Lean body mass (LBM) agglomerates the bulk of nitrogen (N)-containing molecules following well-identified age and sex evolutionary patterns best appraised in clinical practice using the serial measurement of plasma transthyretin (TTR). Methionine (Met), the sole essential amino acid bearing a sulfur (S) atom, presides at the initiation of protein synthesis while maintaining stable body tissue S:N molar ratios of approximately 1:14.5. In protein- depleted states, N- and Met-deficiencies operate as limiting factors for LBM protein synthesis and accretion, causing growth retardation and subnormal TTR plasma values. In inflammatory disorders, LBM is subjected to cytokine-induced tissue breakdown reflecting the S:N ratio found in healthy tissues whereas the liver secretion of TTR declines in proportion. Both malnutrition and inflammation are characterized by stepwise LBM downsizing and reduced bioavailability of Met body stores setting in motion molecular mechanisms safeguarding Met homeostasis at the expense of augmented homocysteine (Hcy) values in biological fluids. Divergent TTR and Hcy alterations indicate that rising Hcy values measured in plasma and cerebrospinal fluid should be regarded as the dark side of efficient compensatory processes. As a result, the neuroprotective activities normally exerted by TTR are weakened, whereas the oxidative burden generated by supranormal Hcy concentrations are strengthened. The combination of protein malnutrition and inflammatory disorders of any cause maximizes the risk of incurable neurodegenerative effects.

G*Power (Erdfelder, Faul, & Buchner, 1996) was designed as a general stand-alone power analysis program for statistical tests commonly used in social and behavioral research. G*Power 3 is a major extension of, and improvement over, the previous versions. It runs on widely used computer platforms (i.e., Windows XP, Windows Vista, and Mac OS X 10.4) and covers many different statistical tests of the t, F, and chi2 test families. In addition, it includes power analyses for z tests and some exact tests. G*Power 3 provides improved effect size calculators and graphic options, supports both distribution-based and design-based input modes, and offers all types of power analyses in which users might be interested. Like its predecessors, G*Power 3 is free.

The NINCDS-ADRDA and the DSM-IV-TR criteria for Alzheimer's disease (AD) are the prevailing diagnostic standards in research; however, they have now fallen behind the unprecedented growth of scientific knowledge. Distinctive and reliable biomarkers of AD are now available through structural MRI, molecular neuroimaging with PET, and cerebrospinal fluid analyses. This progress provides the impetus for our proposal of revised diagnostic criteria for AD. Our framework was developed to capture both the earliest stages, before full-blown dementia, as well as the full spectrum of the illness. These new criteria are centred on a clinical core of early and significant episodic memory impairment. They stipulate that there must also be at least one or more abnormal biomarkers among structural neuroimaging with MRI, molecular neuroimaging with PET, and cerebrospinal fluid analysis of amyloid beta or tau proteins. The timeliness of these criteria is highlighted by the many drugs in development that are directed at changing pathogenesis, particularly at the production and clearance of amyloid beta as well as at the hyperphosphorylation state of tau. Validation studies in existing and prospective cohorts are needed to advance these criteria and optimise their sensitivity, specificity, and accuracy.

In this Seminar, we highlight the main developments in the field of Alzheimer's disease. The most recent data indicate that, by 2050, the prevalence of dementia will double in Europe and triple worldwide, and that estimate is 3 times higher when based on a biological (rather than clinical) definition of Alzheimer's disease. The earliest phase of Alzheimer's disease (cellular phase) happens in parallel with accumulating amyloid β, inducing the spread of tau pathology. The risk of Alzheimer's disease is 60-80% dependent on heritable factors, with more than 40 Alzheimer's disease-associated genetic risk loci already identified, of which the APOE alleles have the strongest association with the disease. Novel biomarkers include PET scans and plasma assays for amyloid β and phosphorylated tau, which show great promise for clinical and research use. Multidomain lifestyle-based prevention trials suggest cognitive benefits in participants with increased risk of dementia. Lifestyle factors do not directly affect Alzheimer's disease pathology, but can still contribute to a positive outcome in individuals with Alzheimer's disease. Promising pharmacological treatments are poised at advanced stages of clinical trials and include anti-amyloid β, anti-tau, and anti-inflammatory strategies.Copyright © 2021 Elsevier Ltd. All rights reserved.

The aging population is a significant social, medical and economic problem due to increasing prevalence of chronic diseases in elderly population. Alzheimer's disease (AD) is the most common form of dementia and the most common neurodegenerative disease. It is characterized by a progressive deterioration of memory and cognitive function. So far, there is neither an effective prevention nor cure for dementia, so more and more attention is paid to the prevention of this group of diseases, particularly to the appropriate diet. Preventive intervention gives the best results if introduced before the first symptoms of dementia, i.e., around the age of 50. This is when the nutritional status, number of synapses, cognition, and neuropathological changes in the nervous system compensate each other, which increases the chances of staying healthy for a longer period of time. It has been proven that dietary habits, which lead to the development of cardiovascular and metabolic diseases, significantly increase the risk of dementia. On the other hand, a Mediterranean diet rich in antioxidants, fiber and omega-3 polyunsaturated fatty acids may have a protective effect on the neurodegenerative process. The beneficial effect of many nutrients on the course of AD has been demonstrated. These include: glutathione, polyphenols, curcumin, coenzyme Q10, vitamins B6, B12, folic acid, unsaturated fatty acids, lecithin, UA, caffeine and some probiotic bacteria. A diet rich in saturated fatty acids and branched-chain amino acids (BCAA) promotes the progression of dementia. Dietary intervention should be introduced as early as possible to minimize the risk of developing dementia. The Mediterranean and DASH diets have been documented to protect against AD. However, the MIND diet is reported to be much more effective in preventing cognitive decline/dementia than either the Mediterranean or DASH diets alone.© Copyright by the National Institute of Public Health - National Institute of Hygiene.

The association between body mass index (BMI) and Alzheimer's disease (AD) remains controversial. Genetic and environmental factors are now considered contributors to AD risk. However, little is known about the potential interaction between genetic risk and BMI on AD risk.To study the causal relationship between BMI and AD, and the potential interaction between AD genetic risk and BMI on AD risk.Using the UK Biobank database, 475,813 participants were selected for an average follow-up time of more than 10 years.1) there was a nonlinear relationship between BMI and AD risk in participants aged 60 years or older (p for non-linear < 0.001), but not in participants aged 37-59 years (p for non-linear = 0.717) using restricted cubic splines; 2) for participants aged 60 years and older, compared with the BMI (23-30 kg/m) group, the BMI (< 23 kg/m) group was associated with a higher AD risk (HR = 1.585; 95% CI 1.304-1.928, p < 0.001) and the BMI (> 30 kg/m) group was associated with a lower AD risk (HR = 0.741; 95% CI 0.618-0.888, p < 0.01) analyzed using the Cox proportional risk model; 3) participants with a combination of high AD genetic risk score (AD-GRS) and BMI (< 23 kg/m) were associated with the highest AD risk (HR = 3.034; 95% CI 2.057-4.477, p < 0.001). In addition, compared with the BMI (< 23 kg/m), the higher BMI was associated with a lower risk of AD in participants with the same intermediate or high AD-GRS; 4) there was a reverse causality between BMI and AD when analyzed using bidirectional Mendelian randomization (MR).There was a reverse causality between BMI and AD analyzed using MR. For participants aged 60 years and older, the higher BMI was associated with a lower risk of AD in participants with the same intermediate or high AD genetic risk. BMI (23-30 kg/m) may be a potential intervention for AD.© 2022. The Author(s).

Mini Nutritional Assessment-Short Form (MNA-SF) is used to assess nutritional status in older adults, but it is not known whether it can be used to define frailty. This study was aimed to investigate whether or not MNA-SF can identify frailty status as defined by Fried's criteria.A total of 1,003 outpatients (aged 65 years or older) were included in the study. All patients underwent comprehensive geriatric assessment. Frailty status was evaluated by Fried's criteria: unintentional weight loss, exhaustion, low levels of activity, weakness, and slowness. One point is assigned for each criterion, and frailty status is identified based on the number of points scored: 0 points, not frail; 1-2 points, pre-frail; ≥3 points, frail. A total score of MNA-SF <8, 8-11, and >11 indicates malnutrition, risk of malnutrition, and no malnutrition, respectively.Of the 1,003 outpatients (mean age 74.2±8.5 years), 313 participants (31.2%) were considered frail and 382 (38.1%) pre-frail. Among frail and pre-frail patients, 49.2% and 25.1% were at risk of malnutrition and 22.0% and 1.6% were malnourished, respectively. MNA-SF with a cut-off point of 11.0 had a sensitivity of 71.2% and a specificity of 92.8% for the detection of frail participants, and with a cut-off point of 13 had a sensitivity of 45.7% and a specificity of 78.3% for the detection of pre-frailty. The area under the curve for MNA-SF was estimated to be 0.906 and 0.687 for frailty and pre-frailty, respectively.MNA-SF can be useful for frailty screening in older adults.

There are a few studies showing how nutritional parameters are affected according to dementia subtypes. The aim of this study was to compare the parameters characterizing nutritional status and micronutrient levels according to different dementia subtypes.Cross-sectional study.Four hundred forty outpatients aged 65 years or older.Newly diagnosed patients with dementia, who underwent comprehensive geriatric assessment (CGA), were retrospectively evaluated. The data on CGA including nutritional status (body mass index), Mini-Nutritional Assessment-Short Form, albumin, and micronutrients (vitamin B12, folate, and vitamin D) were recorded.Of the 396 patients, 195 were diagnosed with Alzheimer type dementia, 70 dementia with Lewy body (DLB), 25 with vascular dementia (VaD), 51 with frontotemporal dementia (FTD), and 55 with normal pressure hydrocephalus. The mean age of the study group was 76.87 ± 8.15 years. The prevalence of malnutrition and the risk of malnutrition were 17.17% and 43.18% in patients, with dementia, respectively. The results of ordinal logistic analysis adjusted by age, sex, and all comorbidities, showed that patients with DLB and VaD were more likely to develop malnutrition [odds ratios 6.834 and 5.414, respectively (P < .001)], whereas FTD had a lower risk of developing malnutrition than the other dementia subtypes (odds ratio 2.883, P = .002).There was no difference in terms of other parameters including vitamin B12, folate, and vitamin D (P > .05).and Implication: There is a close relationship between dementia and malnutrition. Clinical approaches to minimize malnutrition in persons with dementia should include regular screening for malnutrition and its risk factors, avoidance of dietary restrictions, and support of persons at risk for malnutrition with oral nutritional supplements. Moreover, the influence of nutritional status varies in different types of dementia. Nutritional status may be worse in DLB and VaD compared with other types of dementia, whereas nutritional status in FTD is less.Copyright © 2020 AMDA — The Society for Post-Acute and Long-Term Care Medicine. Published by Elsevier Inc. All rights reserved.

This systematic review and meta-analysis assesses the prevalence of protein-energy malnutrition risk across different health-care settings in European older adults, using 22 malnutrition screening tools recently validated for use in older adults. Systematic searches were performed in six electronic databases (2006 through 2017). Included were studies which reported malnutrition risk in adults aged ≥65y in Europe. Frequency of high and moderate malnutrition risk for each malnutrition screening tool was collated. Meta-analyses of malnutrition risk using a random-effects model were performed where data from at least 10 study samples were available. Of 21,465 studies, 196 studies were available for data extraction, representing 223 study samples from 24 European countries and 583,972 older adults. Pooled prevalence rates of high malnutrition risk across all countries and malnutrition screening tools were 28.0% (n = 127 study samples), 17.5% (n = 30), and 8.5% (n = 32), for the hospital, residential care and community settings respectively. Using meta-regression, prevalence rates were higher in adults aged >80y (p < 0.0001), in women (p = 0.03) and in patients with one or multiple comorbidities (p < 0.0001). Prevalence rates differed by country, from 15.2% in Spain to 37.7% in Switzerland, and by screening tool, from 14.9% using MNA-SF to 40.6% using NRS-2002. In conclusion, the prevalence of high malnutrition risk in European older adults varies widely between countries and across health-care settings. Malnutrition risk is associated with older age, gender and presence of disease. As prevalence rates differ depending on the screening tool used, the use of one preferred malnutrition screening tool per setting is strongly recommended.Copyright © 2019. Published by Elsevier B.V.

To evaluate the combined action of folic acid and vitamin B12 supplementation on cognitive performance and inflammation in patients with Alzheimer's disease (AD).This was a randomized, single-blind, placebo-controlled trial.Patients (n=120) diagnosed clinically as probable AD and in stable condition from Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative Diseases.Individuals were randomly divided into the intervention group (n=60, folic acid 1.2 mg/d + vitamin B12 50 μg/d) and the placebo group (n=60). Cognitive performance, blood folate, vitamin B12, one carbon cycle metabolite, and inflammatory cytokine levels were measured at baseline and after 6 months. The data were analyzed using linear mixed models for repeated measures.A total of 101 participants (51 in the intervention group and 50 in the placebo group) completed the trial. Folic acid plus vitamin B12 supplementation had a beneficial effect on the MoCA total scores (P=0.029), naming scores (P=0.013), orientation scores (P=0.004), and ADAS-Cog domain score of attention (P=0.008), as compared to those of the control subjects. Moreover, supplementation significantly increased plasma SAM (P<0.001) and SAM/SAH (P<0.001), and significantly decreased the levels of serum Hcy (P<0.001), plasma SAH (P<0.001), and serum TNFα (P<0.001) compared to in the control subjects.Folic acid and vitamin B12 supplementation showed a positive therapeutic effect in AD patients who were not on a folic acid-fortified diet. The findings of this study help to delineate nutrient intervention as far as public health management for the prevention of dementia is concerned.

Alzheimer's disease (AD) is the most common cause of dementia. In recent years, several studies have robustly shown that neuroinflammation plays a crucial role in the pathophysiology of this disease. The co-localization of amyloid-β plaques near activated glial cells and the increased levels of inflammatory cytokines in AD patients indicate the involvement of the neuroinflammatory process in AD progression. Considering that pharmacological treatment remains a challenge for the management of this disease, compounds with anti-inflammatory and antioxidant properties are promising therapeutic strategies. In this context, vitamin D has gained attention in the last few years due to its neuroprotective property and the high prevalence of vitamin D deficiency in the population. Herein, in this narrative review we present the possible contribution of the antioxidant and anti-inflammatory properties of vitamin D for its neuroprotective effects, and the clinical and preclinical data dealing with the effects of vitamin D in AD, focusing mainly on the neuroinflammatory process.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.