Dementia, osteoporosis and fragility fractures: Intricate epidemiological relationships, plausible biological connections, and twisted clinical practices.

Dementia, osteoporosis, and fragility fractures are chronic diseases, often co-existing in older adults. These conditions pose severe morbidity, long-term disability, and mortality, with relevant socioeconomic implications. While in the research arena, the discussion remains on whether dementia is the cause or the consequence of fragility fractures, healthcare professionals need a better understanding of the interplay between such conditions from epidemiological and physiological standpoints. With this review, we summarized the available literature surrounding the relationship between cognitive impairment, dementia, and both low bone mineral density (BMD) and fragility fractures. Given the strength of the bi-directional associations and their impact on the quality of life, we shed light on the biological connections between brain and bone systems, presenting the main mediators, including gut microbioma, and pathological pathways leading to the dysregulation of bone and brain metabolism. Ultimately, we synthesized the evidence about the impact of available pharmacological treatments for the prevention of fragility fractures on cognitive functions and individuals' outcomes when dementia coexists. Vice versa, the effects of symptomatic treatments for dementia on the risk of falls and fragility fractures are explored. Combining evidence alongside clinical practice, we discuss challenges and opportunities related to the management of older adults affected by cognitive impairment or dementia and at high risk for fragility fracture prevention, which leads to not only an improvement in patient health-related outcomes and survival but also a reduction in healthcare cost and socio-economic burden.

Body mass index and mild cognitive impairment-to-dementia progression in 24 months: a prospective study.

BACKGROUND/OBJECTIVES: Mild cognitive impairment (MCI), often considered as an early stage of dementia, is heterogeneous, and not all subjects with MCI progress into clinically diagnosed dementia. Low body weight (and body mass index, BMI) as well as losing weight while in MCI stadium have been proposed as possible risk factors of MCI-to-dementia conversion. SUBJECTS/METHODS: A prospective, 2-year observation of 102 MCI subjects has been conducted. Data on MCI subtype, somatic and neuropsychiatric co-morbidity and demographic characteristics (including age, gender and education), were collected. In addition, baseline and yearly BMI were calculated. RESULTS: Data of 83 out of the originally included 102 subjects were available after 2 years; 27 of those (32.5%) progressed to dementia. In univariate analysis, multiple-deficit MCI subtype (as compared with pure amnestic), higher age, the presence of diabetes and apathy, and lower baseline BMI (and losing weight on 2-year follow-up) were associated with conversion to dementia. Variables retained in the multivariate backward stepwise logistic regression model for conversion after 24 months of observation included lower baseline BMI (odds ratio, OR (95% cofidence interval, CI): 0.6 (0.4-0.9)), weight loss on 2-year follow-up (OR (95% CI): 1.3 (1.1-1.5)), male gender (OR (95% CI): 0.1 (0.01-0.9)) and presence of apathy (OR (95% CI): 70.7 (5.6-699)). Apathetic subjects had lower BMI and higher weight loss after controlling for potential confounders (age, gender, years of education and baseline ADAS-cog (Alzheimer's Disease Assessment Scale-cognitive subscale) score). CONCLUSION: MCI subjects presenting with apathy, low initial BMI and losing weight on follow-up have a significantly greater risk of developing dementia. Nutritional and behavioural assessment should be considered as additional tools in evaluating the risk of dementia among MCI subjects.

Evaluation of the influence of metabolic processes and body composition on cognitive functions: Nutrition and Dementia Project (NutrDem Project).

The global increase in the prevalence of dementia and its associated comorbidities and consequences has stimulated intensive research focused on better understanding of the basic mechanisms and the possibilities to prevent and/or treat cognitive decline or dementia. The etiology of cognitive decline and dementia is very complex and is based upon the interplay of genetic and environmental factors. A growing body of epidemiological evidence has suggested that metabolic syndrome and its components may be important in the development of cognitive decline. Furthermore, an abnormal body mass index in middle age has been considered as a predictor for the development of dementia. The Nutrition and Dementia Project (NutrDem Project) was started at the Department of Old Age Psychiatry and Psychotic Disorders with close cooperation with Department of Medical Psychology. The aim of this study is to determine the effect of dietary patterns, nutritional status, body composition (with evaluation of visceral fat) and basic regulatory mechanisms of metabolism in elderly patients on cognitive functions and the risk of cognitive impairment (mild cognitive impairment and/or dementia).

["7 Minute Screening. Part II: the evaluation of the test sensitivity and specificity as compared to Mini-Mental State examination]. / "7 minute screen" (7-minutowy test przesiewowy). Czesc II: Ocena czulosci i swoistosci testu i porównanie z Mini Mental State.

In the paper an evaluation of basic accuracy parameters (sensitivity and specificity) of the polish version of "7 Minute Screen" as a screening tool for Alzheimer's disease is presented as well as its comparison to Mini Mental State.