Explore the vast range of titles available.

There is rising public health concern surrounding dual sensory impairment (DSI), or comorbid hearing and vision impairments. Its global prevalence and the magnitude of its association with cognitive decline (CD) is unclear. Three databases were searched for epidemiological studies examining DSI prevalence or its association with CD. Independent reviewers selected studies, extracted data, and evaluated bias. Random‐effects meta‐analyses were performed. Projections were estimated using United Nations data. The population attributable fraction of DSI‐associated CD was calculated. Among 43 studies with 5,246,796 participants, clinically assessed DSI prevalence was 5.50% (95% confidence interval [CI] = 2.88%–10.26%), with regional/ethnic/age variations. DSI prevalence is projected to increase by 27.2% from 2025 to 2050. Approximately 59.83% (95%CI = 41.03–76.12) of DSI patients had cognitive impairment. Baseline DSI was associated with incident CD (odds ratio [OR] = 1.72, 95%CI = 1.37–2.15). Globally, 3.81% (95%CI = 1.05–10.55) of incident CD may be attributed to DSI. DSI is globally prevalent, growing, and associated with CD, highlighting the need for better health policy and resource allocation. Highlights The global prevalence of DSI is 5.50%, with geographical, ethnical and age variations. The prevalence of DSI rises with age and is projected to increase by 27.2% by 2050. Approximately 60% of individuals with DSI may have measurable cognitive impairment. DSI was associated with a 72% greater longitudinal risk of incident CD. Globally, 3.81% of CD cases may be attributable to DSI.

A wide range of cognitive deficits, including memory loss associated with hippocampal dysfunction, have been widely reported in cancer survivors who received chemotherapy. Changes in both white matter and gray matter volume have been observed following chemotherapy treatment, with reduced volume in the medial temporal lobe thought to be due in part to reductions in hippocampal neurogenesis. Pre-clinical rodent models confirm that common chemotherapeutic agents used to treat various forms of non-CNS cancers reduce rates of hippocampal neurogenesis and impair performance on hippocampally-mediated learning and memory tasks. We review the pre-clinical rodent literature to identify how various chemotherapeutic drugs affect hippocampal neurogenesis and induce cognitive impairment. We also review factors such as physical exercise and environmental stimulation that may protect against chemotherapy-induced neurogenic suppression and hippocampal neurotoxicity. Finally, we review pharmacological interventions that target the hippocampus and are designed to prevent or reduce the cognitive and neurotoxic side effects of chemotherapy.

Chemotherapy‐induced cognitive impairment (“chemobrain”) is a frequent side‐effect in cancer survivors treated with paclitaxel (PTX). The mechanisms responsible for PTX‐induced cognitive impairment remain obscure, and there are no effective treatments or prevention strategies. Here, we test the hypothesis that PTX induces endothelial senescence, which impairs microvascular function and contributes to the genesis of cognitive decline. We treated transgenic p16‐3MR mice, which allows the detection and selective elimination of senescent cells, with PTX (5 mg/kg/day, 2 cycles; 5 days/cycle). PTX‐treated and control mice were tested for spatial memory performance, neurovascular coupling (NVC) responses (whisker‐stimulation‐induced increases in cerebral blood flow), microvascular density, blood–brain barrier (BBB) permeability and the presence of senescent endothelial cells (by flow cytometry and single‐cell transcriptomics) at 6 months post‐treatment. PTX induced senescence in endothelial cells, which associated with microvascular rarefaction, NVC dysfunction, BBB disruption, neuroinflammation, and impaired performance on cognitive tasks. To establish a causal relationship between PTX‐induced senescence and impaired microvascular functions, senescent cells were depleted from PTX‐treated animals (at 3 months post‐treatment) by genetic (ganciclovir) or pharmacological (treatment with the senolytic drug ABT263/Navitoclax) means. In PTX treated mice, both treatments effectively eliminated senescent endothelial cells, rescued endothelium‐mediated NVC responses and BBB integrity, increased capillarization and improved cognitive performance. Our findings suggest that senolytic treatments can be a promising strategy for preventing chemotherapy‐induced cognitive impairment. Graphical representation depicting the proposed mechanism of chemotherapy‐induced cognitive impairment. PTX treatment induces endothelial senescence, which impairs microvascular function and contributes to cognitive decline. PTX‐treated mice exhibit microvascular rarefaction, neuroinflammation, and impaired cognitive performance. Senescent cells are eliminated from PTX‐treated animals using genetic or pharmacological means, which results in the restoration of endothelium‐mediated neurovascular coupling responses and blood‐brain barrier (BBB) integrity, increased capillarization, and improved cognitive performance.

Background Sensory impairments significantly contribute to functional decline in aging populations, yet their relationship with the newly defined cardiovascular-kidney-metabolic (CKM) syndrome remains poorly understood. This study examined the longitudinal associations between CKM syndrome stages and incident sensory impairments among middle-aged and older Chinese adults. Methods Data were derived from 12,815 participants (aged ≥ 45 years) in the China Health and Retirement Longitudinal Study (2011–2018), with a median follow-up of 6.5 years. CKM stages (0–4) were defined according to the 2023 American Heart Association framework. Incident hearing impairment (HI), vision impairment (VI), and dual sensory impairment (DSI) were assessed using validated self-reports. To address confounding, weighted marginal structural models (MSM) were employed using inverse probability of treatment weighting (IPTW). Sensitivity was further evaluated using E-value calculations and alternative reference groups. Results After IPTW adjustment, advanced CKM syndrome (Stage 4) was significantly associated with increased odds of incident HI (OR = 1.36, 95% CI: 1.05–1.74) and DSI (OR = 1.50, 95% CI: 1.04–2.15) compared with Stage 0 (optimal health). Although the association for VI was not statistically significant (OR = 1.29, 95% CI: 0.93–1.77), significant dose-response trends were observed across the CKM continuum for HI, VI (both P trend = 0.005), and DSI ( P trend < 0.001). Subgroup analyses revealed more pronounced associations among older adults, rural residents, and those with lower educational attainment. Sensitivity analyses and moderately high E-values supported the robustness of these findings against potential residual confounding. Conclusions Advanced CKM syndrome is longitudinally associated with higher odds of sensory impairments, particularly DSI, in a graded manner. These findings suggest that incorporating sensory health into CKM management frameworks may be crucial for mitigating the burden of functional decline in aging populations.

Chemotherapy-induced cognitive impairment (CICI) is a common detrimental effect of cancer treatment, occurring in up to 75% of cancer patients. The widely utilized chemotherapeutic agent doxorubicin (DOX) has been implicated in cognitive decline, mostly via cytokine-induced neuroinflammatory and oxidative and mitochondrial damage to brain tissues. C-phycocyanin (CP) has previously been shown to have potent anti-inflammatory, antioxidant, and mitochondrial protective properties. Therefore, this present study was aimed to investigate the neuroprotective effects of CP against DOX-elicited cognitive impairment and explore the underlying mechanisms. CP treatment (50 mg/kg) significantly improved behavioral deficits in DOX-treated mice. Furthermore, CP suppressed DOX-induced neuroinflammation and oxidative stress, mitigated mitochondrial abnormalities, rescued dendritic spine loss, and increased synaptic density in the hippocampus of DOX-treated mice. Our results suggested that CP improves established DOX-induced cognitive deficits, which could be explained at least partly by inhibition of neuroinflammatory and oxidant stress and attenuation of mitochondrial and synaptic dysfunction.

The glymphatic system maintains brain homeostasis through cerebrospinal fluid transport and waste clearance. Its potential involvement in chemotherapy‐related cognitive impairment remains largely unexplored due to limited in vivo evidence. In this prospective longitudinal study, 126 female breast cancer patients underwent multiparametric brain MRI and neuropsychological assessments at three time points: baseline (bc1), after the first cycle of neoadjuvant chemotherapy (bc2), and upon completion of neoadjuvant chemotherapy (bc3). Glymphatic function was assessed using four MRI‐derived metrics: choroid plexus (CP) volume, perivascular space (PVS) volume fraction, free water (FW), and Diffusion Tensor Imaging–Along the Perivascular Space (DTI‐ALPS) index. Brain tissue segmentation was conducted to quantify the volume fractions of gray matter (GM) in cortex and subcortex, white matter (WM), and cerebrospinal fluid (CSF) relative to intracranial volume. Neuropsychological assessments included the Self‐Rating Anxiety Scale (SAS), the Functional Assessment of Cancer Therapy–Cognitive Function (FACT‐Cog), and a battery of objective cognitive tests. Longitudinal changes and interrelationships were analyzed using linear mixed‐effects models, correlation analyses, and cross‐lagged panel analysis. During chemotherapy, CP volume increased (p < 0.001), while PVS volume fraction decreased (p = 0.003); no significant changes were found in FW or DTI‐ALPS. GM volumes in both cortex and subcortex declined (both p = 0.02). SAS scores increased (p = 0.02), and FACT‐Cog scores decreased (p < 0.001), with no significant changes in objective test scores. From bc2 to bc3, increases in CP volume were negatively correlated with reductions in PVS volume fraction (r = −0.40, p < 0.001). From bc1 to bc3, reductions in PVS volume fraction were associated with decreases in both cortical GM volumes (r = 0.32, p < 0.001). At bc2, cortical GM atrophy was correlated with increased SAS scores (r = −0.30, p = 0.002). Cross‐lagged panel analysis showed that CP enlargement at bc2 preceded PVS volume fraction reduction at bc3 (β = −1.66, p = 0.007). During neoadjuvant chemotherapy, breast cancer patients exhibited a unique pattern of glymphatic system alterations, suggesting its potential as an imaging marker of treatment‐related brain changes. Using longitudinal multiparametric glymphatic MRI metrics, we found early choroid plexus enlargement and subsequent perivascular space narrowing in breast cancer patients undergoing neoadjuvant chemotherapy. These changes were associated with brain atrophy, suggesting a sequential disruption of glymphatic pathways that may contribute to chemotherapy‐related brain changes.

Background: Cerebral visual impairment (CVI) is a common sequala of early brain injury, damage, or malformation and is one of the leading individual causes of visual dysfunction in pediatric populations worldwide. Although patients with CVI are heterogeneous both in terms of underlying etiology and visual behavioural manifestations, there may be underlying similarities in terms of which white matter pathways are potentially altered. This exploratory study used diffusion tractography to examine potential differences in volume, quantitative anisotropy (QA), as well as mean, axial, and radial diffusivities (mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD), respectively) focusing on the dorsal and ventral visual stream pathways in a cohort of young adults with CVI compared to typically sighted and developing controls. Methods: High angular resolution diffusion imaging (HARDI) data were acquired in a sample of 10 individuals with a diagnosis of CVI (mean age = 17.3 years, 2.97 standard deviation (SD), range 14–22 years) and 17 controls (mean age = 19.82 years, 3.34 SD, range 15–25 years). The inferior longitudinal fasciculus (ILF), inferior fronto-occipital fasciculus (IFOF), vertical occipital fasciculus (VOF), and the three divisions of the superior longitudinal fasciculus (SLF I, II, and III) were virtually reconstructed and average tract volume (adjusted for intracranial volume), MD, AD, and RD were compared between CVI and control groups. As a secondary analysis, an analysis of variance (ANOVA) was carried out to investigate potential differences based on etiology (i.e., CVI due to periventricular leukomalacia (CVI-PVL) and CVI due to other causes (CVI-nonPVL)). Results: We observed a large degree of variation within the CVI group, which minimized the overall group differences in tractography outcomes when examining the CVI sample as a unitary group. In our secondary analysis, we observed significant reductions in tract volume in the CVI-PVL group compared to both controls and individuals with CVI due to other causes. We also observed widespread significant increases in QA, MD, and AD in CVI-PVL compared to the control group, with mixed effects in the CVI-nonPVL group. Conclusions: These data provide preliminary evidence for aberrant development of key white matter fasciculi implicated in visual perceptual processing skills, which are often impaired to varying degrees in individuals with CVI. The results also indicate that the severity and extent of the white matter changes may be due in part to the underlying cause of the cerebral visual impairments. Additional analyses will need to be done in a larger sample alongside behavioural testing to fully appreciate the relationships between white matter integrity, visual dysfunction, and associated causes in individuals with CVI.

Objectives To investigate glymphatic function in Alzheimer’s disease (AD) using the diffusion tensor image analysis along the perivascular space (DTI-ALPS) method and to explore the associations between DTI-ALPS index and perivascular space (PVS) volume, as well as between DTI-ALPS index and cognitive function. Methods Thirty patients with PET-CT-confirmed AD (15 AD dementia; 15 mild cognitive impairment due to AD) and 26 age- and sex-matched cognitively normal controls (NCs) were included in this study. All participants underwent neurological MRI and cognitive assessments. Bilateral DTI-ALPS indices were calculated. PVS volume fractions were quantitatively measured at three locations: basal ganglia (BG), centrum semiovale, and lateral ventricle body level. DTI-ALPS index and PVS volume fractions were compared among three groups; correlations among the DTI-ALPS index, PVS volume fraction, and cognitive scales were analyzed. Results Patients with AD dementia showed a significantly lower DTI-ALPS index in the whole brain ( p  = 0.009) and in the left hemisphere ( p  = 0.012) compared with NCs. The BG-PVS volume fraction in patients with AD was significantly larger than the fraction in NCs ( p  = 0.045); it was also negatively correlated with the DTI-ALPS index ( r  =  − 0.433, p  = 0.021). Lower DTI-ALPS index was correlated with worse performance in the Boston Naming Test ( β  = 0.515, p  = 0.008), Trail Making Test A ( β  =  − 0.391, p  = 0.048), and Digit Span Test ( β  = 0.408, p  = 0.038). Conclusions The lower DTI-ALPS index was found in patients with AD dementia, which may suggest impaired glymphatic system function. DTI-ALPS index was correlated with BG-PVS enlargement and worse cognitive performance in certain cognitive domains. Clinical relevance statement Diffusion tensor image analysis along the perivascular space index may be applied as a useful indicator to evaluate the glymphatic system function. The impaired glymphatic system in patients with Alzheimer’s disease (AD) dementia may provide a new perspective for understanding the pathophysiology of AD. Key Points • Patients with Alzheimer’s disease dementia displayed a lower diffusion tensor image analysis along the perivascular space (DTI-ALPS) index, possibly indicating glymphatic impairment. • A lower DTI-ALPS index was associated with the enlargement of perivascular space and cognitive impairment. • DTI-ALPS index could be a promising biomarker of the glymphatic system in Alzheimer’s disease dementia.

Mild behavioral impairment (MBI) describes later life acquired, sustained neuropsychiatric symptoms (NPS) in cognitively normal individuals or those with mild cognitive impairment (MCI), as an at-risk state for incident cognitive decline and dementia. We developed an operational definition of MBI and tested whether the presence of MBI was related to caregiver burden in patients with subjective cognitive decline (SCD) or MCI assessed at a memory clinic. MBI was assessed in 282 consecutive memory clinic patients with SCD (n = 119) or MCI (n = 163) in accordance with the International Society to Advance Alzheimer's Research and Treatment – Alzheimer's Association (ISTAART–AA) research diagnostic criteria. We operationalized a definition of MBI using the Neuropsychiatric Inventory Questionnaire (NPI-Q). Caregiver burden was assessed using the Zarit caregiver burden scale. Generalized linear regression was used to model the effect of MBI domains on caregiver burden. While MBI was more prevalent in MCI (85.3%) than in SCD (76.5%), this difference was not statistically significant (p = 0.06). Prevalence estimates across MBI domains were affective dysregulation (77.8%); impulse control (64.4%); decreased motivation (51.7%); social inappropriateness (27.8%); and abnormal perception or thought content (8.7%). Affective dysregulation (p = 0.03) and decreased motivation (p=0.01) were more prevalent in MCI than SCD patients. Caregiver burden was 3.35 times higher when MBI was present after controlling for age, education, sex, and MCI (p < 0.0001). MBI was common in memory clinic patients without dementia and was associated with greater caregiver burden. These data show that MBI is a common and clinically relevant syndrome.

Objectives: (1) To characterise neurodevelopmental outcome of neonates with necrotizing enterocolitis (NEC); (2) to define whether NEC increases risk of neurodevelopmental impairment in very low birth weight neonates; (3) to investigate whether stage of disease or need for surgery increase risk of poor outcome. Design: A systematic review was performed. Searches identified 182 relevant papers. Ten studies compared extremely low birthweight neonates with NEC to infants of similar age and gestation who did not develop NEC. Data are reported as OR (95% CIs, p values for test for overall effect) and compared by χ2. Results: 7843 children (821 with NEC) were included in the meta-analysis. Median follow-up was 20 months (range 12 to 156). Overall, 45% of children who had neonatal NEC were neurodevelopmentally impaired. Infants with NEC were significantly more likely than infants of similar age and gestation who did not develop NEC to be neurodevelopmentally impaired (1.6 (1.3 to 2.0), p = 0.0001) including a higher risk of cerebral palsy (1.5 (1.2 to 2.0), p = 0.001), visual (2.3 (1.0 to 5.1), p = 0.04), cognitive (1.7 (1.4 to 2.2), p<0.0001) and psychomotor impairment (1.7 (1.3 to 2.2), p<0.0001). The odds ratio of neurodevelopmental impairment was also 2.3 times higher in neonates with Bell’s stage III disease or requiring surgery ((1.5 to 3.6), p = 0.0001). Conclusions: NEC is associated with significantly worse neurodevelopmental outcome than prematurity alone. Presence of advanced NEC and need for surgery increase the risk of neurological impairment.