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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.

INTRODUCTION Identifying individuals at risk of developing dementia is crucial for early intervention. Mild cognitive impairment (MCI) and subjective memory complaints (SMCs) are considered its preceding stages. This study aimed to assess the utility of functional near‐infrared spectroscopy (fNIRS) in identifying individuals with MCI and SMC. METHODS One hundred fifty‐one participants were categorized into normal cognition (NC); amnestic MCI (aMCI); non‐amnestic MCI (naMCI); and mild, moderate, and severe SMC groups. Task‐related prefrontal hemodynamics were measured using fNIRS during a visual memory span task. RESULTS Results showed significantly lower oxyhemoglobin (HbO) levels in aMCI, but not in naMCI, compared to the NC. In addition, severe SMC had lower HbO levels than the NC, mild, and moderate SMC. Receiver operating characteristic analysis demonstrated 69.23% and 69.70% accuracy in differentiating aMCI and severe SMC from NC, respectively. DISCUSSION FNIRS may serve as a potential non‐invasive biomarker for early detection of dementia. Highlights Only amnestic mild cognitive impairment (aMCI), but not non‐amnestic MCI, showed lower oxyhemoglobin (HbO) than normal individuals. Reduced HbO was observed in those with severe subjective memory complaints (SMCs) compared to normal cognition (NC), mild, and moderate SMCs. Functional near‐infrared spectroscopy measures were associated with performance in memory assessments. Prefrontal hemodynamics could distinguish aMCI and severe SMC from NC.

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.

Chemotherapy-induced cognitive impairment (CICI), often referred to as “chemobrain,” is a common and sometimes persistent consequence of cancer treatment, characterized by deficits in memory, attention, executive function, and processing speed; it disproportionately affects older adults and women, suggesting a role for aging- and sex-related biological factors, including estrogen depletion. This work examines the potential of dietary phenolic compounds as multi-target modulators of mechanisms underlying CICI. A narrative synthesis of preclinical and clinical evidence was conducted, focusing on major phenolic subclasses (flavonoids, phenolic acids, stilbenes, lignans, and secoiridoids) and their effects on pathways implicated in chemotherapy-related neurotoxicity. The reviewed data indicate that phenolic compounds can influence redox balance, neuroinflammatory responses, mitochondrial function, synaptic plasticity, and estrogen-related signaling, with effects that appear to be structure-dependent; however, evidence remains heterogeneous and largely derived from experimental models rather than studies in humans. Overall, the current findings suggest that selected phenolic compounds could mitigate vulnerability to CICI, particularly in higher risk groups such as older individuals and women with low estrogen levels. These compounds represent promising and safe adjunctive strategies, although further well-designed clinical studies are needed to confirm their efficacy and clarify the underlying mechanisms.

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.

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.

IntroductionBreast cancer is the most common form of cancer in women. A considerable number of women with breast cancer who have been treated with chemotherapy subsequently develop neurological symptoms such as concentration and memory difficulties (also known as ‘chemobrain’). Currently, there are no validated therapeutic approaches available to treat these symptoms. Cognitive training holds the potential to counteract cognitive impairment. Combining cognitive training with concurrent transcranial direct current stimulation (tDCS) could enhance and maintain the effects of this training, potentially providing a new approach to treat post-chemotherapy subjective cognitive impairment (PCSCI). With this study, we aim to investigate the effects of multi-session tDCS over the left dorsolateral prefrontal cortex in combination with cognitive training on cognition and quality of life in women with PCSCI.Methods and analysisThe Neuromod-PCSCI trial is a monocentric, randomised, double-blind, placebo-controlled study. Fifty-two women with PCSCI after breast cancer therapy will receive a 3-week tDCS-assisted cognitive training with anodal tDCS over the left dorsolateral prefrontal cortex (target intervention), compared with cognitive training plus sham tDCS (control intervention). Cognitive training will consist of a letter updating task. Primary outcome will be the performance in an untrained task (n-back task) after training. In addition, feasibility, safety and tolerability, as well as quality of life and performance in additional untrained tasks will be investigated. A follow-up visit will be performed 1 month after intervention to assess possible long-term effects. In an exploratory approach, structural and functional MRI will be acquired before the intervention and at post-intervention to identify possible neural predictors for successful intervention.Ethics and disseminationEthical approval was granted by the ethics committee of the University Medicine Greifswald (BB236/20). Results will be available through publications in peer-reviewed journals and presentations at national and international conferences.Trial registration numberClinicalTrials.gov; NCT04817566, registered on 26 March 2021.