Barbara Strasser’s research while affiliated with Ludwig Boltzmann Institute for Cancer Research and other places

Hand-grip strength was evaluated in 757 recreational downhill skiers and compared to 1021 community-dwellers. Findings are reported for age and sex categories consistent with community-dwelling norms. Effect size (Cohen's d) was calculated to estimate the clinical relevance of strength differences between populations. Most male and half of the female age categories of downhill skiers demonstrated higher grip strength of the dominant hand (moderate to large effect size) compared to the reference population. Hand-grip strength in skiers declined with age at a similar rate as in the reference population. Relative grip strength (per kg body mass) was significantly and positively correlated with physical activity (hours/week), and with the number of ski days per year, and negatively with body mass. Thus, hand-grip strength may be related to the type, volume and intensity of exercise regularly performed. These results can help to assess whether the individual hand-grip strength is above or below average with regard to the normal population and the skier population as well and will support advice for training and/or rehabilitation.

Background The amount of regular physical activity (PA) can modulate the prevalence of traditional risk factors for cardiovascular disease (CVD) such as obesity, systemic hypertension, hypercholesterolemia, and type 2 diabetes (T2D). However, how different PA levels either below (< 600 MET min/week), within (600–1200 MET min/week), or above (> 1200 MET min/week) the range of the minimal WHO recommendations impact the age- and sex-dependent prevalence of these risk factors remains to be elucidated. Methods This cross-sectional study was performed to evaluate these relationships using population-based self-reported data collected in a central European country (Austria, 2019). The sample included a total of 15,461 persons (7166 males: 16–95 + years, BMI 26.6 ± 4.4; 8295 females: 16–95 + years, BMI 25.1 ± 5.0). Besides various lifestyle factors (e.g., dietary habits, smoking, and alcohol consumption), variables of particular interest were the age- and sex-dependent amount of weekly PA and prevalence of risk factors for CVD. Sex-specific logistic regression analyses were applied to estimate adjusted odds ratios (ORs) for the associations between self-reported PA and risk factor prevalence. Results Relatively small beneficial effects were found regarding the prevalence of risk factors for CVD when achieving PA levels corresponding to 600–1200 MET min/week as compared to those who did not meet these recommendations. However, exceeding the WHO recommendations provided much more pronounced benefits, especially in younger and older age groups. Adjusted ORs revealed that high volumes of PA (> 1200 MET min/week) were associated with a 32–43% reduction in the prevalence of obesity and T2D compared to those who did not achieve the WHO recommendations (< 600 MET min/week), as well as with a lower prevalence of systemic hypertension only in women and a lower prevalence of hypercholesterolemia only in men. Conclusions Exceeding minimal WHO recommendations for PA promises large beneficial effects, particularly on the prevalence of obesity and T2D. Demonstrated sex differences in PA levels and their association with cardiovascular risk factors may provide an important basis for preventive health counseling.

This investigation delves into the interplay between large neutral amino acids (LNAA) and metabolic syndrome (MetS) in midlife adults, examining their collective influence on brain structure. While LNAA, such as tryptophan and phenylalanine, are known to bolster cognition in youth, these relationships often reverse later in life. Our study hypothesized an earlier reversal of these benefits in middle-aged adults with MetS, potentially signaling premature brain aging. Eighty participants between 40–61 years underwent MetS component quantification, LNAA measurement via high-performance liquid chromatography, and brain imaging to evaluate white matter hyperintensities (WMH) volume and medial temporal lobe (MTL) cortical thickness. Our linear regression analyses, adjusting for sex, age, and education, revealed that phenylalanine levels moderated the relationship between MetS and WMH volume (F(6, 69) = 3.134, p < 0.05, R² = 0.214), suggesting the brain impact of MetS may be partly due to phenylalanine catabolism byproducts. LNAA metabolites did not significantly modulate the MetS-MTL cortical thickness relationship. These findings suggest that better understanding of the role of phenylalanine in the pathogenesis of cerebrovascular disease in midlife may be essential to developing early interventions to protect cognitive health. Further research is crucial to elucidate the longitudinal influence of LNAA and MetS on brain health, thereby informing strategies to mitigate cognitive decline.

Introduction: Large neutral amino acids (LNAAs) tryptophan and phenylalanine have been implicated in the pathogenesis of neurodegenerative diseases. Given limited research on the effects of LNAA on brain health across different life stages, vascular risk, and genetic backgrounds, our study aimed to explore the interaction of LNAA levels, metabolic syndrome (MetS), and the presence of the apolipoprotein E ε4 (ApoE ε4) allele brain integrity at midlife. Methods: Sixty-eight adults aged 40-61 underwent a health assessment to calculate the number of MetS components, quantify LNAA, measure white matter hyperintensity (WMH) volume, and genotype ApoE ε4. Multivariate linear regression analyses were performed to test the joint effect of LNAA, MetS, and ApoE ε4 on WMH while adjusting for sex, age, and education. Results: Significant 3-way interactions were observed between serum tryptophan (β = 0.042, SE = 0.018, p < 0.05) and phenylalanine (β = 0.044, SE = 0.013, p < 0.01) levels, number of MetS components, and ApoE ε4 alleles status on WMH volume. Neither individual LNAA levels nor MetS components alone predicted WMH volume. Conclusions: The study highlights significant 3-way interactions between LNAA, MetS, and genetic risk factors in the pathology of WMH, particularly in individuals genetically predisposed to Alzheimer's disease. These interactions suggest differential impacts of LNAA on WMH volume dependent on both genetic and metabolic factors. Results emphasize the need for personalized metabolic and genetic profile assessments in neurodegenerative disease management.

Prominent pathological features of Huntington’s disease (HD) are aggregations of mutated Huntingtin protein (mHtt) in the brain and neurodegeneration, which causes characteristic motor (such as chorea and dystonia) and non-motor symptoms. However, the numerous systemic and peripheral deficits in HD have gained increasing attention recently, since those factors likely modulate disease progression, including brain pathology. While whole-body metabolic abnormalities and organ-specific pathologies in HD have been relatively well described, the potential mediators of compromised inter-organ communication in HD have been insufficiently characterized. Therefore, we applied an exploratory literature search to identify such mediators. Unsurprisingly, dysregulation of inflammatory factors, circulating mHtt, and many other messenger molecules (hormones, lipids, RNAs) were found that suggest impaired inter-organ communication, including of the gut–brain and muscle–brain axis. Based on these findings, we aimed to assess the risks and potentials of lifestyle interventions that are thought to improve communication across these axes: dietary strategies and exercise. We conclude that appropriate lifestyle interventions have great potential to reduce symptoms and potentially modify disease progression (possibly via improving inter-organ signaling) in HD. However, impaired systemic metabolism and peripheral symptoms warrant particular care in the design of dietary and exercise programs for people with HD.

Introduction: Two large neutral amino acids (LNAA), tryptophan and tyrosine, are precursors to cerebral neurotransmitters and are involved in cognitive function. Higher levels of LNAA in young adults are associated with improved cognition, although these associations appear to reverse over time. Given that exposure to metabolic syndrome (MetS) may induce premature cognitive aging, the current project aims to fill the gap in the literature by examining the effect of LNAA on cognitive performance in midlife adults with metabolic risks. Methods: Eighty-eight adults, ages 40-61 years, participated in this cross-sectional study. LNAA metabolites were quantified, MetS components were measured using high-performance liquid chromatography, and MetS components were assessed in the laboratory. Composite verbal memory and executive functioning scores were computed using principal component analysis. We used linear regression models to test the interaction between LNAA and MetS while covarying for sex, age, and education. Results: The kynurenine/tryptophan ratio moderated the relation between MetS and verbal memory, even after adjusting for relevant covariates. Tyrosine metabolites were not significant moderators of the association between MetS and executive functioning. Conclusion: Our findings suggest that the detected weaker memory performance in adults with a high number of MetS components may be related to relative tryptophan depletion and possible decreases in serotonin production. Further investigation is warranted to examine the potential role of LNAA in associations between cognitive performance and metabolic risks over time.

This investigation delves into the interplay between large neutral amino acids (LNAA) and metabolic syndrome (MetS) in midlife adults, examining their collective influence on brain structure and cognitive function. While LNAA, such as tryptophan and phenylalanine, are known to bolster cognition in youth, our study hypothesizes a reversal of these benefits in older adults with MetS, potentially signaling premature cognitive aging. Eighty participants between 40–61 years underwent MetS component quantification, LNAA measurement via high-performance liquid chromatography, and brain imaging to evaluate white matter hyperintensity (WMH) volume and medial temporal lobe (MTL) cortical thickness. Our linear regression analysis, adjusting for sex, age, and education, revealed that phenylalanine levels moderated the relationship between MetS and WMH volume ( F (6, 69) = 3.134, p < 0.05, R ² = 0.214), suggesting that MetS's cognitive impact may be partly due to phenylalanine catabolism byproducts. However, LNAA metabolites did not significantly modulate the MetS-MTL cortical thickness relationship. The findings suggest that LNAA metabolic dysregulation, marked by elevated levels in the presence of MetS, could correlate with brain structural compromises, particularly in the form of MTL cortical thinning and increased WMH load, detectable in midlife. This nuanced understanding of LNAA's role in cognitive health amid cardiovascular risk factors is pivotal, proposing a potential biomarker for early intervention. Further research is crucial to elucidate the longitudinal influence of LNAA and MetS on brain health, thereby informing strategies to mitigate cognitive decline.

Objective Tryptophan is an essential amino acid and precursor to several compounds of neurobiological significance, including serotonin, melatonin, and nicotinamide adenine dinucleotide. However, the tryptophan-kynurenine metabolic pathway exhibits “double-edged sword” effects on neurons with neuroprotective metabolites and neurotoxic intermediates. Given its involvement in neurodegenerative diseases and recent reports of alterations in the pathway in response to obesity, we set out to investigate the potential moderating effect of the kynurenine/tryptophan ratio (KTR) on the relationship between adiposity and verbal memory performance in midlife. Our study is important in providing insight into mechanisms underlying the association between adiposity and cognition through the life course and sheds light on the role of metabolic risk factors before senescence. With the current epidemic of obesity and the expected age-related increase in dementia incidence, even a small association between obesity and cognitive decline may have far-reaching public health implications. Participants and Methods A total of 110 middle-aged adults aged 40-61 years participated in this cross-sectional study. Serum levels of kynurenine and tryptophan, body adiposity measured through bioimpedance, and non-contextual verbal memory performance on the California Verbal Learning Test, Second Edition (CVLT-II) were evaluated. Using factor analysis, the composite score of memory indices from Short Delay Free Recall, Long Delay Free Recall, and Long Delay Recognition tasks were calculated. We used linear regression models with the interaction between KTR and adiposity. Sex, age, years of education, and physical activity were included as covariates, as they predict cognitive performance. Results Higher KTR was associated with greater adiposity (p < 0.01). Linear regression analyses for assessing interaction effects indicated that KTR moderated the relation between adiposity and composite memory score (F(7, 100) = 5.22, p < 0.001, R2 = 0.27). These results were robust across individual memory indices and composite memory scores. These findings remained significant even with adjusting for relevant covariates. Interestingly, the marginal effects of adiposity on composite memory score were estimated to be statistically significant and negative (higher adiposity = poorer memory) only when KTR was low (< 0.03). Conclusions The present study indicates that KTR may influence the association between adiposity and verbal memory in midlife as KTR moderated the relationship between adiposity and composite memory score even after adjusting for relevant covariates. In contrast to the notion that high KTR is related to increases in neurotoxic metabolites such as quinolinic acid, individuals with high adiposity and low KTR exhibited the weakest memory performance. Unfortunately, our study did not include measurements of quinolinic acid or kynurenic acid, which may have neuroprotective and anti-inflammatory properties. Future studies expanding the number of measured KT metabolites could shed light on the interactions between obesity and KTR on memory function in midlife.