Social connections have a significant impact on health across age groups, including older adults. Loneliness and social isolation are known risk factors for Alzheimer’s disease and related dementias (ADRD). Yet, we did not find a review focused on meta-analyses and systematic reviews of studies that had examined associations of social connections with cognitive decline and trials of technology-based and other social interventions to enhance social connections in people with ADRD.

We conducted a scoping review of 11 meta-analyses and systematic reviews of social connections as possible determinants of cognitive decline in older adults with or at risk of developing ADRD. We also examined eight systematic reviews of technology-based and other social interventions in persons with ADRD.

The strongest evidence for an association of social connections with lower risk of cognitive decline was related to social engagement and social activities. There was also evidence linking social network size to cognitive function or cognitive decline, but it was not consistently significant. A number of, though not all, studies reported a significant association of marital status with risk of ADRD. Surprisingly, evidence showing that social support reduces the risk of ADRD was weak. To varying degrees, technology-based and other social interventions designed to reduce loneliness in people with ADRD improved social connections and activities as well as quality of life but had no significant impact on cognition. We discuss strengths and limitations of the studies included.

Social engagement and social activities seem to be the most consistent components of social connections for improving cognitive health among individuals with or at risk for ADRD. Socially focused technology-based and other social interventions aid in improving social activities and connections and deserve more research.

People with posttraumatic stress disorder (PTSD) may have cognitive decline, a risk which can be particularly threatening at old age. However, it is yet unclear whether initial cognitive decline renders one more susceptible to subsequent PTSD following exposure to traumatic events, whether initial PTSD precedes cognitive decline or whether the effects are reciprocal.

This study examined the bidirectional longitudinal associations between cognitive function and PTSD symptoms and whether this association is mediated by depressive symptoms.

The study used data from two waves of the Israeli component of the Survey of Health, Ageing, and Retirement in Europe (SHARE), collected in 2013 and 2015. This study focused on adults aged 50 years and above (N = 567, mean age = 65.9 years). Each wave used three measures of cognition (recall, fluency, and numeracy) and PTSD symptoms following exposure to war-related events. Data were analyzed using mediation analysis with path analysis.

Initial PTSD symptoms predicted cognitive decline in recall and fluency two years later, while baseline cognitive function did not impact subsequent PTSD symptoms. Partial mediation showed that older adults with more PTSD symptoms had higher depressive symptoms, which in turn were linked to subsequent cognitive decline across all three measures.

This study reveals that PTSD symptoms are linked with subsequent cognitive decline, supporting approaches addressing this direction. It further indicates that part of this effect can be explained by increased depressive symptoms. Thus, treatment for depressive symptoms may help reduce cognitive decline due to PTSD.

Olfactory dysfunction and depression are common in later life, and both have been presented as risk factors for dementia. Our purpose was to investigate the associations between these two risk factors and determine if they had an additive effect on dementia risk.

Olfactory function was assessed using the Brief Smell Identification Test (BSIT), and depression was classified using a combination of the 15-item Geriatric Depression Scale (GDS) score and current antidepressant use. Cross-sectional associations between depression and olfactory function were examined using correlations. Cox regression analyses were conducted to examine the longitudinal relationship between olfaction and depression and incident dementia across 12-years of follow-up.

Participants were 780 older adults (aged 70–90 years; 56.5% female) from the Sydney Memory and Ageing Study (MAS) without a diagnosis of dementia at baseline.

Partial correlation revealed a nonsignificant association between baseline depression and olfactory function after accounting for covariates (r = −.051, p = .173). Cox regression showed that depression at baseline (hazard ratio = 1.706, 95% CI 1.185–2.456, p = .004) and lower BSIT scores (HR = .845, 95%CI .789–.905, p < .001) were independently associated with a higher risk of incident dementia across 12 years. Entering both predictors together improved the overall predictive power of the model.

Lower olfactory identification scores and depressive symptoms predict incident dementia over 12 years. The use of BSIT scores and depression in conjunction provides a greater ability to predict dementia than either used alone. Assessment of olfactory function and depression screening may provide clinical utility in the early detection of dementia.

Older adults commonly take benzodiazepines (BZDs) that may have long-term adverse cognitive effects. We investigated whether BZD use was related to developing mild cognitive impairment (MCI) or dementia in cognitively normal older adults in the community.

A population-based cohort (n = 1959) of adults aged 65 and over, recruited from communities of low socioeconomic status.

BZD use, Clinical Dementia Rating (CDR), anxiety symptoms, depression symptoms, sleep difficulties, and APOE genotype.

We examined time from study entry to MCI (CDR = 0.5) and time from study entry to dementia (CDR ≥ 1) in participants who were cognitively normal at baseline (CDR = 0). We used survival analysis (Cox model), adjusted for age, sex, education, sleep, anxiety, and depression. For all the models, we included an interaction term between BZD use and APOE*4.

Taking BZDs was significantly associated with higher risk of developing MCI, but not of developing dementia. The effect was not affected by APOE genotype.

In a population-based sample of cognitively normal older adults, BZD use is associated with developing MCI, but not dementia. BZD use may be a potentially modifiable risk factor for MCI.