Poor sleep quality may trigger cognitive deficits after recovery from COVID-19.

Objective: In the present study, we aimed to assess the cognition of post-COVID-19 condition (PCC) participants in relation to their subjective sleep quality (Pittsburgh Sleep Quality Index, PSQI) and to analyse possible moderators of this effect, such as quality of life (European Quality of Life-5 Dimensions, EQ-5D), fatigue (Chadler Fatigue Questionnaire, CFQ), cognitive reserve (Cognitive Reserve Questionnaire, CRC), and subjective cognitive complaints (Memory Failures of Everyday Questionnaire, MFE-30). Methods: We included 373 individuals with PCC and 126 healthy controls (HCs) from the NAUTILUS Project (NCT05307549 and NCT05307575) who were assessed with a comprehensive neuropsychological battery and various questionnaires. Results: We found that PCC participants with poor sleep quality had a 4.3% greater risk of immediate verbal memory deficits than those with good sleep quality, as indicated by the greater odds ratio (OR) of 1.043 and confidence interval (CI) of 1.023-1.063. Additionally, their risk of immediate verbal memory disorders was multiplied by 2.4 when their EQ-5D score was low (OR 0.33; CI 0.145-0.748), and they had a lower risk of delayed visual memory deficits with a greater CRC (OR 0.963; CI 0.929-0.999). With respect to processing speed, PCC participants with poor sleep quality had a 6.7% greater risk of deficits as the MFE increased (OR 1.059; CI 1.024-1.096), and the risk of slowed processing speed tripled with a lower EQ-5D (OR 0.021; CI 0.003-0.141). Conclusion: These results indicate that poor subjective sleep quality is a potential trigger for cognitive deficits. Therapeutic strategies to maximize sleep quality could include reducing sleep disturbances and perhaps cognitive impairment in PCC individuals.

Sleep quality in individuals with post-COVID-19 condition: Relation with emotional, cognitive and functional variables.

The study aimed to assess sleep quality in PCC patients and its predictors by analysing its relationship with emotional, cognitive and functional variables, as well as possible differences based on COVID-19 severity. We included 368 individuals with PCC and 123 healthy controls (HCs) from the NAUTILUS Project (NCT05307549 and NCT05307575). We assessed sleep quality (Pittsburgh Sleep Quality Index, PSQI), anxiety (Generalized Anxiety Disorder, GAD-7), depression (Patient Health Questionnaire, PHQ-9), global cognition (Montreal Cognitive Assessment, MoCA), everyday memory failures (Memory Failures of Everyday Questionnaire, MFE-30), fatigue (Chadler Fatigue Questionnaire, CFQ), quality of life (European Quality of Life-5 Dimensions, EQ-5D), and physical activity levels (International Physical Activity Questionnaire, IPAQ). 203 were nonhospitalized, 83 were hospitalized and 82 were admitted to the intensive care unit (ICU). We found statistically significant differences in the PSQI total score between the PCC and HC groups (p < 0.0001), but there were no differences among the PCC groups. In the multiple linear regressions, the PHQ-9 score was a predictor of poor sleep quality for mild PCC patients (p = 0.003); GAD-7 (p = 0.032) and EQ-5D (p = 0.011) scores were predictors of poor sleep quality in the hospitalized PCC group; and GAD-7 (p = 0.045) and IPAQ (p = 0.005) scores were predictors of poor sleep quality in the group of ICU-PCC. These results indicate that worse sleep quality is related to higher levels of depression and anxiety, worse quality of life and less physical activity. Therapeutic strategies should focus on these factors to have a positive impact on the quality of sleep.

Inflammatory agents partially explain associations between cortical thickness, surface area, and body mass in adolescents and young adulthood.

BACKGROUND/OBJECTIVES: Excessive body mass index (BMI) has been linked to a low-grade chronic inflammation state. Unhealthy BMI has also been related to neuroanatomical changes in adults. Research in adolescents is relatively limited and has produced conflicting results. This study aims to address the relationship between BMI and adolescents' brain structure as well as to test the role that inflammatory adipose-related agents might have over this putative link. METHODS: We studied structural MRI and serum levels of interleukin-6, tumor necrosis factor alpha (TNF-α), C-reactive protein and fibrinogen in 65 adolescents (aged 12-21 years). Relationships between BMI, cortical thickness and surface area were tested with a vertex-wise analysis. Subsequently, we used backward multiple linear regression models to explore the influence of inflammatory parameters in each brain-altered area. RESULTS: We found a negative association between cortical thickness and BMI in the left lateral occipital cortex (LOC) and the right precentral gyrus as well as a positive relationship between surface area and BMI in the left rostral middle frontal gyrus and the right superior frontal gyrus. In addition, we found that higher fibrinogen serum concentrations were related to thinning within the left LOC (ß = -0.45, p < 0.001), while higher serum levels of TNF-α were associated to a greater surface area in the right superior frontal gyrus (ß = 0.32, p = 0.045). Besides, we have also identified a trend that negatively correlates the cortical thickness of the left fusiform gyrus with the increases in BMI. It was also associated to fibrinogen (ß = -0.33, p = 0.035). CONCLUSIONS: These results suggest that adolescents' body mass increases are related with brain abnormalities in areas that could play a relevant role in some aspects of feeding behavior. Likewise, we have evidenced that these cortical changes were partially explained by inflammatory agents such as fibrinogen and TNF-α.

Allostatic load and executive functions in overweight adults.

BACKGROUND/OBJECTIVE: Overweight is linked to inflammatory and neuroendocrine responses potentially prompting deregulations in biological systems harmful to the brain, particularly to the prefrontal cortex. This structure is crucial for executive performance, ultimately supervising behaviour. Thus, in the present work, we aimed to test the relationship between allostatic load increase, a surrogate of chronic physiological stress, and core executive functions, such as cognitive flexibility, inhibitory control, and working memory. METHOD: Forty-seven healthy-weight and 56 overweight volunteers aged from 21 to 40 underwent medical and neuropsychological examination. RESULTS: Overweight subjects exhibited a greater allostatic load index than healthy-weight individuals. Moreover, the allostatic load index was negatively related to inhibitory control. When separated, the link between allostatic load index and cognitive flexibility was more marked in the overweight group. CONCLUSIONS: An overweight status was linked to chronic physiological stress. The inverse relationship between the allostatic load index and cognitive flexibility proved stronger in this group. Set-shifting alterations could sustain rigid-like behaviours and attitudes towards food.

Allostatic load and disordered white matter microstructure in overweight adults.

Overweight and stress are both related to brain structural abnormalities. The allostatic load model states that frequent disruption of homeostasis is inherently linked to oxidative stress and inflammatory responses that in turn can damage the brain. However, the effects of the allostatic load on the central nervous system remain largely unknown. The current study aimed to assess the relationship between the allostatic load and the composition of whole-brain white matter tracts in overweight subjects. Additionally, we have also tested for grey matter changes regarding allostatic load increase. Thirty-one overweight-to-obese adults and 21 lean controls participated in the study. Our results showed that overweight participants presented higher allostatic load indexes. Such increases correlated with lower fractional anisotropy in the inferior fronto-occipital fasciculi and the right anterior corona radiata, as well as with grey matter reductions in the left precentral gyrus, the left lateral occipital gyrus, and the right pars opercularis. These results suggest that an otherwise healthy overweight status is linked to long-term biological changes potentially harmful to the brain.

Affected connectivity organization of the reward system structure in obesity.

With the prevalence of obesity rapidly increasing worldwide, understanding the processes leading to excessive eating behavior becomes increasingly important. Considering the widely recognized crucial role of reward processes in food intake, we examined the white matter wiring and integrity of the anatomical reward network in obesity. Anatomical wiring of the reward network was reconstructed derived from diffusion weighted imaging in 31 obese participants and 32 normal-weight participants. Network wiring was compared in terms of the white matter volume as well as in terms of white matter microstructure, revealing lower number of streamlines and lower fiber integrity within the reward network in obese subjects. Specifically, the orbitofrontal cortex and striatum nuclei including accumbens, caudate and putamen showed lower strength and network clustering in the obesity group as compared to healthy controls. Our results provide evidence for obesity-related disruptions of global and local anatomical connectivity of the reward circuitry in regions that are key in the reinforcing mechanisms of eating-behavior processes.

Reward processing in obesity, substance addiction and non-substance addiction.

Similarities and differences between obesity and addiction are a prominent topic of ongoing research. We conducted an activation likelihood estimation meta-analysis on 87 studies in order to map the functional magnetic resonance imaging (fMRI) response to reward in participants with obesity, substance addiction and non-substance (or behavioural) addiction, and to identify commonalities and differences between them. Our study confirms the existence of alterations during reward processing in obesity, non-substance addiction and substance addiction. Specifically, participants with obesity or with addictions differed from controls in several brain regions including prefrontal areas, subcortical structures and sensory areas. Additionally, participants with obesity and substance addictions exhibited similar blood-oxygen-level-dependent fMRI hyperactivity in the amygdala and striatum when processing either general rewarding stimuli or the problematic stimuli (food and drug-related stimuli, respectively). We propose that these similarities may be associated with an enhanced focus on reward--especially with regard to food or drug-related stimuli--in obesity and substance addiction. Ultimately, this enhancement of reward processes may facilitate the presence of compulsive-like behaviour in some individuals or under some specific circumstances. We hope that increasing knowledge about the neurobehavioural correlates of obesity and addictions will lead to practical strategies that target the high prevalence of these central public health challenges.

Neural responses to visual food cues: insights from functional magnetic resonance imaging.

The aim of this paper is to describe the patterns of functional magnetic resonance imaging activation produced by visual food stimuli in healthy participants, as well as in those with anorexia nervosa, bulimia nervosa, binge eating disorder and obesity. We conducted a systematic review of studies published in the last decade on normal and abnormal eating. This review suggested the existence of neural differences in response to the sight of food between healthy individuals, those with an eating disorder and obese subjects. Differences were identified in two brain circuits: (i) limbic and paralimbic areas associated with salience and reward processes and (ii) prefrontal areas supporting cognitive control processes.

Functional connectivity in obesity during reward processing.

Obesity is a health problem that has become a major focus of attention in recent years. There is growing evidence of an association between obesity and differences in reward processing. However, it is not known at present whether these differences are linked exclusively to food, or whether they can be detected in other rewarding stimuli. We compared responses to food, rewarding non-food and neutral pictures in 18 young adults with obesity and 19 normal-weight subjects using independent component analysis. Both groups modulated task-related activity in a plausible way. However, in response to both food and non-food rewarding stimuli, participants with obesity showed weaker connectivity in a network involving activation of frontal and occipital areas and deactivation of the posterior part of the default mode network. In addition, obesity was related with weaker activation of the default mode network and deactivation of frontal and occipital areas while viewing neutral stimuli. Together, our findings suggest that obesity is related to a different allocation of cognitive resources in a fronto-occipital network and in the default mode network.

Depression in Parkinson's disease: clinical correlates and outcome.

Depression has been shown to be more common in Parkinson's disease (PD) than in other chronic and disabling disorders. Neurochemical and functional disturbances are important etiopathogenic factors. The prevalence and clinical features associated with depression in PD remain controversial. The purpose of this study is to estimate the prevalence of depressive symptoms in our patients, as related to other clinical data, and to assess clinical outcomes of these symptoms. A series of PD patients were evaluated over a 9-year period, using the Unified Parkinson's Disease Rating Scale (UPDRS), Hoehn and Yahr stage (HY), Schwab and England Scale (SE), Mini-Mental State Examination (MMSE), and Yesavage Geriatric Depression Scale (GDS). Presence of depressive symptoms was considered if GDS score was higher than 10: mild-moderate (MD) for GDS scores between 11 and 20 and moderate-severe (SD) for GDS scores greater than 20. Three hundred and fifty-three patients were included in this study and additional follow up information was obtained for 184 patients. MD and SD were found in 40.2 and 16.7% of PD patients, respectively. Female gender, high HY, high UPDRS total and subtotal, and low MMSE and SE scores were significantly associated with depressive symptoms. According to changes in GDS score, 34% of patients remained stable, 35% showed an improvement, and 30.9% worsened in the follow up study. Gender, age, age of onset, HY, UPDRS, and PD duration are not related to depression outcome.