Impaired Cognitive Performance Research Articles

IL-6 LEVELS AND COGNITIVE COMPLICATIONS IN PATIENTS WITH TYPE 2 DIABETES MELLITUS: A CROSS SECTIONAL STUDY

Objective: It is important to monitor and manage macrovascular and microvascular complications, which are significant causes of mortality and morbidity in type 2 diabetes (T2DM). Diabetes-related cognitive impairment is an important complication that has recently attracted more attention, but its pathophysiology and clinical features are not known. The aim of this study was to evaluate the potential role of inflammation in diabetes-related cognitive impairment. Material and Method: A total of 122 participants (67 patients with T2DM and 55 controls) took part in this cross-sectional observational clinical study. Cognitive performance was assessed using the Montreal Cognitive Assessment (MoCA) test. IL-6 levels were measured using the ELISA method on blood samples obtained from the participants. Result and Discussion: Although IL-6 levels increased with diabetes and cognitive impairment, there was no significant difference between the groups (p>0.05). Except for attention and orientation, we observed significantly more impaired cognitive performance in T2DM patients. The MoCA total score was significantly correlated with age, education level, fasting glucose, HbA1c, and vitamin D levels (p<0.05). Our results found no evidence that IL-6 is involved in the pathophysiology of cognitive impairment in T2DM, but these findings the importance of cognitive screening in monitoring complications associated with diabetes.

Adaptive cognitive tasks for mental fatigue: An innovative paradigm for cognitive loading in human performance

ObjectivesMental fatigue (MF) can impair cognitive and physical performance in sport. We tested the hypothesis that a shorter adaptive Time Load Dual Back (TLDB) task induces MF faster than a longer Stroop; and subsequently impairs cognitive and intermittent running performance. DesignThis study employed a randomized within-participant design. Methods25 trained individuals performed a Yo-Yo test after one of four experimental conditions (30-min Stroop, 20-min and 10-min TLDB tasks, and active control). Cognitive performance was assessed using the Psychomotor Vigilance Task (PVT) before and after the experimental conditions. Measures of mood, workload, MF, RPE, heart rate (HR), heart rate variability (HRV) and blood lactate were collected. ANOVAs determined the effect of the 4 conditions. ResultsStroop and 20-min TLDB conditions impaired running performance similarly (p = .015), while no differences are reported for 10-min TLDB and Control. No significant differences in physiological parameters were reported during the Yo-Yo test although RPE was significantly higher in the Stroop and 20-min TLDB conditions (p = .014). Stroop and both TLDBs conditions impaired PVT's cognitive performance (p = .029), MF (p = .012), mental demand (p < .001), HR (p = .021) and HRV (p = .033); with 20-min TLDB task having the higher significant impact. Mood alterations were similar between Stroop and TLDB conditions. ConclusionsIntermittent running (Yo-Yo) and cognitive (PVT) performances, and subjective ratings were impaired by 30-min Stroop and 20-min TLDB tasks; while 10-min TLDB did not to impair performance. Shorter adaptive modes seem to be more effective in inducing MF and could have relevant clinical applications to assess conditions such as traumatic brain injury and concussion.

Cognitive performance of grey mouse lemurs (Microcebus murinus) during a discrimination learning task: Effect of the emotional valence of stimuli.

Emotions are omnipresent in many animals' lives. It is a complex concept that encompasses physiological, subjective, behavioural and cognitive aspects. While the complex relationship between emotion and cognition has been well studied in humans and in some nonhuman primates, it remains rather unexplored for other nonhuman primate species, such as lemurs. In our study, we evaluated the performance of N = 48 grey mouse lemurs (Microcebus murinus) in a discrimination learning task using visual emotional stimuli. We tested whether the type of visual stimulus (positive, negative or neutral) influenced the cognitive performance of mouse lemurs. Individuals had to learn to discriminate between two platforms according to the associated visual stimuli and to jump to the target platform (leading to a reward). Our main finding was that emotional stimuli, whether positive or negative in valence, impaired cognitive performance when used as a target. Specifically, the lowest success rate occurred when the target was associated with the emotional stimuli, and the highest success rate occurred when it was associated with neutral stimuli. Our results show a similar pattern to that found in other primate species and support the adaptive role of emotion. Our results also support that individual differences could be a factor impacting the relation between emotion and cognition. This study is the first to explore how emotions interfere with the cognitive abilities of a lemur species and highlights the importance of acknowledging emotion in mouse lemurs as well as studying the emotion-cognition interaction in a wider range of primate species.

Adding a sustained attention task to a physically demanding cycling exercise exacerbates neuromuscular fatigue and impairs cognitive performance in both normoxia and hypoxia.

Both cognitive motor dual-tasks (CMDT) protocols and hypoxic environments have been associated with significant impairments in cognitive and physical performance. We aimed to determine the effects of hypoxia on cognitive performance and neuromuscular fatigue during a highly physically demanding CMDT. Fifteen young adults completed a first session involving a cognitive task (CTLCOG) followed by cycling exercise (CTLEX) in normoxia. After that, they randomly participated in CMDT sessions in normoxia (DTNOR) and hypoxia (DTHYP). The physical exercise consisted of 20min cycling at a "hard" perceived effort, and the cognitive task consisted of 15min sustained attention to response time task (SART). Concurrent psycho-physiological measurements included: quadriceps neuromuscular fatigue (peripheral/central components from femoral nerve electrostimulation), prefrontal cortex (PFC) oxygenation by near-infrared spectroscopy, and perception of effort. SART performance significantly decreased in DTNOR (-15.7 ± 15.6%, P < 0.01) and DTHYP (-26.2 ± 16.0%, P < 0.01) compared to CTLCOG (-1.0 ± 17.7%, P = 0.61). Peripheral fatigue similarly increased across conditions, whereas the ability of the central nervous system to activate the working muscles was impaired similarly in DTNOR (-6.1 ± 5.9%, P < 0.001) and DTHYP (-5.4 ± 7.3%, P < 0.001) compared to CTLEX (-1.1 ± 0.2%, P = 0.52). Exercise-induced perception of effort was higher in DTHYP vs. DTNOR and in DTNOR vs. CTLEX. This was correlated with cognitive impairments in both normoxia and hypoxia. PFC deoxygenation was more pronounced in DTHYP compared to DTNOR and CTLEX. In conclusion, performing a sustained attention task together with physically challenging cycling exercise promotes central neuromuscular fatigue and impairs cognitive accuracy; the latter is particularly noticeable when the CMDT is performed in hypoxia.

Neutrophil-to-lymphocyte ratio and longitudinal cognitive performance in Parkinson's disease.

Previous studies have suggested a link between peripheral inflammation and cognitive outcomes in the general population and individuals with Parkinson's disease (PD). We sought to test the association between peripheral inflammation, measured by the neutrophil-to-lymphocyte ratio (NLR), cognitive performance, and mild cognitive impairment (MCI) status in individuals with PD. A retrospective, longitudinal analysis was carried out using data from the Parkinson's Progression Markers Initiative (PPMI), including 422 participants with PD followed over 5 years. Cognitive performance was assessed using a neuropsychological battery including the Montreal Cognitive Assessment (MoCA) and tests of verbal learning, visuospatial function, processing speed, and executive function. Mixed-effect regression models were used to analyze the association between NLR, cognitive performance, and MCI status, controlling for age, sex, education, APOE genotype, and motor severity. There was a negative association between NLR and MoCA, even after adjusting for covariates (b = -0.12, p = 0.033). MoCA scores for individuals in the high NLR category exhibited a more rapid decline over time compared to the low NLR group (b = -0.16, p = 0.012). Increased NLR was associated with decreased performance across all cognitive domains. However, NLR was not associated with MCI status over 5 years of follow-up. This study demonstrates a link between elevated NLR and cognitive performance in PD, but not with MCI status over 5 years. This suggests that NLR is more strongly associated with day-to-day cognitive performance than with incident MCI, but this requires further study in more heterogeneous cohorts.

Impact of sleep deprivation on stress levels and cognitive performance in young and middle-aged adults at a Medical University in Ajman, UAE

BACKGROUND: Inadequate sleep is a widespread public health concern, impacting physical and mental health, as well as cognitive well-being. This study explores the link between sleep quality, the inflammatory marker interleukin-6 (IL-6), and cognitive function in two age groups (18-25 years and 35 years and above) at Gulf Medical University. MATERIALS AND METHODS: Sleep quality was assessed using the Pittsburgh questionnaire, and salivary IL-6 levels were measured. Cognitive function was evaluated using the National Aeronautics and Space Administration-Psychomotor Vigilance Test (NASA-PVT), focusing on mean reaction time (RT), lapses, fastest 10% RT, and slowest 10% RT. Descriptive and inferential statistics were used to analyze the data. The descriptive statistics used were frequency, percentage mean, and standard deviation (SD). The inferential statistics used was the unpaired t-test. The level of significance was taken as P ≤ 0.05. Statistical Package for the Social Sciences (SPSS) 28 was used to analyze the data. RESULTS: Approximately 75% of young adults and 80% of middle-aged adults reported good sleep quality. Sleep disturbances were reported by 65% of young adults and 95% of middle-aged adults. In both age groups, individuals with poor sleep exhibited higher IL-6 levels, but all IL-6 values remained within the reference range. NASA-PVT results indicated that individuals with poor sleep had higher mean RT and lapses compared to those with good sleep. In the older age group, both mean RT and lapses were higher than in the younger group, suggesting potential age-related effects on psychomotor vigilance. CONCLUSION: Our findings suggest a connection between poor sleep quality, elevated IL-6 levels, and impaired cognitive performance.

No Impairment in Bone Turnover or Executive Functions in Well-Treated Preschoolers with Phenylketonuria-A Pilot Study.

Patients with phenylketonuria (PKU) present signs of impaired executive functioning and bone health in adolescence and adulthood, depending in part on the success of therapy in childhood. Therefore, nine children with well-treated PKU (4-7 years old, 22.2% ♀, seven with a full set of data, two included into partial analysis) and 18 age-, gender- and season-matched controls were analyzed for differences in executive functioning and bone parameters in plasma. Plasma was analyzed with commercially available kits. Cognitive performance in tonic alertness, visuo-spatial working memory, inhibitory control and task switching was assessed by a task battery presented on a touch screen. Regarding cognition, only the performance in incongruent conditions in inhibitory control was significantly better in children with PKU than in controls. No further differences in cognitive tests were detected. Furthermore, no significant difference in the bone turnover markers osteocalcin, undercarboxylated osteocalcin and CTX were detected between children with PKU and controls, while children with PKU had a significantly higher vitamin D concentration (69.44 ± 12.83 nmol/L vs. 41.87 ± 15.99 nmol/L, p < 0.001) and trended towards lower parathyroid hormone concentrations than controls (48.27 ± 15.16 pg/mL vs. 70.61 ± 30.53 pg/mL, p = 0.066). In this small group of well-treated preschoolers with PKU, no impairments in cognitive performance and bone turnover were observed, while vitamin D supplementation of amino acid supplements seems to be sufficient to achieve good vitamin D status.

Adult-onset deactivation of autophagy leads to loss of synapse homeostasis and cognitive impairment, with implications for alzheimer disease

ABSTRACT A growing number of studies link dysfunction of macroautophagy/autophagy to the pathogenesis of diseases such as Alzheimer disease (AD). Given the global importance of autophagy for homeostasis, how its dysfunction can lead to specific neurological changes is puzzling. To examine this further, we compared the global deactivation of autophagy in the adult mouse using the atg7iKO with the impact of AD-associated pathogenic changes in autophagic processing of synaptic proteins. Isolated forebrain synaptosomes, rather than total homogenates, from atg7iKO mice demonstrated accumulation of synaptic proteins, suggesting that the synapse might be a vulnerable site for protein homeostasis disruption. Moreover, the deactivation of autophagy resulted in impaired cognitive performance over time, whereas gross locomotor skills remained intact. Despite deactivation of autophagy for 6.5 weeks, changes in cognition were in the absence of cell death or synapse loss. In the symptomatic APP PSEN1 double-transgenic mouse model of AD, we found that the impairment in autophagosome maturation coupled with diminished presence of discrete synaptic proteins in autophagosomes isolated from these mice, leading to the accumulation of one of these proteins in the detergent insoluble protein fraction. This protein, SLC17A7/Vglut, also accumulated in atg7iKO mouse synaptosomes. Taken together, we conclude that synaptic autophagy plays a role in maintaining protein homeostasis, and that while decreasing autophagy interrupts normal cognitive function, the preservation of locomotion suggests that not all circuits are affected similarly. Our data suggest that the disruption of autophagic activity in AD may have relevance for the cognitive impairment in this adult-onset neurodegenerative disease. Abbreviations: 2dRAWM: 2-day radial arm water maze; AD: Alzheimer disease; Aβ: amyloid-beta; AIF1/Iba1: allograft inflammatory factor 1; APP: amyloid beta precursor protein; ATG7: autophagy related 7; AV: autophagic vacuole; CCV: cargo capture value; Ctrl: control; DLG4/PSD-95: discs large MAGUK scaffold protein 4; GFAP: glial fibrillary acidic protein; GRIN2B/NMDAR2b: glutamate ionotropic receptor NMDA type subunit 2B; LTD: long-term depression; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; m/o: months-old; PNS: post-nuclear supernatant; PSEN1/PS1: presenilin 1; SHB: sucrose homogenization buffer; SLC32A1/Vgat: solute carrier family 32 member 1; SLC17A7/Vglut1: solute carrier family 17 member 7; SNAP25: synaptosome associated protein 25; SQSTM1/p62: sequestosome 1; SYN1: synapsin I; SYP: synaptophysin ; SYT1: synaptotagmin 1; Tam: tamoxifen; VAMP2: vesicle associated membrane protein 2; VCL: vinculin; wks: weeks.

Mild Dehydration Triggered by Exercise Reduces Cognitive Performance in Children, But Does Not Affect Their Motor Skills

Objective Children face the risk of dehydration in varying amounts during the day due to reasons such as physical activity, sweating, eating salty foods and drinking carbonated beverages. It is assumed that dehydration can lead to impaired motor skills and cognitive performance since it affects brain function. However, inconsistencies in study results, test times and problems caused by heat stress make new research mandatory. In our research, we examined the effects of exercise-induced mild dehydration on motor skills and cognitive performance in active/sedentary boys who do/do not do regular physical activities in their daily lives. Methods The study included 112 boys who do regular physical activity (n:57; 12.40 ± 0.49age) and sedentary (n:55; 12.49 ± 0.50age). The children were given a 12-h hydration program. Mild dehydration was created by giving exercises after hydration measurements. In case of hydration and mild dehydration, Bruininks-Oseretsky Motor Proficiency and d2 attention test were applied to the children. For comparison, Repeated Measures ANOVA and Bonferroni post-hoc test was performed at the second level. Results According to the hydration and mild dehydration comparison results, there was no difference in total score of Fine Motor Skill Sensitivity, Fine Motor Skill Integration, Hand Dexterity and Bidirectional Coordination, Balance, Running Speed and Agility, Hand-Arm Coordination, Strength, and BOT-2 in children. There was a decrease in both groups in terms of Focused Attention, Processing Speed, Accuracy, Concentration Performance and Attention Span. Conclusion As a result, mild dehydration is associated with daily physical activity in children (physical education classes, etc.) or it can easily occur due to food/beverage preferences. It may affect children’s performance of school curriculum and extracurricular activities. It shows that maintaining optimal hydration is important.

Targeted TGF-βR2 Knockdown in the Retrotrapezoid Nucleus Mitigates Respiratory Dysfunction and Cognitive Decline in a Mouse Model of Cerebral Amyloid Angiopathy with and without Stroke.

Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid-beta peptides within cerebral blood vessels, leading to neurovascular complications. Ischemic strokes result from acute disruptions in cerebral blood flow, triggering metabolic disturbances and neurodegeneration. Both conditions often co-occur and are associated with respiratory dysfunctions. The retrotrapezoid nucleus (RTN), which is crucial for CO2 sensing and breathing regulation in the brainstem, may play a key role in breathing disorders seen in these conditions. This study aims to investigate the role of Transforming Growth Factor Beta (TGF-β) signaling in the RTN on respiratory and cognitive functions in CAA, both with and without concurrent ischemic stroke. Adult male Tg-SwDI (CAA model) mice and C57BL/6 wild-type controls underwent stereotaxic injections of lentivirus targeting TGF-β2R2 in the RTN. Stroke was induced by middle cerebral artery occlusion using a monofilament. Respiratory functions were assessed using whole-body plethysmography, while cognitive functions were evaluated through the Barnes Maze and Novel Object Recognition Test (NORT). Immunohistochemical analysis was conducted to measure TGF-βR2 and GFAP expressions in the RTN. CAA mice exhibited significant respiratory dysfunctions, including reduced respiratory rates and increased apnea frequency, as well as impaired cognitive performance. TGF-βR2 knockdown in the RTN improved respiratory functions and cognitive outcomes in CAA mice. In CAA mice with concurrent stroke, TGF-βR2 knockdown similarly enhanced respiratory and cognitive functions. Immunohistochemistry confirmed reduced TGF-βR2 and GFAP expressions in the RTN following knockdown. Our findings demonstrate that increased TGF-β signaling and gliosis in the RTN contribute to respiratory and cognitive dysfunctions in CAA and CAA with stroke. Targeting TGF-βR2 signaling in the RTN offers a promising therapeutic strategy to mitigate these impairments. This study is the first to report a causal link between brainstem gliosis and both respiratory and cognitive dysfunctions in CAA and stroke models.

The role of cognitive flexibility on higher level executive functions in mild cognitive impairment and healthy older adults

BackgroundMild Cognitive Impairment (MCI) is a preclinical condition between healthy and pathological aging, which is characterized by impairments in executive functions (EFs), including cognitive flexibility. According to Diamond’s model, cognitive flexibility is a core executive function, along with working memory and inhibition, but it requires the development of these last EFs to reach its full potential. In this model, planning and fluid intelligence are considered higher-level EFs. Given their central role in enabling individuals to adapt their daily life behavior efficiently, the goal is to gain valuable insight into the functionality of cognitive flexibility in a preclinical form of cognitive decline. This study aims to investigate the role of cognitive flexibility and its components, set-shifting and switching, in MCI. The hypotheses are as follows: (I) healthy participants are expected to perform better than those with MCI on cognitive flexibility and higher-level EFs tasks, taking into account the mediating role of global cognitive functioning; (II) cognitive flexibility can predict performance on higher-level EFs (i.e., planning and fluid intelligence) tasks differently in healthy individuals and those diagnosed with MCI.MethodsNinety participants were selected and divided into a healthy control group (N = 45; mean age 64.1 ± 6.80; 66.6% female) and an MCI group (N = 45; mean age 65.2 ± 8.14; 40% female). Cognitive flexibility, fluid intelligence, planning, and global cognitive functioning of all participants were assessed using standardized tasks.ResultsResults indicated that individuals with MCI showed greater impairment in global cognitive functioning and EFs performance. Furthermore, the study confirms the predictive role of cognitive flexibility for higher EFs in individuals with MCI and only partially in healthy older adults.

Prefrontal activity and heart rate variability during cognitive tasks may show different changes in young and older adults with and without mild cognitive impairment.

Age-related decline in cognitive function is often linked to changed prefrontal cortex (PFC) activity and heart rate variability (HRV). Mild cognitive impairment (MCI), a transitional stage between normal aging and dementia, might have further degeneration beyond aging. This study aimed to investigate the differences between young and older adults with or without MCI in cognitive functions, task-induced PFC activation and HRV changes. Thirty-one healthy young adults (YA), 44 older adults (OA), and 28 older adults with MCI (OA-MCI) were enrolled and compared in this cross-sectional study. Each participant received a one-time assessment including cognitive and executive functions, as well as the simultaneous recording of PFC activity and HRV during a cognitive task paradigm. We observed age-related decrease in global cognitive functions, executive functions, HRV, and increase in PFC activity. The MCI further deteriorated the global cognitive and executive performances, but not the HRV or the prefrontal activation. Older people showed lower performances in general cognitive function and executive function, compensatory increase of PFC activity, and reduced HRV. Older people with MCI had further deterioration in cognitive performance, but not in PFC activation and HRV.

Cigarette smoking and cognitive task performance: Experimental effects of very-low nicotine-content cigarettes.

Reductions in the nicotine content of cigarettes decrease smoking rate and dependence severity, but effects on cognition are less well established. The potential impacts of very-low nicotine-content (VLNC) cigarettes on cognitive task performance must be evaluated, especially in vulnerable populations. The aim of the present study is to experimentally examine the effects of VLNC cigarettes on cognitive performance. Adults who smoked daily (n = 775) from three vulnerable populations (socioeconomically disadvantaged reproductive-age women, individuals with opioid use disorder, affective disorders) were examined. Participants were randomly assigned to normal nicotine content (NNC; 15.8 mg nicotine/g tobacco) or VLNC (2.4 mg/g or 0.4 mg/g) cigarettes for 12 weeks. Response inhibition (stop-signal task), working memory (n-back task; n of 2-n of 0), and cognitive interference (nicotine Stroop task) were assessed at baseline, 2, 6, and 12 weeks. Results were analyzed using mixed-model repeated-measures analyses of variance. Extended exposure to VLNC cigarettes produced no significant changes in any measure of cognitive performance compared to NNC cigarettes. Over weeks, response times on the n-back task decreased across doses. No significant effects were observed on the stop-signal or nicotine Stroop tasks. All three vulnerable populations performed comparably on all three cognitive tasks. Extended exposure to VLNC cigarettes produced no impairments in cognitive performance on any of the assessed tasks compared to NNC cigarettes. These findings are consistent with the larger literature detailing other consequences following exposure to VLNC cigarettes and are encouraging for the adoption of a nicotine-reduction policy. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Alzheimer-like behavior and synaptic dysfunction in 3 × Tg-AD mice are reversed with calcineurin inhibition.

Alzheimer's disease is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance. Current treatments are unable to achieve satisfactory therapeutic effects or reverse the progression of the disease. Calcineurin has been implicated as part of a critical signaling pathway for learning and memory, and neuronal calcineurin may be hyperactivated in AD. To investigate the effects and underlying mechanisms of FK506, a calcineurin inhibitor, on Alzheimer-like behavior and synaptic dysfunction in the 3 × Tg-AD transgenic mouse model of Alzheimer's disease, we investigated the effect of FK506 on cognitive function and synaptic plasticity in the 3 × Tg-AD transgenic mouse model of Alzheimer's disease. The results showed that FK506 treatment ameliorated cognitive deficits, as indicated by the decreased latency in the water maze, and attenuated tau hyperphosphorylation in 3 × Tg-AD mice. Treatment with FK506 also reduced the levels of certain markers of postsynaptic deficits, including PSD-95 and NR2B, and reversed the long-term potentiation deficiency and dendritic spine impairments in 3 × Tg-AD mice. These findings suggest that treatment with calcineurin inhibitors such as FK506 can be an effective therapeutic strategy to rescue synaptic deficit and cognitive impairment in familial Alzheimer's disease and related tauopathies.

Accelerated epigenetic age is associated with whole-brain functional connectivity and impaired cognitive performance in older adults

While chronological age is a strong predictor for health-related risk factors, it is an incomplete metric that fails to fully characterize the unique aging process of individuals with different genetic makeup, neurodevelopment, and environmental experiences. Recent advances in epigenomic array technologies have made it possible to generate DNA methylation-based biomarkers of biological aging, which may be useful in predicting a myriad of cognitive abilities and functional brain network organization across older individuals. It is currently unclear which cognitive domains are negatively correlated with epigenetic age above and beyond chronological age, and it is unknown if functional brain organization is an important mechanism for explaining these associations. In this study, individuals with accelerated epigenetic age (i.e. AgeAccelGrim) performed worse on tasks that spanned a wide variety of cognitive faculties including both fluid and crystallized intelligence (N = 103, average age = 68.98 years, 73 females, 30 males). Additionally, fMRI connectome-based predictive models suggested a mediating mechanism of functional connectivity on epigenetic age acceleration-cognition associations primarily in medial temporal lobe and limbic structures. This research highlights the important role of epigenetic aging processes on the development and maintenance of healthy cognitive capacities and function of the aging brain.

Mitochondrial dysfunction is associated with cognitive impairment in adults with OSA without dementia

Study objectivesIncreased reactive oxygen species associated with loss of mitochondrial function affect synaptic activity, which is an important mechanism underlying cognitive decline. This study assesses the role of mitochondrial proteins in neuron-derived exosomes (NDEs) on cognitive impairment in patients with obstructive sleep apnea (OSA) without dementia. MethodsAnalyses were conducted in 268 study participants with complete polysomnography data, cognitive tests, and important clinical data available. NDEs were isolated immunochemically for enzyme-linked immunosorbent assay quantification of mitochondrial proteins, i.e., humanin and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c), and synaptic protein, i.e., neurogranin (NRGN). A mediation analysis of the relationship between sleep parameters and cognition was performed using humanin, MOTS-c, and NRGN values as a mediating factor. Twenty-two patients with moderate to severe OSA who received CPAP therapy were followed up, and humanin, MOTS-c and NRGN levels were reassessed after 1 year of treatment. ResultsAll participants were divided into the OSA + MCI group (n = 91), OSA-MCI group (n = 89), MCI group (MCI without OSA) (n = 38) and control group (normal cognitive state without OSA) (n = 50). The mean CD63-normalized NDE levels of humanin, MOTS-c, and NRGN in the OSA + MCI group were higher than those in the OSA-MCI and control groups. The NDE levels of humanin, MOTS-c, and NRGN in the MCI group were lower than those in controls. The odds of cognitive impairment in patients with OSA were higher with higher NDE levels of humanin, MOTS-c, and NRGN (odds ratio (OR): 2.100, 95 % confidence interval (CI): 1.646–2.679, P < 0.001; OR: 5.453, 95 % CI: 3.112–9.556, P < 0.001; OR: 3.115, 95 % CI: 2.163–4.484, P < 0.001). The impaired cognitive performance was associated with higher NDE levels of humanin (β: 0.505, SE: 0.048, P < 0.001), MOTS-c (β: 0.580, SE: 0.001, P < 0.001), and NRGN (β: 0.585, SE: 0.553, P < 0.001). The relationship between sleep parameters (mean SaO2 and T90) and MoCA scores was mediated by the NDE levels of humanin, MOTS-c, and NRGN with the proportion of mediation varying from 35.33 % to 149.07 %. Receiver operating characteristic curve revealed an area under the curve of 0.905 for humanin, 0.873 for MOTS-c, and 0.934 for NRGN to predict MCI in OSA patients without dementia. Increased humanin, MOTS-c, and NRGN levels significantly decreased after CPAP treatment. ConclusionsMitochondrial dysfunction is implicated in cognitive impairment in OSA patients without dementia, and mainly mediates the association between intermittent hypoxia and cognitive impairment in adults with OSA without dementia. Mitochondrial dysfunction can be partially reversible by CPAP treatment. Mitochondrial proteins can be used as markers of cognitive impairment in patients with OSA.

Low-carbohydrate diet as a disease modifier for relapse prevention of treatment-resistant depression. Spotlight on neuroplasticity and brain-derived neurotrophic factor

Depression is the most common mental disorder with a high treatment resistance rate that can affect patients at any age. Individuals who obtain insufficient and unsatisfactory responses after two treatment steps are considered as treatment-resistant-depression (TRD), and therefore seek other both pharmacological and nonpharmacological modalities that may offer not only alleviation of depressive symptoms, but also prevent relapse of the disease. Dietary interventions, whether focusing on supplementation or dietary restrictions seem to match these criteria. Low-carbohydrate-diet (LCHD), which is a close family to ketogenic diet, has been shown to improve neuroplasticity by increasing production of brain-derived neurotrophic factor (BDNF) that has been decreased in patients with depression, yet naive to depression treatment. Furthermore, links between neuroplasticity deterioration and diet rich in sweetened beverages have been demonstrated as impaired cognitive performance and increased risk of depression. Here, we hypothesize that BDNF could be the common end-point intervention in TRD, that could be relatively easily achieved by reduction in carbohydrate consumption.

Changes in essentialist beliefs about cognitive aging predicts changes in mental health: Evidence from a 10-year longitudinal study.

The belief that aging-related cognitive decline is inevitable is associated with impaired cognitive performance of older adults. Little is, however, known about the association between changes in essentialist beliefs about cognitive aging and mental health in the long term and among both younger and older adults. From a theoretical perspective, it would be expected that changes in essentialist beliefs about cognitive aging predict changes in mental health among older adults compared to younger adults. These differential associations have not yet been prospectively investigated. Using longitudinal data, the association between changes in essentialist beliefs about cognitive aging and mental health outcomes and the moderation effect of age were assessed. Mental health includes well-being and mental illness (depression, anxiety, and panic symptoms). Data from adult participants (n = 4,963 with a mean age of 55.41 years, range 28-84 years) in a U.S. national longitudinal study were analyzed. A series of two-wave latent change score models indicated that changes in essentialist beliefs about cognitive aging are associated with changes in well-being and mental illness. Age did not moderate the relationship between changes in essentialist beliefs about aging and changes in mental health (i.e., mental illness and well-being). The present study highlights change-to-change dynamics between essentialist beliefs about cognitive aging and mental health, regardless of age. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

The Role of Sensory Impairment in Cognitive Health Appraisal: A Study of Older Korean Americans Living in Subsidized Senior Housing.

We examined how the association between cognitive performance and cognitive health appraisal would be moderated by vision and/or hearing impairment. Data were collected from 315 older Korean-American residents in subsidized senior housing in Los Angeles (M age = 79.4years). Linear regression models examined the direct and interactive effects of cognitive performance, vision impairment, and hearing impairment on cognitive health appraisal. Negative appraisal of cognitive health was associated with lower cognitive performance and poorer ratings for vision and hearing. Moreover, we found a significant interaction between cognitive performance and hearing impairment (β = .13, p < .05), as well as a three-way interaction among cognitive performance, vision impairment, and hearing impairment (β = .12, p < .05). The association between objective and subjective measures of cognition was weakened when hearing was impaired. Such a pattern was further evident when both vision and hearing were impaired.

Preoperative recovery sleep ameliorates postoperative cognitive dysfunction aggravated by sleep fragmentation in aged mice by enhancing EEG delta-wave activity and LFP theta oscillation in hippocampal CA1

Sleep fragmentation (SF) is a common sleep problem experienced during the perioperative period by older adults, and is associated with postoperative cognitive dysfunction (POCD). Increasing evidence indicates that delta-wave activity during non-rapid eye movement (NREM) sleep is involved in sleep-dependent memory consolidation and that hippocampal theta oscillations are related to spatial exploratory memory. Recovery sleep (RS), a self-regulated state of sleep homeostasis, enhances delta-wave power and memory performance in sleep-deprived older mice. However, it remains unclear whether RS therapy has a positive effect on cognitive changes following SF in older mouse models. Therefore, this study aimed to explore whether preoperative RS can alleviate cognitive deficits in aged mice with SF. A model of preoperative 24-h SF combined with exploratory laparotomy-induced POCD was established in 18-month-old mice. Aged mice were treated with preoperative 6-h RS following SF and postoperative 6-h RS following surgery, respectively. The changes in hippocampus-dependent cognitive function were investigated using behavioral tests, electroencephalography (EEG), local field potential (LFP), magnetic resonance imaging, and neuromorphology. Mice that underwent 24-h SF combined with surgery exhibited severe spatial memory impairment; impaired cognitive performance could be alleviated by preoperative RS treatment. In addition, preoperative RS increased NREM sleep; enhanced EEG delta-wave activity and LFP theta oscillation in the hippocampal CA1; and improved hippocampal perfusion, microstructural integrity, and neuronal damage. Taken together, these results provide evidence that preoperative RS may ameliorate the severity of POCD aggravated by SF by enhancing delta slow-wave activity and hippocampal theta oscillation, and by ameliorating the reduction in regional cerebral blood flow and white matter microstructure integrity in the hippocampus.