The effect of social networks on the relation between Alzheimer's disease pathology and level of cognitive function in old people: a longitudinal cohort study

Summary

Background

Few data are available about how social networks reduce the risk of cognitive impairment in old age. We aimed to measure this effect using data from a large, longitudinal, epidemiological clinicopathological study.

Methods

89 elderly people without known dementia participating in the Rush Memory and Aging Project underwent annual clinical evaluation. Brain autopsy was done at the time of death. Social network data were obtained by structured interview. Cognitive function tests were Z scored and averaged to yield a global and specific measure of cognitive function. Alzheimer's disease pathology was quantified as a global measure based on modified Bielschowsky silver stain. Amyloid load and the density of paired helical filament tau tangles were also quantified with antibody-specific immunostains. We used linear regression to examine the relation of disease pathology scores and social networks to level of cognitive function.

Findings

Cognitive function was inversely related to all measures of disease pathology, indicating lower function at more severe levels of pathology. Social network size modified the association between pathology and cognitive function (parameter estimate 0·097, SE 0·039, p=0·016, R²=0·295). Even at more severe levels of global disease pathology, cognitive function remained higher for participants with larger network sizes. A similar modifying association was observed with tangles (parameter estimate 0·011, SE 0·003, p=0·001, R²=0·454). These modifying effects were most pronounced for semantic memory and working memory. Amyloid load did not modify the relation between pathology and network size. The results were unchanged after controlling for cognitive, physical, and social activities, depressive symptoms, or number of chronic diseases.

Interpretation

These findings suggest that social networks modify the relation of some measures of Alzheimer's disease pathology to level of cognitive function.

Introduction

Several clinicopathological studies over the past two decades have shown that many elderly people with extensive pathology of Alzheimer's disease do not clinically manifest cognitive impairment.1, 2, 3, 4 This ability to tolerate the pathology of this disease without obvious clinical consequences is increasingly referred to as cognitive or neural reserve.1, 5 Identification of factors associated with neural reserve has important implications for disease prevention. For example, one such factor is education. Clinicopathological studies suggest that the relation between quantitative measures of Alzheimer's disease pathology and level of cognition differ by duration of formal education.⁶ Another potential factor that could modify this relation is social networks. Social networks have been related to a reduced risk of death and a reduction in a wide variety of adverse health outcomes in old people.⁷ Several studies have also examined the relation between the extent of social ties and cognitive function and dementia. Most,8, 9, 10 but not all,¹¹ showed that people with more extensive social networks were at reduced risk of cognitive impairment. Little is known about the cellular, molecular, and neuropathology of social networks and potential neurobiological mechanisms underlying this association. Although social networks could be directly related to the accumulation of Alzheimer's disease pathology, it seems more likely that social network size is related to reserve capacity capable of reducing the likelihood that the disease pathology will be clinically expressed as cognitive impairment. We aimed to test this hypothesis using data from the Rush Memory and Aging Project—a large, longitudinal, epidemiological, clinicopathological study of ageing and Alzheimer's disease.