Introduction: Hospital‐associated deconditioning (HAD) or post‐hospital syndrome is well recognized as reduced functional performance after an acute hospitalization. Recommendations for the management of HAD are still lacking, partly due to a poor understanding of the underlying processes. We aimed to review existing data on risk factors, pathophysiology, measurement tools, and potential interventions.Materials and methods: We conducted a systematic review from bibliographical databases in English, Spanish and French with keywords such as ‘post‐hospitalization syndrome’ or ‘deconditioning’. We selected studies that included people aged 60 years or older. Three researchers independently selected articles and assessed their quality.Results: From 4421 articles initially retrieved, we included 94 studies. Most were related to risk factors, trajectories and measures, and focused on the physical aspects of deconditioning. Risk factors for HAD included age, nutritional status, mobility, and pre‐admission functional status, but also cognitive impairment and depression. Regarding interventions, almost all studies were devoted to physical rehabilitation and environmental modifications. Only one study focused on cognitive stimulation.Discussion: In the last decade, studies on HAD have mostly focused on the physical domain. However, neurological changes may also play a role in the pathophysiology of HAD. Beyond physical interventions, cognitive rehabilitation and neurological interventions should also be evaluated to improve deconditioning prevention and treatment in the hospital setting.

Objectives: Brain health is an important focus for coming decades due to population ageing. Although the term ‘brain health’ is increasingly used in lay and professional settings, a clear definition of the term is lacking. We conducted an analysis of the concept of brain health to inform policy, practice, and research.Methods: We applied a hybrid concept analysis method involving three stages: (1) a review of the extant literature for definitions of brain health; (2) field work, involving an international survey of ‘brain health’ researchers and practitioners; and (3) a final analysis, integrating the findings into a working definition and model.Results: Our review of the literature identified 13 articles defining brain health, six of which proposed their own definition. Our survey revealed that the term ‘brain health’ was used in diverse ways based on different theoretical frameworks. From the review and survey, we extracted attributes, antecedents, and consequences of brain health. These were synthesized into a definition of brain health as a life‐long, multidimensional, dynamic state consisting of cognitive, emotional and motor domains underpinned by physiological processes and can be objectively measured and subjectively experienced. It is influenced by eco‐biopsychosocial determinants.Conclusion: This working definition of brain health is a foundation for developing policy, practice, research and advocacy. The definition needs to be operationalised through further development of empirical referents, including cross‐cultural understanding, adaptation and validation.

Background: Public health restrictions due to the COVID‐19 (SARS CoV‐2) pandemic have disproportionately affected informal caregivers of people living with long term health conditions. We aimed to explore levels of care burden, loneliness, and social isolation among caregivers of people with enduring physical and brain health conditions in English‐speaking regions worldwide, by investigating outcomes before and during the COVID‐19 pandemic.Methods: A cross‐sectional anonymous online survey data from 2287 English‐speaking caregivers of people with long term health conditions from four English‐speaking regions (UK, Ireland, USA, New Zealand) included measures of care burden, loneliness, and social isolation, reported before and during the COVID‐19 pandemic. Analyses were descriptive, followed by an ordinal regression model for predictors of burden.Results: Compared to pre‐pandemic levels, all caregivers experienced a significant increase in burden, loneliness, and isolation. Caregivers of people with both brain health and physical conditions were the most burdened and had the highest levels of loneliness and isolation compared to caregivers of people with either a brain health or physical condition only. The increase in care burden among caregivers of people with brain health challenges was associated with caregiver's gender, moderate and severe emotional loneliness, magnitude and frequency of isolation during the pandemic, and care circumstances (cohabitation with the care recipient, restrictions on the ability to provide care).Conclusions: Health and social care interventions should target caregivers' care circumstances and psychological outcomes, particularly in women, accounting for the significant additional burden of care, loneliness, and isolation resulting from pandemic‐related restrictions.

INTRODUCTION Midlife hypertension has been consistently linked with increased risk of cognitive decline and Alzheimer’s disease (AD). Observational studies and randomized trials show that the use of antihypertensive therapy is associated with a lesser incidence or prevalence of cognitive impairment and dementia. However, whether anti-hypertensive agents specifically target the pathological process of AD remains elusive. AREAS COVERED This review of literature provides an update on the clinical and preclinical arguments supporting anti-AD properties of antihypertensive drugs. The authors focused on validated all classes of antihypertensive treatments such as angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), calcium channel blockers (CCB), β-blockers, diuretics, neprilysin inhibitors, and other agents. Three main mechanisms can be advocated: action on the concurrent vascular pathology, action on the vascular component of Alzheimer’s pathophysiology, and action on non-vascular targets. EXPERT OPINION In 2019, while there is no doubt that hypertension should be treated in primary prevention of vascular disease and in secondary prevention of stroke and mixed dementia, the place of antihypertensive agents in the secondary prevention of “pure” AD remains an outstanding question.

Hospital-associated deconditioning is a broad term, which refers non-specifically to declines in any function of the body secondary to hospitalisation. Older people, particularly those living with frailty, are known to be at greatest risk. It has historically been most commonly used as a term to describe declines in muscle mass and function (i.e. acute sarcopenia). However, declines in physical function do not occur in isolation, and it is recognised that cognitive deconditioning (defined by delayed mental processing as part of a spectrum with fulminant delirium at one end) is commonly encountered by patients in hospital. Whilst the term ‘deconditioning’ is descriptive, it perhaps leads to under-emphasis on the inherent organ dysfunction that is associated, and also implies some ease of reversibility. Whilst deconditioning may be reversible with early intervention strategies, the long-term effects can be devastating. In this article, we summarise the most recent research on this topic including new promising interventions and describe our recommendations for implementation of tools such as the Frailty Care Bundle.

Cerebral microbleeds (CMBs) could contribute to cognitive impairment in the general population and in patients with dementia. We designed a study to (i) develop a murine model of CMBs, (ii) assess whether CMBs affect cognition in this model and (iii) assess whether this model is sensitive to pharmacological modulation. Male C57Bl6/J mice were stereotactically administered collagenase to induce cortical lesion analysed by MRI at 24 h. CMB-mice were assessed at six weeks post-lesion for cognitive performances (Barnes maze and Touchscreen automated paired-associated learning (PAL) task) and for cerebral metabolism (in vivo PET/CT with fluorodeoxyglucose (FDG)). CMB-model sensitivity to pharmacological modulation was assessed by administering atorvastatin (5 mg/kg/day) over the follow-up period. CMB mice were compared to naïve littermates. Collagenase at 0.8 µU/µl appeared suitable to induce reproducible and reliable CMBs. At six weeks, a decline in learning, spatial and visuospatial memory was significantly observed in CMB-mice. Brain metabolism was impaired in all cortex, striatum and the ipsilateral dentate gyrus. A significant improvement in cognition performances was depicted under atorvastatin. In this novel murine model of CMBs, we validated that CMBs lowered cognitive performances and affected regional metabolism. We also proved that this CMB-model is sensitive to pharmacological modulation.