The lack of accelerated decline in proximity to death after excluding persons with dementia or preclinical dementia suggests that part of the terminal decline effect demonstrated in previous investigations may reflect preclinical dementia deficits. Further, accelerated cognitive decline might be a more reliable indicator of preclinical dementia than a low cognitive score due to confounds associated with cross-sectional cognitive performance.

Background: Poor social health is likely associated with cognitive decline and risk of dementia; however, studies show inconsistent results. Additionally, few studies separate social health components or control for mental health. Objective: To investigate whether loneliness and social support are independently associated with cognitive decline and risk of dementia, and whether depressive symptoms confound the association. Methods: We included 4,514 participants from the population-based Rotterdam Study (RS; aged 71±7SD years) followed up to 14 years (median 10.8, interquartile range 7.4–11.6), and 2,112 participants from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K; aged 72±10SD years) followed up to 10 years (mean 5.9±1.6SD). At baseline, participants were free of major depression and scored on the Mini-Mental State Examination (MMSE) ≥26 for RS and ≥25 for SNAC-K. We investigated loneliness, perceived social support, and structural social support (specifically marital status and number of children). In both cohorts, dementia was diagnosed and cognitive function was repeatedly assessed with MMSE and a global cognitive factor (g-factor). Results: Loneliness was prospectively associated with a decline in the MMSE in both cohorts. Consistently, persons who were lonely had an increased risk of developing dementia (RS: HR 1.34, 95%CI 1.08–1.67; SNAC-K: HR 2.16, 95%CI 1.12–4.17). Adjustment for depressive symptoms and exclusion of the first 5 years of follow-up did not alter results. Neither perceived or structural social support was associated with cognitive decline or dementia risk. Conclusion: Loneliness, not social support, predicted cognitive decline and incident dementia independently of depressive symptoms.

Background/Aim: Alzheimer’s disease (AD) is one of the most important causes of old-age cognitive impairment. We aimed to examine the influence of history of vascular disease on cognition in preclinical and early AD. Methods: Participants from a population-based study were assessed twice with a test of global cognition. The study sample was nondemented at baseline. Three years later, 138 persons were diagnosed with AD and 783 persons remained nondemented. History of vascular disease (heart disease, cerebrovascular disease) was assessed at both occasions. Results: Analyses of covariance revealed significant main effects of group (AD; comparison group) and vascular disease (present; absent) at baseline and follow-up (p < 0.01). At follow-up, a significant interaction indicated that the AD group was more negatively affected by vascular disease (p < 0.01). The fastest rate of cognitive decline was observed for those persons with preclinical AD who had new recordings of vascular disease. Conclusions: History of vascular disease has a negative impact on cognition in old age. This effect is most pronounced in persons in the earliest clinical phases of AD. Treatment of vascular risk factors in early AD might postpone time of diagnosis and slow down dementia progression.

A considerable proportion of the terminal-decline effect is accounted for by the impact of preclinical dementia. However, for tasks that are relatively resistant to age-related change, such effects might be detected independently of preclinical dementia.