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34 records · Page 2Linked to original sources
PubMed2026

Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.

BACKGROUND: Cerebral small vessel disease (CSVD) is increasingly recognized as a disorder involving microvascular dysfunction, impaired perivascular clearance, and inflammatory processes. However, how systemic inflammatory burden, neurovascular coupling (NVC), glymphatic MRI markers, vascular lesion burden, and cognition are interrelated remains unclear. MATERIALS AND METHODS: In this prospective study, 155 patients with CSVD and 70 healthy controls (HCs) underwent multimodal MRI. NVC was quantified using the cerebral blood flow/fractional amplitude of low-frequency fluctuations ratio. Glymphatic function was assessed via the diffusion tensor image analysis along the perivascular space (ALPS) index, choroid plexus volume (CPV), and perivascular space (PVS) fractions. Structural equation modeling (SEM) was employed to evaluate the direct and indirect effects of inflammatory markers on vascular burden and cognitive performance. RESULTS: Patients with CSVD exhibited significantly diminished NVC (specifically in the right median cingulate and left frontal gyri) and impaired glymphatic function (lower ALPS-index; higher CPV and PVS fractions) compared to HCs. SEM revealed that inflammatory biomarkers exerted both a direct effect on vascular burden and a substantial indirect effect (accounting for 66.3% of the total effect) mediated through two pathways: a single-mediation path via glymphatic function (42.8%) and a serial-mediation path via NVC and glymphatic function (23.5%). Increased vascular burden was significantly associated with poorer cognitive performance. CONCLUSION: Inflammation drives CSVD progression and cognitive decline primarily through the disruption of NVC and glymphatic clearance mechanisms. These findings highlight glymphatic dysfunction as a critical mediator of inflammation-related structural brain damage.

Humans↗
PubMed1979

[Chronic inflammatory neuromyopathies in adults treated for gluten-sensitive enteropathy. A report on three cases with microvascular nerve and muscle lesions (author's transl)].

Neuromyopathies developed in three patients with gluten-sensitive enteropathy, a long time after they had been cured of their digestive disease by following a gluten-free diet. These cases differed radically from typical deficiency neuropathies by the presence of microvascular inflammatory lesions in nerves and muscles. The semiological findings were similar in all 3 cases, and were distinguished by the association of signs eveking lesions of the largest myelinated nerves fibers to the posterior rami with lesions in the muscles. Corticotherapy improved the condition but did not affect its chronic course. Nerve and muscle biopsies revealed the presence of segmentary microrascularitis, mainly lymphohistiocytic. The probable mechanism of these histological changes is alterations in the circulating immune-complexes, usually found in gluten-sensitive enteropathy, producing various types of associated disorders. Some of these immune-complexes would not be related straight to digestive intolerance to gluten, but would persist during the gluten-free diet period, and could be responsible for the micro-angiitis.

Adult↗
PubMed2026

Cochlear Implantation in Sickle Cell Disease: A Systematic Review of Feasibility and Outcomes.

INTRODUCTION: Sickle cell disease (SCD) is associated with systemic complications, including sensorineural hearing loss (SNHL) from microvascular occlusion and chronic inflammation. Although reports link SCD to higher rates of SNHL, current evidence is limited by small sample size, varied audiologic methods, and lack of standardized screening. This systematic review summarizes available literature on SNHL and cochlear implantation (CI) in SCD. METHODS: A literature search of PubMed MEDLINE, Embase, Scopus, Web of Science, and CINAHL identified 79 citations. After removal of duplicates, 35 records were screened in Rayyan. Studies published between January 1, 2000, and June 30, 2025, were eligible if they reported patients with SCD who developed hearing loss and underwent CI. Nine full texts were reviewed, and 4 met the inclusion criteria. Screening and review were performed independently by 2 authors per PRISMA guidelines. RESULTS: Across 4 case reports, a total of 5 patients with SCD underwent CI, ranging in age from 2 to 42 years. Four presented with bilateral severe-to-profound SNHL and one with unilateral loss. Implantation was technically feasible in all cases, including patients with cochlear fibrosis or ossification requiring modified insertion techniques. Postoperative outcomes were favorable: all patients demonstrated reliable device function and low impedances. Only 60% showed meaningful auditory benefit, characterized by improved functional speech perception in 2 patients (40%) and access to the speech frequency range with hearing testing going from moderate/profound hearing loss to mild hearing loss in 3 patients (60%). Complications occurred in 2 patients (40%): one developed unilateral middle ear infection leading to meningitis, and another experienced a postoperative pulmonary embolism requiring anticoagulation. The remaining 3 patients (60%) had uncomplicated recoveries with reported improved hearing from moderate/profound hearing loss to mild hearing loss post implantation. CONCLUSION: While CI appears feasible in SCD, our findings suggest that additional data are needed to assess its effectiveness in this patient population. However, evidence is limited to case reports, and complications such as thromboembolism and rapid cochlear fibrosis highlight the need for close perioperative management. More comprehensive studies with larger sample size are required to define surgical risk, optimize management, and establish best practices for timely implantation in this population.

Humans↗
PubMed2025

Measures of retinal health successfully capture risk for Alzheimer's disease and related dementias at midlife.

BackgroundIdentification of at-risk individuals who would benefit from early intervention for Alzheimer's disease and related dementias (ADRD) is critical as new treatments are developed. Measures of retinal health could offer accessible and low-cost indication of pre-morbid disease risk, but their association with ADRD risk is unknown.ObjectiveTo determine whether midlife retinal neuronal and microvascular measures are associated with ADRD risk-index scores and individual domains of ADRD risk.MethodsData were from the Dunedin Multidisciplinary Health and Development Study, a population-representative longitudinal New Zealand-based birth cohort study. 94.1% (N&#x2009;=&#x2009;938) of living Study members were seen at age 45 (2017-2019). Retinal neuronal (retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GC-IPL)) and microvascular (arterioles and venules) measures were used as predictors. Outcome measures were four top ADRD risk indexes (CAIDE, LIBRA, Lancet, and ADU-ADRI), and a comprehensive midlife ADRD risk index, the DunedinARB.ResultsPoorer retinal microvascular health (narrower arterioles and wider venules) was associated with greater ADRD risk (&#x3b2;s&#x2009;=&#x2009;0.16-0.31; ps&#x2009;<&#x2009;0.001). Thinner RNFL was modestly associated with higher ADRD risk (&#x3b2;s&#x2009;=&#x2009;0.05-0.08; ps&#x2009;=&#x2009;0.02-0.13). Follow-up tests of distinct domains of ADRD risk indicated that while RNFL associations reflected cardiometabolic risk only, microvascular measures were associated with diverse ADRD risk factors.ConclusionsMeasures of retinal health, particularly microvascular measures, successfully capture ADRD risk across several domains of known risk factors, even at the young midlife age of 45 years. Retinal microvascular imaging may be an accessible, scalable, and relatively low-cost method of assessing ADRD risk among middle-aged adults.

Humans↗
PubMed2026

Artificial Intelligence in Predicting Systemic Complications From Retinal Findings: A New Frontier in Precision Medicine.

Innovations in retinal imaging technologies and growing evidence from retinal imaging of systemic and neurodegenerative diseases have begun to explore the utility of retinal imaging in diagnosing these conditions. Since the retina shares embryological origins with the central nervous system and reflects systemic microvascular characteristics, it is well positioned for noninvasive observation of patients' systemic and neural health. Moreover, accessibility of retinal imaging has improved with the increasing number of ophthalmology clinics. Rapid improvements in various deep learning (DL) tools have also catalyzed the automation of retinal imaging analysis. Systems that utilize DL for retinal imaging are being developed to assist with disease recognition, clinical judgment, and prognostic assessment of systemic health. Various imaging modalities are being integrated with existing genomic and clinical data to estimate an individual's predisposition to certain conditions. Contrary to many existing reviews, the objective of this review is to synthesize the most recent clinical and technological evidence on DL-based diagnostic systems for retinal imaging, with a focus on how different network architectures and their combinations have been developed, validated, and applied across systemic disease detection and prediction. Specifically, this review examines the datasets, model validation approaches, and automated diagnostic systems reported in recent literature. It discusses the extent to which these advancements address existing barriers toward real-time diagnostic application across clinical disciplines. Integrating retinal imaging with DL is an innovative and promising approach to precision medicine and health risk reduction.

artificial intelligence↗
PubMed1975

In vivo microscopic observations of the pathogenesis of acute mouse viral hepatitis.

In vivo microscopy of the liver was undertaken to determine the extent of involvement of the hepatic microvascular system in mice infected with viral hepatitis (MHV-3). It was found that the major effects of the disease were produced in localized areas where parenchyma, sinusoids and blood were obliterated. However, immediately peripheral to these lesions blood flow and vessels were unaffected other than by localized hypertrophy of Küpffer cells. While each lesion produced a sinusoidal block to blood flow, portal hypertension did not occur even in the presence of extensive focal and confluent necrosis.

Animals↗
PubMed2025

Integrative oral and gut microbiome profiling highlights microbial correlates of complications in type 1 diabetes: a cross-sectional analysis.

BACKGROUND/OBJECTIVE: Chronic vascular complications are the primary threat in long-standing type 1 diabetes (T1D) patients. We examined the associations between oral-gut microbiome dysbiosis and these complications, offering novel insights into therapeutic strategies and underlying mechanisms. METHODS: This cross-sectional study enrolled 75 T1D participants (disease duration&#x2009;&#x2265;&#x2009;10&#xa0;years) and 43 healthy controls who underwent comprehensive clinical assessment, including blood glucose, lipid profile, and complication-related examinations. Fecal and oral rinse samples were collected for shotgun metagenomic sequencing. T1D participants were stratified by the presence of microvascular (retinopathy, nephropathy, or neuropathy) or macrovascular complications separately. Microbial differences across groups were assessed. RESULTS: Significant differences in oral and gut microbiota compositions were observed between T1D participants with and without complications (both microvascular and macrovascular). A core set of 26 gut and 8 oral microbial species was specifically associated with vascular complications. Butyrate-producing gut bacteria (Blautia wexlerae, Anaerobutyricum hallii, Roseburia inulinivorans, A. soehngenii) and specific oral Neisseria species were enriched in T1D without complications individuals, suggesting protective effects against complications. Mediation analysis indicated associations consistent with partial mediation between certain microbial species and the relationships of glycemic control or insulin resistance (HbA1c, glucose risk index, estimated glucose disposal rate) with complication risk. Moreover, potential oral-gut microbiome interconnections were implicated in complication development. Finally, classification models integrating both oral and gut microbial features significantly outperformed models based on either site alone in distinguishing T1D patients with complications. CONCLUSIONS: Distinct oral and gut microbiome features are associated with chronic vascular complications in T1D. These findings highlight the potential of microbiome-targeted strategies for understanding and preventing T1D-related complications.

Humans↗
PubMed1977

Effects of alveolar hypoxia on lung fluid and protein transport in unanesthetized sheep.

To determine whether hypoxia directly affects pulmonary microvascular filtration of fluid or permeability to plasma proteins, we measured steady state lung lymph flow and protein transport in eight unanesthetized sheep breathing 10% O2 in N2 for 4 hours. We also studied three sheep breathing the same gas mixture for 48 hours. We surgically prepared the sheep to isolate and collect lung lymph and to measure average pulmonary arterial (Ppa) and left atrial (Pla) pressures. We placed a balloon catheter in the left atrium to elevate Pla. After recovery, the sheep breathed air through a tracheostomy for 2-4 hours, followed by 4 or 48 hours of hypoxia. In 13 4-hour studies, the average arterial PO2 fell from 97 to 38 torr; Ppa rose from 20 to 33 cm H2O; and lung lymph flow and lymph protein flow were unchanged. We also found that during 48-hour hypoxia, with a sustained elevation in Ppa and a decline in Pla, lymph flow and protein flow did not increase. In four sheep, we also raised Pla for 4 hours, followed by 4 hours of hypoxia with elevated Pla. Again, despite the added stress of elevated Pla, we found that lymph flow and lymph protein flow remained constant during hypoxia. We conclude that severe alveolar hypoxia, for 4 or 48 hours, alone or with increased pulmonary microvascular pressure, produced no change in lung fluid filtration or protein permeability, a finding supported by normal postmortem histology and extravascular lung water content.

Acute Disease↗
PubMed1978

Thiamine deficiency encephalopathy in a specific-pathogen-free cat colony.

Thiamine deficiency encephalopathy occurred in a specific-pathogen-free cat colony where the diet consisted exclusively of commercially canned diet. This product was described by the manufacturer as a complete diet for cats. The clinical diagnosis was confirmed by the demonstration of bilaterally symmetrical hemorrhage and microvascular fibrinoid necrosis in the brain and low erythrocyte transketolase levels. Treatment of clinically ill cats with vitamin B complex was followed by recovery within 24 hours.

Animals↗
PubMedDate not supplied

[Delayed radionecrosis of the cerebral hemispheres following betatron electron beam irradiation for scalp cancer. Pathological and clinical findings in one case (author's transl)].

Three years following an irradiation by the Betatron's electron beam of an epithelioma in left parieto occipital area of the scalp in a female patient aged 77, early suffering from high blood pressure, a fatal pseudo-tumoral brain necrosis occurs presenting as a rapidly increasing from of Wernicke's aphasia. The necropsy shows intense radionecrosis lesions of the brain and the bone, free of any parenchymatous malignant proliferation note-worthy for the striking density of microvascular changes as previously described in radiation therapy. The case observed some years ago, allows to definite again the limits doses of the extracranial irradiations now estimated at 1760 rets. That is the "Nominal Standard Dose" (NSD) measured by rets and taking into account the number of seances (N) and the duration of irradiation (T) which would be to take the place of "the total dose" (D) (rads). These dosimetric criteria themselves must be adjusted to the age and the vascular features of each patient.

Age Factors↗
PubMed2026

Advanced glycation end products drive blood-brain barrier lipid dysregulation via RAGE-ABCA1 signaling to promote neurovascular dysfunction in Alzheimer's disease.

Neurovascular dysfunction is an early and critical contributor to Alzheimer's disease (AD), yet the molecular mechanisms linking vascular pathology to metabolic dysregulation remain incompletely understood. Advanced glycation end products (AGEs), which accumulate during aging and metabolic stress, have been implicated in AD pathology; however, their role in cerebrovascular lipid homeostasis is unclear. Here, we demonstrate that AGE accumulation within cerebral microvessels promotes lipid droplet (LD) formation in endothelial cells through receptor for AGE (RAGE)-dependent disruption of cholesterol efflux pathways. In aged APP transgenic mice and human AD brains, we observe increased AGE deposition concomitant with elevated RAGE, DGAT1, and perilipin expression, alongside reduced ABCA1 levels. In human brain endothelial cells, AGE exposure induces lipid metabolic reprogramming characterized by enhanced LD accumulation, upregulation of lipogenic machinery, and suppression of cholesterol efflux. Mechanistically, RAGE silencing restores ABCA1 expression and attenuates LD formation, identifying RAGE as a key upstream regulator. Pharmacological activation of ABCA1 reverses AGE-induced lipid accumulation and reduces RAGE expression, highlighting a therapeutic axis. Furthermore, AGE exposure disrupts blood-brain barrier (BBB) integrity and impairs amyloid-&#x3b2; transport in an in vitro BBB model. In vivo, aging is associated with progressive microvascular LD accumulation, linking metabolic dysfunction to vascular pathology. Together, our findings establish an AGE-RAGE-ABCA1 signaling axis that drives endothelial lipid dysregulation and BBB impairment, providing a mechanistic framework connecting metabolic stress to neurovascular dysfunction in AD.

Journal Article↗
PubMed2025

Stage-dependent proteomic alterations in aqueous humor of diabetic retinopathy patients based on data-independent acquisition and parallel reaction monitoring.

BACKGROUND: Diabetic retinopathy (DR), a microvascular complication of diabetes mellitus (DM), represents the predominant cause of preventable vision loss in working-age populations globally. While the pathophysiological mechanisms underlying DR progression remain incompletely understood, our study employs comprehensive proteomic profiling of aqueous humor (AH) to identify stage-specific biomarkers and therapeutic targets in type 2 diabetes mellitus (T2DM) patients across DR progression. METHODS: Utilizing data-independent acquisition (DIA) mass spectrometry, we quantified AH proteomes in a discovery cohort comprising 24 subjects: 18 T2DM patients stratified by DR severity [6 non-DR, 6 non-proliferative DR (NPDR), 6 proliferative DR (PDR)] and 6 cataract controls without diabetes (non-DM). Validation cohort analysis (including 10 AH samples in each group) was performed using parallel reaction monitoring (PRM) strategy for verification of target proteins. Comprehensive bioinformatics analyses included gene set enrichment analysis (GSEA), weighted gene co-expression network analysis (WGCNA), Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis, protein-protein interaction (PPI) network construction, receiver operating characteristic (ROC) curve analysis, and ConnectivityMap (Cmap)-based drug prediction. RESULTS: Proteomic profiling identified 739 quantifiable AH proteins (62% extracellular) with clear separation among the four clinical stages in the discovery cohort. GSEA uncovered altered expression of proteins mainly related to complement and coagulation cascades, folate metabolism, and the selenium micronutrient network in patients with DR. WGCNA-derived protein modules yielded 83 PRM-validated targets, including 5 hub proteins differentiating NPDR from non-DR and 33 hub proteins showed significant upregulation in PDR versus NPDR comparison. Clinical correlation analysis identified F2, FGG, FGB, RBP4, AMBP, VTN, C8A, CPB2, and C2 associated with clinical traits. C6, FAM3C, SPP1, and JCHAIN levels were altered post-anti-VEGF treatment. Pharmacological prediction identified potential therapeutic compounds, including perindopril, triciribine, and XAV-939 for NPDR, and topiramate, triciribine, and vecuronium for PDR. CONCLUSION: This study established a comprehensive AH proteomic signature of DR progression, offering insights into the pathogenesis of DR and highlighting potential biomarkers and novel therapeutic targets.

Humans↗