Frontiers in Aging Neuroscience最新文献

Lung diseases induce changes in brain structure and function, leading to a range of cognitive, emotional, and motor deficits. The concept of the lung-brain axis has been proposed through neuroanatomy, endocrine, and immune pathway, while a considerable number of studies also explored the existence of the lung-brain axis from a neuroimaging perspective. This survey summarizes studies exploring the relationship between lung disease and brain structure and function from neuroimaging perspective, particular in magnetic resonance imaging (MRI). We have collated existing lung diseases studies and categorized them into four types: chronic obstructive pulmonary disease (COPD), coronavirus disease 2019 (COVID-19), lung cancer and other lung diseases. The observed structural and functional changes in the brain and cognitive dysfunction induced by lung diseases are discussed. We also present distinct pattern of brain changes in various lung diseases. Neuroimaging changes in COPD are concentrated in the frontal lobes, including gray matter atrophy, white matter damage, and reduced perfusion. Patients with COVID-19 exhibit extensive microhemorrhages and neuroinflammation, brain regions functionally connected to the primary olfactory cortex show greater changes. For lung cancer patients, brain changes are mainly attributed to the neurotoxicity of radiotherapy and chemotherapy, with damage concentrated in subcortical structures, patients with cancer pain demonstrate hyperconnectivity in motor and visual networks. The survey also discusses the pathological mechanisms revealed in neuroimaging studies and clinical significance of current studies. Finally, we analyzed current limitations, mainly in terms of small sample size, non-standardized criteria, reliance on correlation analyses, lack of longitudinal studies, and absence of reliable biomarkers. We suggest future research directions should include leveraging artificial intelligence for biomarker development, conducting longitudinal and multicenter studies, and investigating the systemic effects of lung disease on the brain and neuromodulation strategies.

Objective: To assess the therapeutic effect of tDCS on cognitive function in patients with Parkinson's disease.

Methods: From the start of the library's construction until June 24, 2024, we searched the following databases for literature: PubMed, Embase, Web of Science, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang, China Science and Technology Journal Database (VIP), and China Biomedical Literature Database (CBM). We also looked through the references in the articles. The improvement of overall cognition in patients with Parkinson's disease with tDCS was the primary outcome indicator. The improvement of executive function, memory, attention, language, quality of life, and depression with tDCS were the secondary outcome indicators. Two researchers extracted data independently, with a third researcher mediating in the event of a dispute. The Cochrane risk of bias tool was used to evaluate the quality of the included literature.

Results: A total of 23 articles encompassing 874 subjects were included. tDCS has shown significant efficacy on overall cognition (SMD = 0.73, 95% CI = 0.57 to 0.89, I² = 0%, P < 0.00001), particularly in the areas of executive function (SMD = -0.32, 95% CI = -0.56 to -0.07, I² = 0%, P = 0.01) and language function (SMD = 0.5, 95% CI = 0.2 to 0.8, I² = 0%, P = 0.001). Furthermore, the clinical efficacy of tDCS was enhanced with a stimulation intensity of 2 mA (SMD = 0.76, 95% CI = 0.58 to 0.93, I² = 7%, P < 0.00001), a stimulation duration of ≥25 min (SMD = 0.70, 95% CI = 0.49 to 0.91, I² = 6%, P < 0.00001), and a minimum of 10 stimulation sessions (SMD = 0.74, 95% CI = 0.56 to 0.92, I² = 0%, P < 0.00001). Furthermore, tDCS has shown efficacy in alleviating depressive mood (SMD = -0.46, 95% CI = -0.79 to -0.13, I² = 0%, P = 0.006).

Conclusion: tDCS demonstrated substantial efficacy in enhancing overall cognition in patients with PD. The efficacy of tDCS was obvious in executive function, language, and depressive mood. Nonetheless, a substantial quantity of rigorous clinical trials on tDCS for cognitive function in patients with PD remains necessary in the future.

Human studies suggest that heavy alcohol use may be an etiological factor contributing to the development of Alzheimer's disease (AD) neuropathology. Both alcohol use disorder (AUD) and AD share common underlying neuropathology, including proinflammatory high-mobility group box 1 (HMGB1)-mediated neuroimmune signaling and basal forebrain cholinergic neuron degeneration. Adolescent onset of binge drinking represents a significant risk factor for later development of an AUD, and accumulating evidence suggests that adolescent initiation of heavy alcohol use induces HMGB1 signaling and causes degeneration of the basal forebrain cholinergic system that persists into adulthood. However, it is unknown whether adolescent binge drinking confers increased risk for later development of AD-associated neuropathology through persistent induction of proinflammatory HMGB1 neuroimmune signaling. To investigate this question, we first (Experiment 1) assessed AD-associated neuropathology in the post-mortem human basal forebrain of individuals with AUD and an adolescent age of drinking onset relative to age-matched moderate drinking controls (CONs). In Experiment 2, we treated non-transgenic and 5xFAD male and female mice, which overexpress both mutant human APP and PS1, with adolescent intermittent ethanol (AIE; 5.0 g/kg, i.g. 2-days on/2-days off; postnatal day [P]30 - P55), and assessed AD-associated neuropathology in the adult (P100) basal forebrain. In Experiment 3, 5xFAD female mice received AIE treatment followed by glycyrrhizic acid (150 mg/L), an HMGB1 inhibitor, in drinking water from P56 to P100, and basal forebrain tissue was collected on P100 for assessment of AD-associated neuropathology. In the post-mortem human AUD basal forebrain (Experiment 1), we report upregulation of Hmgb1 and the HMGB1 receptors Rage and Tlr4 as well as microglial activation and increased intraneuronal Aβ_1-42 accumulation in association with reduced cholinergic neuron marker expression (ChAT). In the 5xFAD mouse model (Experiment 2), AIE accelerated AD-associated induction of Hmgb1 proinflammatory neuroimmune genes, microglial activation, and reductions of ChAT+ basal forebrain cholinergic neurons in the adult female, but not male, basal forebrain. In Experiment 3, post-AIE treatment with glycyrrhizic acid rescued the AIE-induced acceleration of AD-associated increases in proinflammatory HMGB1 neuroimmune signaling, microglial activation, and persistent reductions of basal forebrain cholinergic neurons in adult 5xFAD female mice. Together, these findings suggest that adolescent binge ethanol exposure may represent an underappreciated etiological factor contributing to onset of AD-associated neuropathology in adulthood through HMGB1- mediated neuroimmune signaling.

Background: Motor vehicle accidents remain a leading cause of accidental death worldwide. Death and injury rates are particularly high for both young inexperienced drivers and elderly drivers. Understanding the behavioral changes that are associated with maturation and aging could inform assessments of driving performance and lead to new measures identifying at-risk drivers. To shed further light on such effects, this study aims to characterize simulated driving behavior across and within age groups using a large driving simulation dataset.

Methods: The analyzed dataset consisted of 112 participants [47/112 (42%) female] between the ages of 17 and 85 (average ± standard deviation: 54 ± 22 years). Participants performed navigation in scenarios modeled after the standard licensing test of Ontario, Canada, which included a series of turns at intersections with different levels of complexity (e.g., involving oncoming traffic or pedestrians) and levels of distraction (requiring auditory responses to common-knowledge questions). Behavioral metrics were defined and investigated not only for the full completion of each task but also based on common subtasks (e.g., braking at an intersection), which were then compared across and within age groups (young, middle-aged, old).

Results: Overall, young adults behaved similarly to middle-aged adults for basic tasks but showed differences during traffic navigation subtasks when distracted, such as starting to decelerate significantly later when approaching intersections. Old drivers, on the other hand, drove at lower average speed, stopped earlier at intersections, and left increased distances to pedestrians, but required significantly more time to complete the driving tasks.

Conclusion: With rich detail arising from intra-task quantification, the results were consistent with and additive to previous literature showcasing that compared to middle-aged adults, young adults showed performance suggestive of riskier driving behavior, and old adults showed performance suggestive of caution consequent to declining driving ability. In particular, the intra-task quantification revealed that the driving of young adults was more impacted by the presence of distraction (e.g., delayed decelerating), whereas old adults prioritized safe driving (e.g., correctly braking at intersections) over responding to distractions. The study may be used as motivation for future studies of driving safety and accident prevention, and informed assessment of governmental regulations.

Background: While gait analysis is well-documented, turn performance-which is a more complex task and involves multiple brain regions-has been less explored. This study aims to assess the diagnostic potential of turn dynamics as a novel tool for detecting cognitive decline.

Methods: We recruited 75 participants, including 26 neurotypical (NT) older adults, 25 with amnestic mild cognitive impairment (aMCI), and 24 with mild Alzheimer's disease (AD). Participants completed a dual-task walk and turn (DTWT) test using a dual Kinect setup while counting backwards by ones. Key measures analyzed included spatial-temporal parameters of gait and turn dynamics. Statistical analyses including analyses of variance and linear regression were performed to identify key features as well as to assess their correlation with cognitive performance.

Results: Gait speed and stride time significantly differentiated among groups in DTWT conditions. More notably, turn dynamics, particularly segmental peak speeds and step length, displayed stronger discriminatory power with more significant p-values compared to gait features. Linear regression analysis indicated that turn dynamics had stronger correlations with executive function and working memory, suggesting a more pronounced relationship between cognitive performance and turn features than gait variables.

Conclusion: In contrast to straight walk metrics, this study shows that DTWT turn dynamics are more sensitive to detect cognitive impairment. Consequently, incorporating turning movements into gait analysis techniques could enhance diagnostic protocols in clinical settings, offering a valuable tool for monitoring the progression of conditions associated with cognitive aging.

Background: Cognitive impairment is a common dysfunction following stroke, significantly affecting patients' quality of life. Studies suggest that post-stroke cognitive impairment (PSCI) may be related to neural activity in specific brain regions. However, the neural mechanisms remain to be further explored. This study aimed to investigate the alterations in brain function in patients with PSCI.

Methods: This was a case-control study. Thirty patients with PSCI, thirty with non-PSCI (NPSCI), and thirty age- and gender-matched healthy controls (HCs) were selected in a 1:1:1 ratio. Resting-state functional magnetic resonance imaging (rs-fMRI) were acquired from all participants to study the potential neural mechanisms of PSCI patients by comparing the differences in fractional amplitude of low-frequency fluctuation (fALFF), Kendall's coefficient of concordance-regional homogeneity (KCC-ReHo), and seed-based functional connectivity (FC). Additionally, the Montreal Cognitive Assessment (MoCA) scores of PSCI patients were collected, and Pearson correlation was used to analyze the correlation between functional indicators and cognitive performance in PSCI patients.

Results: fALFF analysis revealed that the PSCI group had decreased zfALFF values in the left caudate, right inferior temporal gyrus (ITG), anterior cingulate cortex (ACC), left putamen, and left superior temporal gyrus. In contrast, increased zfALFF values were observed in the right Cerebellum_6. KCC-ReHo analysis indicated that the PSCI group had decreased SzKCC-ReHo values in the right middle frontal gyrus (MFG) and left postcentral lobe, while increased SzKCC-ReHo values in the left cerebellum_ crus 1, and left cerebellum_4-5. Furthermore, seed-based FC analysis revealed decreased zFC values between brain regions in the PSCI group, especially between the angular gyrus and precuneus. Additionally, correlation analysis showed that the zfALFF value of ACC was positively correlated with MoCA scores in the PSCI group.

Conclusion: This study demonstrated significant changes in the spontaneous neural activity intensity, regional homogeneity, and FC of multiple cognition-related brain regions in PSCI patients, shedding light on the underlying neural mechanisms of brain function in PSCI.

This study investigates the relationship between white matter hyperintensities (WMHs) and longitudinal cognitive decline in older adults. Using data from The Irish Longitudinal Study on Ageing (TILDA), we examined WMH characteristics, including volume, location, and microstructural integrity, in a community-dwelling population of 497 individuals over a six-year period. WMHs were categorised into phenotypes based on their size, fractional anisotropy (FA), and mean diffusivity (MD), with subtypes for periventricular and deep white matter lesions. We hypothesised that larger, microstructurally compromised lesions would be associated with accelerated cognitive decline. We isolated 11,933 WMHs, with an average of 24 WMHs per individual. Of these lesions, 6,056 (51%) were classified as Low Volume - High FA, 3193 (27%) were classified as Low Volume - Low FA and 2684 (22%) were classified as High Volume, Low FA. Our findings demonstrate that high-volume, low FA deep (p = 0.05) and periventricular (p = 0.004) lesions were significantly linked to cognitive decline (X = 12.9, p = 0.004), whereas small periventricular lesions with near normal microstructural properties do not predict cognitive decline. These results suggest that distinct WMH phenotypes may serve as markers for differential risks of cognitive impairment, providing potential targets for early intervention in at-risk populations.

Background: Cognitive impairment is a growing public health concern, particularly in aging populations. Obesity, as measured by various indices, has been linked to cognitive decline, but the relationship between Body Roundness Index (BRI) and cognitive impairment remains unclear. This study aims to evaluate the association between BRI and cognitive impairment in a rural, low-income, low-education population in China and to determine if BRI can be used as an independent predictor of cognitive decline.

Methods: This cross-sectional study included the participants aged 35-95 years from rural Tianjin, China. The mean age of the study population was 64.35 ± 7.58 years. Data were collected through face-to-face interviews, physical examinations, and laboratory tests. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), and BRI was calculated and grouped into quartiles. Univariate and multivariate logistic regression analyses were performed to examine the relationship between BRI and cognitive impairment. Subgroup analyses were conducted to explore interactions between BRI, age, gender, and hypertension. The dose-response relationship was analyzed using restricted cubic spline models.

Results: Of the participants, 36.5% had cognitive impairment. Multivariate analysis showed that women, individuals aged 65 and over, and those with hypertension had a higher risk of cognitive impairment. Participants in the second quartile of BRI had a 31% lower risk of cognitive impairment compared to the first quartile (OR: 0.69, 95% CI: 0.51-0.94, p = 0.017). Subgroup analysis revealed that BRI was significantly associated with cognitive impairment in individuals under 65, but not in older participants. The dose-response relationship between BRI and MMSE score showed an inverted U-shaped curve, with the weakest association observed around a BRI of 4.49.

Conclusion: Body Roundness Index, in conjunction with age, gender, and hypertension, can serve as a useful predictor of cognitive impairment, particularly in younger populations. Early identification of individuals at risk through BRI may facilitate timely interventions, reducing the burden of cognitive decline on patients and healthcare systems.