Ebook: Handbook of Prevention and Alzheimer’s Disease

Advances in Alzheimer’s Disease

Volume 10

Handbook of Prevention and Alzheimer’s Disease

Cyrus A. Raji, MD, PhD

Washington University, St. Louis, MO, USA

Yue Leng, PhD

University of California, San Francisco, CA, USA

J. Wesson Ashford, MD, PhD

VA Palo Alto Health Care System, Palo Alto, CA, USA

Stanford University, Palo Alto, CA, USA

Dharma Singh Khalsa, MD

Alzheimer’s Research and Prevention Foundation, Tucson, AZ, USA

The Handbook of Prevention and Alzheimer’s Disease educates physicians, scientists, and members of industry into a subfield of Alzheimer’s disease (AD) research that has matured in the early 21st Century—the notion that AD can be prevented and modified through changeable factors and related interventions. The idea of AD prevention is not new with reference to strategies noted as early as the 1990s [1], with additional prescriptive approaches arising shortly thereafter [2]. Foundational highly cited work would then follow [3]. AD was first reported almost 120 years ago and remarkably even the article that gave rise to this field noted the presence of large vessel arteriosclerosis in the first identified person with Alzheimer’s, Auguste D [4]. Thus, the concept that modifiable risk factors may be part of AD is virtually part of the origin of this field and make the need for additional work in this area urgent.

The number of modifiable risk factors related to AD continues to increase from the initial seven identified in foundational work [3] to 12 modifiable risk factors [5] with a current projected contribution to 40% of worldwide dementias. Thus, an Alzheimer’s disease ‘preventome’ now exists and will continue to expand as understanding of newer factors and related biomarkers is refined. The outcome of optimizing the AD preventome is an improvement in overall brain health [6]. Such an outcome will reduce risk for AD and improve quality of life by enhancements in brain health. Newer supporting fields will also evolve around these principles such as preventive neuroradiology [7].

The growth of this field is reflected in the fact that we have two volumes: Volume 10 on Prevention and Volume 11 on Intervention. The Prevention volume goes into greater depth than an AD preventome by examining domains of prevention from vascular risk factors to social engagement, sleep health and spirituality. If the journey to end AD can be likened to a long and arduous challenge, understanding every possible part of the overall toolkit of approaches for disease prevention and intervention is essential.

References

[1] Khalsa DS (1998) Integrated medicine and the prevention and reversal of memory loss. Altern Ther Health Med 4, 38–43.

[2] Ashford JW (2002) The top ten treatments for preventing Alzheimer’s disease. LIAF Line: Newsletter of the Long Island Alzheimer’s Foundation.

[3] Barnes DE, Yaffe K (2011) The projected effect of risk factor reduction on Alzheimer’s disease prevalence. Lancet Neurol 10, 819–28.

[4] Alzheimer A (1907) Uber eine eigenartige Erkrankung der Hirnrinde. Allg Zeits f Psychiat 64, 146–148.

[5] Livingston G, Huntley J, Sommerlad A, Ames D, Ballard C, Banerjee S, Brayne C, Burns A, Cohen-Mansfield J, Cooper C, Costafreda SG, Dias A, Fox N, Gitlin LN, Howard R, Kales HC, Kivimäki M, Larson EB, Ogunniyi A, Orgeta V, Ritchie K, Rockwood K, Sampson EL, Samus Q, Schneider LS, Selbæk G, Teri L, Mukadam N (2020) Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet 396, 413–446.

[6] Hachinski V, Avan A, Gilliland J, Oveisgharan S (2021) A new definition of brain health. Lancet Neurol 20, 335–336.

[7] Raji CA, Eyre H, Wei SH, Bredesen DE, Moylan S, Law M, Small G, Thompson PM, Friedlander RM, Silverman DH, Baune BT, Hoang TA, Salamon N, Toga AW, Vernooij MW (2015) Hot topics in research: preventive neuroradiology in brain aging and cognitive decline. Am J Neuroradiol 36, 1803–1809.

Background:

Little is known about the association between physical activity (PA) and cognitive trajectories in older adults.

Objective:

To examine the association between PA and change in memory, language, attention, visuospatial skills, and global cognition, and a potential impact of sex or Apolipoprotein E (APOE) ε4 status.

Methods:

Longitudinal study derived from the population-based Mayo Clinic Study of Aging, including 2,060 cognitively unimpaired males and females aged ≥70 years. Engagement in midlife (ages 50–65) and late-life (last year) PA was assessed using a questionnaire. Neuropsychological testing was done every 15 months (mean follow-up 5.8 years). We ran linear mixed-effect models to examine whether mid- or late-life PA at three intensities (mild, moderate, vigorous) was associated with cognitive z-scores.

Results:

Light intensity midlife PA was associated with less decline in memory function compared to the no-PA reference group (time x light PA; estimate [standard error] 0.047 [0.016], p = 0.004). Vigorous late-life PA was associated with less decline in language (0.033 [0.015], p = 0.030), attention (0.032 [0.017], p = 0.050), and global cognition (0.039 [0.016], p = 0.012). Females who were physically inactive in midlife experienced more pronounced cognitive decline than females physically active in midlife and males regardless of PA (p-values for time interaction terms with midlife PA levels and sex were all p < 0.05 for global cognition). APOE ε4 carriership did not moderate the association between PA and cognition.

Conclusion:

Engaging in PA, particularly of vigorous intensity in late-life, was associated with less pronounced decline in global and domain-specific cognition. This association may differ by sex.

Background:

Physical activity has been associated with better cognitive function and better sleep quality. Yet, whether the beneficial effect of physical activity on cognitive function can be explained by an indirect pathway involving better sleep quality is unclear.

Objective:

To investigate whether sleep quality mediates the association between physical activity and cognitive function in adults 50 years of age or older.

Methods:

86,541 community-dwelling European adults were included in the study. Physical activity and sleep quality were self-reported. Indicators of cognitive function (immediate recall, delayed recall, verbal fluency) were assessed using objective tests. All measures were collected six times between 2004 and 2017. The mediation was tested using multilevel mediation analyses.

Results:

Results showed that self-reported physical activity was associated with better self-reported sleep quality, which was associated with better performance in all three indicators of cognitive function, demonstrating an indirect effect of physical activity on cognitive function through sleep quality. The mediating effect of sleep quality accounted for 0.41%, 1.46%, and 8.88% of the total association of physical activity with verbal fluency, immediate recall, and delayed recall, respectively.

Conclusion:

These findings suggest that self-reported sleep quality partly mediates the association between self-reported physical activity and cognitive function. These results need to be confirmed by device-based data of physical activity and sleep quality.

Background:

Cognitive reserve (CR) has been postulated to contribute to the variation observed between neuropathology and clinical outcomes in Alzheimer’s disease (AD).

Objective:

We investigated the effect of an education-occupation derived CR proxy on biological properties of white matter tracts in patients with amnestic mild cognitive impairment (aMCI) and healthy elders (HC).

Methods:

Educational attainment and occupational complexity ratings (complexity with data, people, and things) from thirty-five patients with aMCI and twenty-eight HC were used to generate composite CR scores. Quantitative magnetic resonance imaging (qMRI) and multi-shell diffusion MRI were used to extract macromolecular tissue volume (MTV) across major white matter tracts.

Results:

We observed significant differences in the association between CR and white matter tract MTV in aMCI versus HC when age, gender, intracranial volume, and memory ability were held constant. Particularly, in aMCI, higher CR was associated with worse tract pathology (lower MTV) in the left and right dorsal cingulum, callosum forceps major, right inferior fronto-occipital fasciculus, and right superior longitudinal fasciculus (SLF) tracts. Conversely higher CR was associated with higher MTV in the right parahippocampal cingulum and left SLF in HC.

Conclusion:

Our results support compensatory CR mechanisms in aMCI and neuroprotective mechanisms in HC and suggest differential roles for CR on white matter macromolecular properties in healthy elders versus prodromal AD patients.

Background:

A protective effect of education on cognitive decline after stroke has been claimed, but evidence from prospective population-based cohorts is very limited. The differential role of literacy and education on dementia after stroke remains unexplored.

Objective:

This research addresses the role of education and literacy in dementia incidence after stroke and transient ischemic attack (TIA).

Methods:

131 participants with stroke or TIA were identified within the population-based NEDICES study (N = 5,278 persons). Participants were fully assessed at baseline (1994–1995) and incident dementia diagnosis was made by expert neurologists (DSM-IV criteria) after a mean follow-up of 3.4 years. Adjusted Cox regression analyses were applied to test the association between education, literacy, and dementia risk.

Results:

Within the 131 subjects with stroke or TIA, 19 (14%) developed dementia at follow-up. The Cox’s regression model (age and sex adjusted) showed that low education (HR = 3.48, 95% CI = 1.28, 9.42, p = 0.014) and literacy (HR = 3.16, 95% CI = 1.08, 9.22, p = 0.035) were significantly associated with a higher dementia risk. Low education was also associated with dementia when main confounders (i.e., cognitive/functional performance) were considered in the Cox’s model. However, after including stroke recurrence, only low/null literacy (versus education) remained as significant predictor of dementia. Finally, low/null literacy showed an effect over-and-above education on dementia risk when both factors were introduced in the adjusted Cox’s regression.

Conclusion:

These findings underline the importance of literacy to estimate cognitive decline after stroke in low-educated populations.

Background:

Age-related cognitive decline is a chronic, progressive process that requires active clinical management as cognitive status changes. Computerized cognitive training (CCT) provides cognitive exercises targeting specific cognitive domains delivered by computer or tablet. Meanwhile, CCT can be used to regularly monitor the cognitive status of patients, but it is not clear whether CCT can reliably assess cognitive ability or be used to diagnose different stages of cognitive impairment.

Objective:

To investigate whether CCT can accurately monitor the cognitive status of patients with cognitive impairment as well as distinguish patients with dementia from patients with mild cognitive impairment (MCI).

Method:

We included 116 patients (42 dementia and 74 MCI) in final analysis. Cognitive ability was assessed by averaging the patient performance on the CCT to determine the Cognitive Index. The validity of the Cognitive Index was evaluated by its correlation with neuropsychological tests, and internal consistency was measured to assess the reliability. Additionally, we determined the diagnostic ability of the Cognitive Index to detect dementia using receiver operating characteristic (ROC) analysis.

Results:

The Cognitive Index was highly correlated with the Montreal Cognitive Assessment (r = 0.812) and the Mini-Mental State Examination (r = 0.694), indicating good convergent validity, and the Cronbach’s alpha coefficient was 0.936, indicating excellent internal consistency. The area under the ROC curve, sensitivity, and specificity of the Cognitive Index to diagnose dementia were 0.943, 83.3%, and 91.9%, respectively.

Conclusions:

CCT can be used to assess cognitive status and detect dementia in patients with cognitive impairment.

Background:

Fluid intelligence (FI) involves abstract problem-solving without prior knowledge. Greater age-related FI decline increases Alzheimer’s disease (AD) risk, and recent studies suggest that certain dietary regimens may influence rates of decline. However, it is uncertain how long-term food consumption affects FI among adults with or without familial history of AD (FH) or APOE4 (ε4).

Objective:

Observe how the total diet is associated with long-term cognition among mid- to late-life populations at-risk and not-at-risk for AD.

Methods:

Among 1,787 mid-to-late-aged adult UK Biobank participants, 10-year FI trajectories were modeled and regressed onto the total diet based on self-reported intake of 49 whole foods from a Food Frequency Questionnaire (FFQ).

Results:

Daily cheese intake strongly predicted better FIT scores over time (FH-: β = 0.207, p < 0.001; ε4–: β = 0.073, p = 0.008; ε4+: β = 0.162, p = 0.001). Alcohol of any type daily also appeared beneficial (ε4+: β = 0.101, p = 0.022) and red wine was sometimes additionally protective (FH+: β = 0.100, p = 0.014; ε4–: β = 0.59, p = 0.039). Consuming lamb weekly was associated with improved outcomes (FH-: β = 0.066, p = 0.008; ε4+: β = 0.097, p = 0.044). Among at risk groups, added salt correlated with decreased performance (FH+: β = –0.114, p = 0.004; ε4+: β = –0.121, p = 0.009).

Conclusion:

Modifying meal plans may help minimize cognitive decline. We observed that added salt may put at-risk individuals at greater risk, but did not observe similar interactions among FH- and AD- individuals. Observations further suggest in risk status-dependent manners that adding cheese and red wine to the diet daily, and lamb on a weekly basis, may also improve long-term cognitive outcomes.

Background:

The relationship between midlife dietary habits and risk of dementia remains unclear.

Objective:

To investigate the association between dietary fish and n-3 polyunsaturated fatty acid (PUFA) consumption in midlife and risk of dementia in later life.

Methods:

This population-based cohort study assessed food frequency (average intake in 1995 and 2000) and cognition (2014-2015) in 1,127 participants (aged 45–64 in 1995). We used logistic regression analyses to calculate odds ratios (ORs) for dementia and mild cognitive impairment (MCI) diagnoses for consumption quartiles of fish, PUFA-rich fish, total n-3 PUFAs, total n-6 PUFAs, types of PUFAs, and n-3/n-6 PUFA ratio. Estimated ORs were adjusted for age; sex; education; smoking status; alcohol consumption frequency; physical activity; histories of cancer, myocardial infarction, and diabetes mellitus; and depression.

Results:

Significantly reduced risks of dementia over non-dementia (MCI plus cognitively normal) were observed in the second (OR = 0.43 (95% CI = 0.20–0.93)), third (OR = 0.22 (95% CI = 0.09–0.54)), and highest quartiles (OR = 0.39 (95% CI = 0.18–0.86)) for fish; the third (OR = 0.39 (95% CI = 0.16–0.92)) and highest quartiles (OR = 0.44 (95% CI = 0.19–0.98)) for eicosapentaenoic acid (EPA); the second (OR = 0.39 (95% CI = 0.18–0.84)), third (OR = 0.30 (95% CI = 0.13–0.70)), and highest quartiles (OR = 0.28 (95% CI = 0.12–0.66)) for docosahexaenoic acid (DHA); and the third (OR = 0.36 (95% CI = 0.16–0.85)) and highest quartiles (OR = 0.42 (95% CI = 0.19–0.95)) for docosapentaenoic acid (DPA).

Conclusion:

High intake of fish in midlife might aid in preventing dementia.

Background:

The efficacy of vitamin E in prevention of diabetes-related complications differs by Haptoglobin (Hp) genotype.

Objective:

To examine the role of Hp genotype in the relationship of vitamin E intake with brain volume in cognitively normal elderly patients with type 2 diabetes.

Methods:

Brain volumes for the superior, middle, and inferior frontal gyri and for the middle temporal gyrus were generated from structural T1 MRI in 181 study participants (Hp 1-1: n = 24, Hp 2-1: n = 77, Hp 2-2: n = 80). Daily vitamin E intake was assessed using the Food Frequency Questionnaire. Analyses of covariance, controlling for demographic and cardiovascular variables was used to evaluate whether the association of daily vitamin E intake with brain volume was modified by Hp genotype.

Results:

Average age was 70.8 (SD = 4.2) with 40% females, and mean Mini-Mental State Examination score of 28.17 (SD = 1.90). A significant interaction was found between vitamin E intake and Hp genotype in inferior frontal gyrus’ volume; p = 0.0108. For every 1 microgram increase in vitamin E intake, the volume of the inferior frontal gyrus decreased by 0.955% for Hp 1-1 (p = 0.0348), increased by 0.429% for Hp 2-1 (p = 0.0457), and by 0.077% for Hp 2-2 (p = 0.6318). There were no significant interactions between vitamin E intake and Hp genotype for the middle (p = 0.6011) and superior (p = 0.2025) frontal gyri or for the middle temporal gyrus (p = 0.503).

Conclusions:

The effect of dietary vitamin E on the brain may differ by Hp genotype. Studies examining the impact of vitamin E on brain-related outcomes should consider Hp genotype.

Background:

Excess weight in adulthood leads to health complications such as diabetes, hypertension, or dyslipidemia. Recently, excess weight has also been related to brain atrophy and cognitive decline. Reports show that obesity is linked with Alzheimer’s disease (AD)-related changes, such as cerebrovascular damage or amyloid-β accumulation. However, to date no research has conducted a direct comparison between brain atrophy patterns in AD and obesity.

Objective:

Here, we compared patterns of brain atrophy and amyloid-β/tau protein accumulation in obesity and AD using a sample of over 1,300 individuals from four groups: AD patients, healthy controls, obese otherwise healthy individuals, and lean individuals.

Methods:

We age- and sex-matched all groups to the AD-patients group and created cortical thickness maps of AD and obesity. This was done by comparing AD patients with healthy controls, and obese individuals with lean individuals. We then compared the AD and obesity maps using correlation analyses and permutation-based tests that account for spatial autocorrelation. Similarly, we compared obesity brain maps with amyloid-β and tau protein maps from other studies.

Results:

Obesity maps were highly correlated with AD maps but were not correlated with amyloid-β/tau protein maps. This effect was not accounted for by the presence of obesity in the AD group.

Conclusion:

Our research confirms that obesity-related grey matter atrophy resembles that of AD. Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.

Until 300,000 years ago, ancestors of modern humans ubiquitously carried the apolipoprotein E (APOE) ε4/ε4 genotype, when the ε3 allele mutated from the ancestral ε4, which elevates the risk of Alzheimer’s disease. Modern humans living today predominantly carry the ε3 allele, which provides protection against heart disease and dementia in long-lived populations. The ancestral ε4 allele has been highly preserved in isolated populations in tropical and Arctic regions with high pathogen burdens, e.g., helminths. Early humans experienced serious enteric infections that exerted evolutionary selection pressure, and factors that mitigate infant and childhood mortality from enteric infections also exert selection pressure. Some bacteria can exploit the host’s defensive inflammatory response to colonize and invade the host. Pathogen-induced inflammation associated with infant and childhood diarrhea can damage the gut wall long after the invading organisms are no longer present. Inflammation not only resides in the mucosal wall, but also induces systemic inflammation. Baseline systemic inflammation is lower in ε4 carriers, yet ε4 carriers display a stronger host inflammatory response that reduces pathogen burdens, increasing infant and early childhood survival. Evolutionary selection of the ε3 allele likely occurred after humans moved into temperate zones with lower pathogen burdens, unrelated to protection from Alzheimer’s disease.

Background:

The effectiveness of glucose-lowering drugs (GLDs) is unknown among patients with dementia.

Objective:

To analyze all-cause mortality among users of six GLDs in dementia and dementia-free subjects, respectively.

Methods:

This was a longitudinal open-cohort registry-based study using data from the Swedish Dementia Registry, Total Population Register, and four supplemental registers providing data on dementia status, drug usage, confounders, and mortality. The cohort comprised 132,402 subjects with diabetes at baseline, of which 11,401 (8.6%) had dementia and 121,001 (91.4%) were dementia-free. Subsequently, comparable dementia – dementia-free pairs were sampled. Then, as-treated and intention-to-treat exposures to metformin, insulin, sulfonylurea, dipeptidyl-peptidase-4 inhibitors, glucagon-like peptide-1 analogues (GLP-1a), and sodium-glucose cotransporter-2 inhibitors (SGLT-2i) were analyzed in the parallel dementia and dementia-free cohorts. Confounding was addressed using inverse-probability weighting and propensity-score matching, and flexible parametric survival models were used to produce hazard ratios (HR) and 95% confidence intervals (CI) of the association between GLDs and all-cause mortality.

Results:

In the as-treated models, increased mortality was observed among insulin users with dementia (HR 1.34 [95% CI 1.24–1.45]) as well as in dementia-free subjects (1.54 [1.10–1.55]). Conversely, sulfonylurea was associated with higher mortality only in dementia subjects (1.19 [1.01–1.42]). GLP-1a (0.44 [0.25–0.78]) and SGLT-2i users with dementia (0.43 [0.23–0.80]) experienced lower mortality compared to non-users.

Conclusion:

Insulin and sulfonylurea carried higher mortality risk among dementia patients, while GLP-1a and SGLT-2i were associated with lower risk. GLD-associated mortality varied between dementia and comparable dementia-free subjects. Further studies are needed to optimize GLD use in dementia patients.

Different investigations lead to the urgent need to generate validated clinical protocols as a tool for medical doctors to orientate patients under risk for a preventive approach to control Alzheimer’s disease. Moreover, there is consensus that the combined effects of risk factors for the disease can be modified according to lifestyle, thus controlling at least 40% of cases. The other fraction of cases are derived from candidate genes and epigenetic components as a relevant factor in AD pathogenesis. At this point, it appears to be of critical relevance the search for molecular biomarkers that may provide information on probable pathological events and alert about early detectable risks to prevent symptomatic events of the disease. These precocious detection markers will then allow early interventions of non-symptomatic subjects at risk. Here, we summarize the status and potential avenues of prevention and highlight the usefulness of biological and reliable markers for AD.

Background:

Vitamin D deficiency is associated with all-cause dementia and Alzheimer’s disease (AD). At the same time, this knowledge is limited specifically for vascular dementia (VaD), while data regarding other subtypes of dementia are even more limited.

Objective:

To investigate the association of 25-hydroxy vitamin D (25(OH)D) status with dementia subtypes in an outpatient geriatric population.

Methods:

In a cross-sectional design, we analyzed data from 1,758 patients of an outpatient memory clinic in The Netherlands. Cognitive disorders were diagnosed by a multidisciplinary team according to international clinical standards. At each first-visit 25(OH)D levels were measured. Data were analyzed using ANCOVA in four models with age, gender, BMI, education, alcohol, smoking, season, polypharmacy, calcium, eGFR, and glucose as co-variates. 25(OH)D was treated as a continuous square rooted (sqr) variable.

Results:

In the fully adjusted model, reduced 25(OH)D serum levels (sqr) were found in AD (estimated mean 7.77 ± 0.11 CI95% 7.55-7.99): and in VaD (estimated mean 7.60 ± 0.16 CI95% 7.28-7.92) patients compared to no-dementia (ND) patients (estimated mean 8.27 ± 0.09 CI95% 8.10-8.45) (ND-AD: p = 0.006, CI95% 0.08-0.92.; ND-VaD p = 0.004 CI95% 0.13-1.22). We did not find differences in 25(OH)D levels of mild cognitive impairment (MCI) or other dementia patients compared to ND patients, nor differences in comparing dementia subtypes.

Conclusion:

We observed significantly lower 25(OH)D serum levels in both AD and VaD patients compared to no-dementia patients, but no significant differences between MCI and Lewy body and mixed dementia subtypes in this cross-sectional study of a geriatric outpatient clinic population.

Background:

Given the advent of large-scale neuroimaging data-driven endeavors for Alzheimer’s disease, there is a burgeoning need for well-characterized neuroimaging databases of healthy individuals. With the rise of initiatives around the globe for the rapid and unrestricted sharing of data resources, there is now an abundance of open-source neuroimaging datasets available to the research community. However, there is not yet a systematic review that fully details the demographic information and modalities actually available in all open access neuroimaging databases around the globe.

Objective:

This systematic review aims to provide compile a list of MR structural imaging databases encompassing healthy individuals across the lifespan. Methods: In this systematic review, we searched EMBASE and PubMed until May 2022 for open-access neuroimaging databases containing healthy control participants of any age, race, with normal development and cognition having at least one structural T1-weighted neuroimaging scan.

Results:

A total of 403 databases were included, for up to total of 48,268 participants with all available demographic information and imaging modalities detailed in Supplementary Table 1. There were significant trends noted when compiling normative databases for this systematic review, notably that 11.7% of databases included reported ethnicity in their participants, with underrepresentation of many socioeconomic groups globally.

Conclusions:

As efforts to improve primary prevention of AD may require a broader perspective including increased relevance of earlier stages in life, and strategies in addressing modifiable risk factors may be individualized to specific demographics, improving data characterization to be richer and more rigorous will greatly enhance these efforts.

Background:

Religious and spiritual interventions may have an effect on Alzheimer’s disease prevention. Kirtan Kriya meditation has been shown to mitigate the deleterious effects of chronic stress on cognition, reverse memory loss, and create psychological and spiritual wellbeing, which may reduce multiple drivers of Alzheimer’s disease risk.

Objective:

To detail a new concept in medicine called Spiritual Fitness, a merging of stress reduction, basic wellbeing, and psycho/spiritual wellbeing to prevent Alzheimer’s disease.

Methods:

The literature on the topics mentioned above is described, including an in-depth discussion on why and how each are critical to advancing the future of Alzheimer’s disease prevention. The many negative effects of chronic stress, and the benefits of Kirtan Kriya, are reviewed. The four pillars of basic wellbeing, six practical aspects of psychological wellbeing, and the four new non-sectarian features of spiritual fitness are then disclosed. Moreover, instructions on practicing Kirtan Kriya are offered in the Supplementary Material.

Conclusion:

Religious and spiritual practices, including Kirtan Kriya, are crucial components in the development of enhanced cognition and well-being, which may help prevent and, in some cases, reverse cognitive decline. The key point of this review is that making a commitment to live a brain longevity lifestyle including spiritual fitness is a critically important way for aging Alzheimer’s disease free. We hope that this article will inspire scientists, clinicians, and patients to embrace this new concept of spiritual fitness and make it a part of every multidomain program for the prevention of cognitive disability.

Background:

African Americans (AA) have a higher Alzheimer’s disease (AD) prevalence and report more perceived stress than White Americans. The biological basis of the stress-AD link is unclear. This study investigates the connection between stress and AD biomarkers in a biracial cohort.

Objective:

Establish biomarker evidence for the observed association between stress and AD, especially in AA.

Methods:

A cross-sectional study (n = 364, 41.8% AA) administering cognitive tests and the perceived stress scale (PSS) questionnaire. A subset (n = 309) provided cerebrospinal fluid for measurement of Aβ₄₂, Tau, Ptau, Tau/Aβ₄₂ (TAR), and Ptau/Aβ₄₂ (PTAR). Multivariate linear regression, including factors that confound racial differences in AD, was performed.

Results:

Higher PSS scores were associated with higher Ptau (β = 0.43, p = 0.01) and PTAR (β = 0.005, p = 0.03) in AA with impaired cognition (mild cognitive impairment).

Conclusion:

Higher PSS scores were associated with Tau-related AD biomarker indices in AA/MCI, suggesting a potential biological connection for stress with AD and its racial disparity.

Background:

Recent studies have shown that long working hours can have adverse consequences on health and possibly trigger biological processes that mediate the relationship between long working hours and cognitive decline.

Objective:

To investigate whether long working hours and the overall duration such exposure is associated with a decline in cognitive function.

Methods:

Data obtained during the Korean Longitudinal Study on Aging (n = 2,518) during the period 2006–2018 were used to explore the relationship between long working hours and cognitive decline. Korean version of the Mini-Mental State Examination (K-MMSE) scores were used to evaluate cognitive function. Cox proportional hazard regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs), which were used to evaluate declines in K-MMSE scores over the 12-year study period.

Results:

Overall HR (95% CI) for a decline in cognitive function in long working hours group was 1.13 (0.73–1.17). When categorized by sex, women with long working hours had an HR (95% CI) of 1.50 (1.05–2.22), K-MMSE scores decreased significantly after working long hours for 5 years (p < 0.01).

Conclusion:

The study furthers understanding of the effects of long working hours on cognitive decline among female workers. Further research is required to determine the effects of long working hours on cognitive functions.

Background:

Social media is a powerful tool for engaging diverse audiences in dementia research. However, there is little data summarizing current content exchange in this context.

Objective:

To inform ethical dementia research engagement on social media, we characterized current practices by analyzing public social media posts.

Methods:

We retrieved Facebook (2-year period, N = 7,896) and Twitter (1-year period, N = 9,323) posts containing dementia research-related keywords using manual and machine learning-based search strategies. We performed qualitative and quantitative content and sentiment analyses on random samples (10%) of the posts.

Results:

Top Facebook users were advocacy (45%) and health organizations (25%). On Twitter, academics/researchers were the largest user group. Prevention was the most frequently coded theme (Facebook 30%; Twitter 26%), followed by treatment (Facebook 15%; Twitter 18%). Diagnostics had the highest Facebook engagement. Sharing knowledge was the primary form of content exchange (Facebook 63%; Twitter 80%). Most shared journal articles were peer-reviewed and open access. Emotional tone was overall more positive on Facebook. Justice was a prominent ethics topic regarding inequalities related to identity and intersecting modes of marginalization in dementia research.

Conclusion:

The findings indicate the importance of social media as an engagement tool of current topics in health research and reveal areas of potential for increased engagement. These data can inform consensus-based best practices for ethical social media application in dementia research.