Functional disability and social participation restriction associated with chronic conditions in middle-aged and older adults

Abstract : Background. We examine the population impact on functional disability and social participation of physical and mental chronic conditions individually and in combination. Methods. Cross-sectional, population-based data from community-dwelling people aged 45 years and over living in the 10 Canadian provinces in 2008–2009 were used to estimate the population attributable risk (PAR) for functional disability in basic (ADL) and instrumental (IADL) activities of daily living and social participation restrictions for individual and combinations of chronic conditions, stratified by age and gender, after adjusting for confounding variables. Results. Five chronic conditions (arthritis, depression, diabetes, heart disease and eye disease) made the largest contributions to ADL-related and IADL-related functional disability and social participation restrictions, with variation in magnitude and ranking by age and gender. While arthritis was consistently associated with higher PARs across gender and most age groups, depression, alone and in combination with the physical chronic conditions, was associated with ADL and IADL disability as well as social participation restrictions in the younger age groups, especially among women. Compared to women, the combinations of conditions associated with higher PARs in men more often included heart disease and diabetes. Conclusions. Our findings suggest that in community dwelling middle-aged and older adults, the impact of combinations of mental and physical chronic conditions on functional disability and social participation restriction is substantial and differed by gender and age. Recognising the differences in the drivers of PAR by gender and age group will ultimately increase the efficiency of clinical and public health interventions

Reminiscence groups for people with dementia and their family carers: pragmatic eight-centre randomised trial of joint reminiscence and maintenance versus usual treatment: a protocol

The growing number of people with dementia, and the increasing cost of care, provides a major incentive to develop and test methods of supporting them in the community for longer. Most attention has been given to pharmacological interventions, but there is increasing recognition that psychosocial interventions may be equally effective, even preferable where medication has negative side-effects. Reminiscence groups, run by professionals and volunteers, which use photographs, recordings and other objects to trigger personal memories are probably the most popular therapeutic approach to working with people with dementia, but there is little evidence for their effectiveness and cost-effectiveness. The recent inclusion of family carers in groups with people with dementia, notably in our own pilot studies, has generated informal evidence that this joint approach improves relationships between people with dementia and their carers, and benefits both

Impaired mitochondrial calcium efflux contributes to disease progression in models of Alzheimer’s disease

Impairments in neuronal intracellular calcium (iCa2+) handling may contribute to Alzheimer’s disease (AD) development. Metabolic dysfunction and progressive neuronal loss are associated with AD progression, and mitochondrial calcium (mCa2+) signaling is a key regulator of both of these processes. Here, we report remodeling of the mCa2+ exchange machinery in the prefrontal cortex of individuals with AD. In the 3xTg-AD mouse model impaired mCa2+ efflux capacity precedes neuropathology. Neuronal deletion of the mitochondrial Na+/Ca2+ exchanger (NCLX, Slc8b1 gene) accelerated memory decline and increased amyloidosis and tau pathology. Further, genetic rescue of neuronal NCLX in 3xTg-AD mice is sufficient to impede AD-associated pathology and memory loss. We show that mCa2+ overload contributes to AD progression by promoting superoxide generation, metabolic dysfunction and neuronal cell death. These results provide a link between the calcium dysregulation and metabolic dysfunction hypotheses of AD and suggest mCa2+ exchange as potential therapeutic target in AD