The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia.

/pdf/the-diagnosis-of-dementia-due-to-alzheimer-s-disease-w5k0egjbz5.pdf

The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

https://hull-repository.worktribe.com/preview/1797952/1-s2.0-S0140673618322797-main.pdf

Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

https://openresearch-repository.anu.edu.au/bitstream/1885/164632/2/01_Bin%2bSayeed_Global%252C_regional%252C_and_national_2018.pdf

Global, regional, and national incidence, prevalence, andyears lived with disability for 354 diseases and injuries for195 countries and territories, 1990–2017: a systematicanalysis for the Global Burden of Disease Study 2017

Approximately two-thirds of individuals diagnosed with Alzheimer’s disease are women. Although women tend to have longer life expectancy than men, this does not entirely explain the differences in the prevalence of dementia and Alzheimer’s disease. Some evidence suggests that men and women have different patterns of risk and protective factors across the lifespan. The goal of this chapter is to summarize the current evidence on sex differences in genetic and modifiable lifestyle factors that are associated with dementia risk. These include demographic factors such education, vascular, metabolic, lifestyle, and psychosocial factors, and sex-specific factors such as menopause and andropause. Potential mechanisms such as neural reserve and resilience are also summarized. The chapter also summarizes the evidence from recent multidomain lifestyle intervention trials, and the intervention response observed in men and women. While there have been insightful advancements in the field, many important questions still remain. Considerations for future research and risk reduction initiatives are also highlighted.

Sex and gender differences in genetic and lifestyle risk and protective factors for dementia

Results and experiences from Scandinavian multi-domain intervention trials (DRs EXTRA and FINGER)

An ageing society, whilst representing a major success of humanity in recent decades, brings a significant increase in the numbers of dementia sufferers, world-wide. There is evidence to suggest that successive cohorts remain cognitively healthy for longer than their forebears and reach an older age before developing dementia. This has been attributed to a combination of life-course factors and testifies to the multifactorial aetiology of Alzheimer’s disease (AD) and other forms of late-onset dementia (LOD). But as longevity increases, more people live long enough to develop LOD, and survive longer with the condition. Consequently, despite (or because of) improvements in population health, LOD is becoming an increasing burden on society. It is a public health imperative to prevent or delay the onset or clinical progression of this multifactorial disorder. The manuscripts in this issue address a range of aetiological risk factors for LOD, novel technologies and study designs, with implications for preventative strategies. Age-specific incidence rates for dementia have fallen by an estimated 13% per decade since 1988 in the United States and Europe (1). Both dementia-free life expectancy and years of survival with dementia have increased (2). Taking into account declining age-specific incidence and increasing life expectancy, the number of cases of dementia is projected to continue to increase over coming decades (3). Reducing the burden of dementia is identified as a key global health priority (4). The aetiologies of AD and other LOD forms are evidently multifactorial, with risk factors identified throughout the life course. The heritability of dementia varies according to type, with that of late-life Alzheimer’s disease reaching highly significant levels (h2 ranging between 0.58 and 0.79) (5). Fetal, perinatal and early childhood factors have been proposed as potentially relevant to risk of late-life common and complex diseases, such as dementia or cardiovascular and metabolic conditions (6). Low educational attainment, midand late-life hypertension, diabetes, obesity, physical inactivity, excessive alcohol consumption, smoking, depression, hearing impairment, brain injury, social isolation and air pollution may account collectively for 40% of dementia cases worldwide (7). Potential explanatory factors which may have contributed to the reduction in age-adjusted dementia incidence across successive cohorts include higher educational attainment, reductions in smoking and more effective management of cardiovascular diseases and diabetes (8). With a complex and multifactorial disorder, the identification of aetiological pathways or risk factors should broaden intervention efforts rather than narrowing them. Dementia may in some cases be prevented by interventions which target individual risk factors, as has been demonstrated in the case of risk reduction of cardiovascular diseases via antihypertensive medication (9). But other single-factor strategies have, to date, been less successful. Trials of pharmaceutical interventions targeting beta-amyloid as potential treatments for AD have yielded predominantly negative results. Some non-pharmaceutical interventions, such as diet, physical exercise and cognitive training, have demonstrated beneficial effects on aspects of cognition though not prevention of dementia (9). Multifactorial aetiology calls for a multidomain approach to intervention, whereby multiple risk factors are addressed concurrently, such as the Finnish Geriatric Intervention Study to prevent cognitive impairment and disability (FINGER) study (10) and the Vascular Care Intervention to Prevent Dementia (preDIVA) study (11). The natural extension of this approach will be the strategy of personalised precision medicine, whereby individuals’ personal profiles of risk factors are identified through careful assessment and targeted through bespoke intervention packages delivered to at-risk individuals. The manuscripts included in this edition relate, in different and complementary ways, to this ambition (12-20). An essential requirement for successful trialling of preventative interventions is the identification and recruitment of at-risk individuals. Mourzi and colleagues present an example of developments in the genetic prediction of the risk and clinical manifestation of dementia in their investigation of the genetics of frailty. Ford et al. discuss the value of neuroimaging in risk prediction and early detection, the pragmatic challenges which limit its widespread adoption at large scale, and the potential for new and emerging technologies to provide solutions to these challenges. Udeh-Momoh et al. present an analysis of the utility and economic viability of plasma amyloid assays in pre-screening for © Serdi and Springer Nature Switzerland AG 2022

Dementia Prevention: A Global Challenge in Urgent Need of Solutions

Statins and dementia prevention: A population-based study (FINRISK)

(MDC/CCL22). MDC was chosen for its ability to target and deliver antigens to professional antigen-presenting cells, and to elicit Th2-type polarized immune responses. Results: We demonstrated that the pMDC3A 1-11-PADRE vaccine induced robust anti-A antibody and Th2 type anti-PADRE T cell responses in 3xTg-AD mouse model. Multiple immunizations of 3-4 mo old mice protected them from age-related behavioral impairment and significantly inhibited development of A plaques. Currently, we further investigate, and will be reporting the quantity of soluble (monomeric/oligomeric) and insoluble forms of A 42/40 peptides as well as phosphorylated tau accumulated in the brains of immune and control animals. Conclusion: Considering our above-mentioned data along with others’ results demonstrating that AD plaques undergo chemical modifications thus making them more resistant to disruption with age while soluble forms of A amyloid are trapped in vasculature in immunized patients, we suggest that anti-A vaccine might be effective as prophylactic, but not therapeutic measure and should be used for vaccination of middle-aged healthy people. However, recent publications demonstrate that A peptide plays an essential role at synapse and in synaptic structurefunctional plasticity. A is shown to mediate a physiological homeostatic mechanism that regulates synaptic activity. Therefore, preventive vaccine should be designed very carefully, and we need to study whether preventive vaccination may have deleterious consequences for patients with mild cognitive impairment, or healthy people. All these issues will be discussed during the presentation.

Miia Kivipelto

Papers

Sex and gender differences in genetic and lifestyle risk and protective factors for dementia

Results and experiences from Scandinavian multi-domain intervention trials (DRs EXTRA and FINGER)

Dementia Prevention: A Global Challenge in Urgent Need of Solutions

Statins and dementia prevention: A population-based study (FINRISK)

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