The proportion of older people has increased rapidly in recent decades such that 12% of the global population in 2015 was 60 years or older.¹ By 2050, this proportion is projected to be greater than one-fifth of the population.¹ Consequently, the number of older adults with cognitive impairment and dementia is increasing rapidly.² Dementia is one of the most common and serious disorders in later life. It is responsible for a large proportion of disability and mortality in older people and imposes a huge burden of long-term care for families and society.³ No effective therapies are available for treating dementia; therefore, the development of dementia prevention strategies has become a priority.^4,5 During the long preclinical phase of dementia, accelerated cognitive decline is regarded as a cardinal marker. Thus, the identification of risk factors for cognitive decline is of great significance for dementia prevention.

Previous studies have suggested that coronary heart disease (CHD) may be associated with accelerated cognitive decline. However, the temporal pattern of cognitive decline before and after incident CHD remains largely unknown. The purpose of this study was to determine the cognitive trajectory before and after incident CHD diagnosis in a national representative cohort age ≥50 years. This study included 7,888 participants (mean age 62.1 ± 10.2 years) with no history of stroke or incident stroke during follow-up from the English Longitudinal Study of Ageing. Participants underwent a cognitive assessment at baseline (wave 1, 2002 to 2003), and at least 1 other time point (from wave 2 [2004 to 2005] to wave 8 [2016 to 2017]). Incident CHD was identified as a diagnosis of myocardial infarction and/or angina during follow-up. Incident CHD was associated with accelerated cognitive decline during a median follow-up of 12 years. The annual rate of cognitive decline before CHD diagnosis among individuals who experienced incident CHD was similar to that of participants who remained CHD-free throughout follow-up. No short-term cognitive decline was observed in participants with CHD diagnosis after the event. In the years following CHD diagnosis, global cognition, verbal memory, and temporal orientation scores declined significantly faster than they did before the event, after multivariable adjustment. Sensitivity analyses yielded similar results. Incident CHD is associated with accelerated cognitive decline after, but not before, the event. Attention should be drawn to the long-term cognitive deterioration related to CHD. Careful monitoring of cognitive function is warranted in CHD patients in the years following the event.

Aims/hypothesis The aim of the study was to evaluate longitudinal associations between HbA_1c levels, diabetes status and subsequent cognitive decline over a 10 year follow-up period. Methods Data from wave 2 (2004–2005) to wave 7 (2014–2015) of the English Longitudinal Study of Ageing (ELSA) were analysed. Cognitive function was assessed at baseline (wave 2) and reassessed every 2 years at waves 3–7. Linear mixed models were used to evaluate longitudinal associations. Results The study comprised 5189 participants (55.1% women, mean age 65.6 ± 9.4 years) with baseline HbA_1c levels ranging from 15.9 to 126.3 mmol/mol (3.6–13.7%). The mean follow-up duration was 8.1 ± 2.8 years and the mean number of cognitive assessments was 4.9 ± 1.5. A 1 mmol/mol increment in HbA_1c was significantly associated with an increased rate of decline in global cognitive z scores (−0.0009 SD/year, 95% CI −0.0014, −0.0003), memory z scores (−0.0005 SD/year, 95% CI −0.0009, −0.0001) and executive function z scores (−0.0008 SD/year, 95% CI −0.0013, −0.0004) after adjustment for baseline age, sex, total cholesterol, HDL-cholesterol, triacylglycerol, high-sensitivity C-reactive protein, BMI, education, marital status, depressive symptoms, current smoking, alcohol consumption, hypertension, CHD, stroke, chronic lung disease and cancer. Compared with participants with normoglycaemia, the multivariable-adjusted rate of global cognitive decline associated with prediabetes and diabetes was increased by −0.012 SD/year (95% CI −0.022, −0.002) and −0.031 SD/year (95% CI −0.046, −0.015), respectively (p for trend <0.001). Similarly, memory, executive function and orientation z scores showed an increased rate of cognitive decline with diabetes. Conclusions/interpretation Significant longitudinal associations between HbA_1c levels, diabetes status and long-term cognitive decline were observed in this study. Future studies are required to determine the effects of maintaining optimal glucose control on the rate of cognitive decline in people with diabetes.

Objective: To assess the relationship between fine particulate matter (PM_2.5) concentration and ischaemic heart disease (IHD) morbidity and mortality. Methods: A time-series study conducted in Beijing from 1 January 2010 to 31 December 2012. Data on 369 469 IHD cases and 53 247 IHD deaths were collected by the Beijing Monitoring System for Cardiovascular Diseases, which covers all hospital admissions and deaths from IHD from Beijing's population of 19.61 million. Results: The mean daily PM_2.5 concentration was 96.2 μg/m³ with a range from 3.9 to 493.9 μg/m³. Only 15.3% of the daily PM_2.5 concentrations achieved WHO Air Quality Guidelines target (25 μg/m³) in the study period. The dose–response relationships between PM_2.5 and IHD morbidity and mortality were non-linear, with a steeper dose–response function at lower concentrations and a shallower response at higher concentrations. A 10 μg/m³ increase in PM_2.5 was associated with a 0.27% (95% CI 0.21 to 0.33%, p<2.00×10⁻¹⁶) increase in IHD morbidity and a 0.25% (95% CI 0.10 to 0.40%, p=1.15×10⁻³) increase in mortality on the same day. During the 3 years, there were 7703 cases and 1475 deaths advanced by PM_2.5 pollution over expected rates if daily levels had not exceeded the WHO target. Conclusions: PM_2.5 concentration was significantly associated with IHD morbidity and mortality in Beijing. Our findings provide a rationale for the urgent need for stringent control of air pollution to reduce PM_2.5 concentration.

Elevated blood pressure (BP) has been linked to impaired cognition and dementia in older adults. However, few studies have accounted for long-term cumulative BP exposure. The aim of this study was to test whether long-term cumulative BP was independently associated with subsequent cognitive decline, incident dementia, and all-cause mortality among cognitively healthy adults. This study used data from the HRS (Health and Retirement Study) and ELSA (English Longitudinal Study of Ageing). Cumulative BP was calculated as the area under the curve using measurements from wave 0 (1998-1999) to wave 4 (2008-2009) in ELSA and wave 8 (2006-2007) to wave 10 (2010-2011) in the HRS. Outcomes included cognitive decline, incident dementia, and all-cause mortality. A total of 7,566 and 9,294 participants from ELSA and the HRS were included (44.8% and 40.2% men and median age 62.0 years [IQR: 55.0-70.0 years] and 65.0 years [IQR: 58.0-72.0 years], respectively). The median follow-up duration was 8.0 years (IQR: 4.0-8.0 years) and 8.0 years (IQR: 6.0-8.0 years), respectively. Elevated cumulative systolic BP and pulse pressure were independently associated with accelerated cognitive decline (P < 0.001 for both), elevated dementia risk (P < 0.001 for both), and all-cause mortality (P < 0.001 for both), while a significant inverse association was observed for diastolic BP. Strong dose-response relationships were identified, with similar results for the 2 cohorts. Long-term cumulative BP was associated with subsequent cognitive decline, dementia risk, and all-cause mortality in cognitively healthy adults aged ≥50 years. Efforts are required to control long-term systolic BP and pulse pressure and to maintain adequate diastolic BP.

Objective To determine the trajectory of cognitive decline before and after incident stroke. Methods By using data from the English Longitudinal Study of Ageing, we studied 9,278 participants without dementia with no history of stroke who underwent cognitive assessment at baseline (wave 1) and at least 1 other time point (waves 2–7). We used linear mixed models to analyze repeated measures and longitudinal data. Results Among the 9,278 participants (56.8% women, mean age 63.1 ± 10.3 years), 471 (5.1%) incident stroke events were identified. Compared with stroke-free participants, multivariable-adjusted rates of prestroke cognitive decline in global cognition, memory, semantic fluency, and temporal orientation of participants who later experienced an incident stroke were increased by −0.029 , −0.016, −0.022, and −0.024 SD/y, respectively. Among the 471 stroke survivors, the multivariable-adjusted acute changes in the 4 cognitive domains were −0.257, −0.150, −0.121, and −0.272 SD, respectively. In the years after stroke, global cognition declined over time and was steeper than its prestroke slope, that is, by −0.064 SD/y after multivariable adjustment. The rates of memory, semantic fluency, and temporal orientation decline were −0.046, −0.033, and −0.037 SD/y, respectively. Conclusions Accelerated prestroke cognitive decline and poststroke cognitive decline were associated with incident stroke over a follow-up period of 12 years. Attention should be paid to the long-term cognitive problems of stroke survivors, and intervention and management of major vascular risk factors should start from early life or midlife to reduce the risk of cerebrovascular disease and the associated cognitive impairment.