal atrophy, and only 20-25% of WT mice which underwent the same light treatment developed atrophic lesions. In addition, synaptophysin expression was detected in the outer nucler layer (ONL) of area related to photoreceptor loss in CCL2(-/-)CX3CR1(GFP/GFP) mice. Markedly increased rhodopsin but reduced cone arrestin expression was observed in retinal outer layers in aged CCL2(-/-)CX3CR1(GFP/GFP) mice. GABA expression was reduced in the inner retina of aged CCL2(-/-)CX3CR1(GFP/GFP) mice. Significantly increased Müller glial and microglial activation was observed in CCL2(-/-)CX3CR1(GFP/GFP) mice compared to age-matched WT mice. Macrophages from CCL2(-/-)CX3CR1(GFP/GFP) mice were less phagocytic, but expressed higher levels of iNOS, IL-1ß, IL-12 and TNF-a under hypoxia conditions. Our results suggest that the deletions of CCL2 and CX3CR1 predispose mice to age- and light-mediated retinal damage. The CCL2/CX3CR1 deficient mouse may thus serve as a model for age-related atrophic degeneration of the RPE, including the dry type of macular degeneration, geographic atrophy.

Risk-Taking Differences Across the Adult Life Span:A Question of Age and Domain

Older adults face important risky decisions about their health, their financial future, and their social environment. We examine age differences in risk-taking behaviors in multiple risk domains across the adult life span.