The stakes are considerable. Cerebrovascular diseases remain a leading cause of death and loss of healthy life in China, with a reported crude mortality rate of 149.6 per 100,000 individuals. Beyond the physical damage, cognitive impairment has emerged as a pervasive complication spanning a spectrum from mild deficits to dementia. Prevalence rates reported across CVD subtypes are striking: roughly 66 percent in stroke and about 54.6 percent in moyamoya disease. Evidence even suggests that among people adhering to optimal lifestyle behaviors, the presence of cognitive impairment significantly elevates the risk of all-cause and cerebrovascular mortality. Yet how impairment manifests across multiple cognitive domains in individual patients has remained poorly understood, often resulting in generalized care plans that fail to meet specific rehabilitation needs.

Traditionally, clinical and nursing research has followed a variable-centered path, relying on global screening instruments such as the Mini-Mental State Examination (MMSE) or the Montreal Cognitive Assessment (MoCA) to categorize patients via dichotomous cut-off scores. While effective for identifying universal risk factors like age, comorbidities, or lesion sites, this approach assumes population homogeneity. It cannot simultaneously analyze individual performance across multiple cognitive domains such as memory, orientation, and language ability. LPA offers a sophisticated alternative by identifying latent subgroups within a population based on response patterns across multiple continuous indicators. Recent studies applying LPA to older adults, stroke survivors, and people with cardiometabolic diseases have consistently identified three cognition profiles: a high-performing group, a severely impaired group, and an intermediate group characterized by domain-specific deficits whose distinguishing features varied across disease populations.

The new study recruited 474 patients from the neurosurgery department of a tertiary referral hospital in southwestern China between November 2023 and September 2025, using convenience sampling and reporting according to the STROBE checklist. Participants were aged 18 or older, diagnosed with CVDs via ICD-10 codes (I60-I68) and confirmed by cranial CT or MRI. Patients with pre-existing dementia attributable to other conditions, severe auditory impairment, psychiatric illness, communication disorders, acute critical medical conditions, or concurrent enrollment in other trials were excluded. The cohort had a median age of 52 years, a near-equal gender split, and was clinically dominated by intracerebral hemorrhage (52.3 percent), moyamoya disease (18.8 percent), and intracranial aneurysms (15.0 percent), with ischemic stroke accounting for only 4.6 percent. The majority underwent surgery (79.7 percent) and received intensive supportive management including analgesia, sedation, and mechanical ventilation.

The methodological core of the study lay in how it prepared the cognitive data. The Chinese version of the MMSE, a 30-item instrument assessing five dimensions of orientation, memory, attention and calculation, recall, and language ability, was administered to all participants. The cohort’s mean total MMSE score was 22.92, indicating overall mild cognitive impairment, with the most significant deficits observed in recall (mean 1.66 out of 3) and orientation (mean 7.72 out of 10), while memory registration and language ability were relatively better preserved. Crucially, the five MMSE domain scores were separately adjusted for age, gender, and years of education using ordinary least-squares linear regression, producing demographically adjusted residual z-scores. These adjusted z-scores, rather than raw scores, served as the continuous indicators in the LPA, ensuring that profiles reflected genuine cognitive differences rather than demographic artifacts.

The analysis, conducted in R using the tidyLPA package, estimated one- through five-profile solutions. Fit statistics told a nuanced story: AIC, BIC, and adjusted BIC decreased as profiles were added, and the Lo-Mendell-Rubin and bootstrapped likelihood ratio tests were significant for the two- through five-profile solutions, meaning the four- and five-profile models showed better statistical fit than the three-profile model. However, the three-profile model showed greater classification certainty, with an entropy of 0.955 compared with 0.859 and 0.815 for the four- and five-profile models. The team retained the three-profile solution as a pragmatic choice based on parsimony and clinical interpretability, and examined local-solution sensitivity using 1,000 randomized hierarchical initializations for each model.

The retained model classified participants into a mild impairment group (82.5 percent, n=391), which performed relatively well across all five cognitive domains; a moderate impairment group (11.4 percent, n=54), which showed lower performance across all domains with the greatest deficits in orientation and attention/calculation while memory was relatively preserved; and a severe impairment group (6.1 percent, n=29), characterized by pervasive deficits across all domains. The three profiles reflected increasing severity of global cognitive impairment. Univariate analyses revealed significant inter-profile differences in gender, educational background, alcohol consumption, disease subtypes, follow-up interval, nutritional risk (NRS-2002), NIHSS score, and length of hospital stay. The severe group had a median MMSE score of just 3, compared with 15 in the moderate group and 27 in the mild group.

Multinomial logistic regression, using the mild impairment group as the reference category, identified two factors independently associated with profile membership. Higher NIHSS scores were associated with higher odds of membership in the moderate impairment profile (OR=1.222, 95 percent CI=1.126-1.326, p<0.001) and in the severe impairment profile (OR=1.397, 95 percent CI=1.254-1.557, p<0.001). Male gender was associated with lower odds of membership in the severe impairment profile (OR=0.218, 95 percent CI=0.067-0.704, p=0.011). The NIHSS association aligns with the scale’s established prognostic utility: a higher score typically correlates with a larger infarct or hematoma volume and a lesion in a more critical location, such as the dominant hemisphere or key cognitive networks, depleting the brain’s cognitive reserve. Population-based evidence from the Oxford Vascular Study suggests severe stroke can bring forward dementia by about 25 years.

The gender finding is more exploratory but mechanistically intriguing. The authors note that females typically demonstrate higher baseline cerebral blood flow than males, potentially rendering them more sensitive to hemodynamic fluctuations following cerebrovascular events. While sex hormones confer neuroprotection in younger physiology, preclinical evidence suggests these effects may become ineffective or even deleterious with advancing age, and 64 percent of the female participants in this study were aged over 50. Sociodemographic factors may also play a role, as women in the cohort had significantly lower educational attainment than men. The authors caution that further studies are needed to assess the biological or social mechanisms underlying this association.

Important limitations temper the conclusions. The cohort’s predominance of hemorrhagic and neurosurgical cases, with ischemic stroke accounting for only 4.6 percent, introduces selection bias that may limit generalizability to broader CVD populations. The cross-sectional design precludes causal inference and cannot characterize individual cognitive trajectories over time. The severe impairment subgroup was small, with an events-per-parameter ratio of 2.4, limiting statistical precision and producing wide confidence intervals. The MMSE itself is a brief screening tool with limited coverage of executive function, processing speed, visuospatial ability, and episodic memory, and demographic adjustment cannot recover information lost to these measurement limitations. The authors call for multicenter, longitudinal studies with larger, more diverse samples to validate the profiles and assess their prognostic utility. Still, the emergence of distinct profiles underscores the multidimensional nature of cognitive impairment captured by the MMSE, challenging the notion of a unitary trajectory of decline and pointing toward targeted nursing assessment and intervention for specific patient subgroups.

Subject of Research: Neurology

Article Title: Cognitive impairment profiles in patients with cerebrovascular diseases: a latent profile analysis

Article References: Yin, Y., Ma, H., Zou, R., Fan, C., Zhu, W., & Zheng, J. (2026). Cognitive impairment profiles in patients with cerebrovascular diseases: a latent profile analysis. Frontiers in Neurology, 17, Article 1840409. https://doi.org/10.3389/fneur.2026.1840409

Image Credits: AI Generated

DOI: 10.3389/fneur.2026.1840409

Keywords: cognitive impairment, cerebrovascular disease, latent profile analysis, stroke, NIHSS, MMSE, neurology, vascular cognitive impairment, Cognitive, impairment, profiles, patients

The research team, led by investigators at Nantong First People’s Hospital and Southeast University in China, enrolled 245 consecutive patients admitted with acute ischemic stroke between June 2023 and December 2024. Of these, 65 were diagnosed with PSD within the first month after their stroke, using the 24-item Hamilton Depression Rating Scale and DSM-5 diagnostic criteria. The study focused on two key metabolic markers: the atherogenic index of plasma (AIP), which reflects lipid metabolism and atherosclerotic risk, and the triglyceride-glucose (TyG) index, a reliable surrogate for insulin resistance. Functional status was assessed using the Barthel Index, a widely adopted tool that measures activities of daily living such as eating, dressing, and walking.

Compared with non-PSD patients, those with PSD showed significantly lower Barthel Index scores and higher TyG and AIP levels. Restricted cubic spline (RCS) analysis indicated a nonlinear relationship between AIP and PSD risk, with the odds ratio increasing more markedly at higher AIP values. The researchers identified an approximate turning point at an AIP value of 0.26, beyond which the risk of depression showed a clear upward trend. This finding suggests that AIP may trigger inflammatory or endocrine cascades only beyond a certain threshold, a pattern that linear models can undershoot.

Multivariate logistic regression identified the Barthel Index (OR = 0.97, 95% CI: 0.95–0.99) and the TyG Index (OR = 2.04, 95% CI: 1.19–3.47) as independent predictors of PSD. These results confirm that both functional impairment and metabolic dysregulation carry distinct associations with post-stroke depression. The Barthel Index reflects not only reduced self-care ability but also the psychological burden and reduced confidence in recovery that accompany physical dependence. Insulin resistance, indexed by TyG, is tightly linked to inflammation and oxidative stress and may provoke depressive symptoms by disrupting neurotransmitter metabolism and neuroplasticity.

The most innovative aspect of the study was the application of partial least squares (PLS) regression combined with K-means clustering to categorize stroke patients based on integrated functional and metabolic indicators, including the Barthel Index, body mass index (BMI), AIP, and TyG Index. This approach revealed four distinct functional–metabolic subtypes: a physiological protection subtype (preserved function with optimal metabolic indices), a subclinical burden subtype (largely intact function with mild metabolic abnormalities), a metabolic susceptibility subtype (acceptable function but markedly elevated TyG and AIP), and a dual-impaired subtype (pronounced functional impairment accompanied by metabolic abnormalities).

Patients in the metabolic susceptibility subtype and the dual-impaired subtype had significantly higher risks of PSD compared to the reference group. The metabolic susceptibility subtype showed an odds ratio of 2.13 (95% CI: 1.02–4.46), while the dual-impaired subtype showed an odds ratio of 2.63 (95% CI: 1.16–5.96). Notably, the dual-impaired subtype exhibited the highest incidence of PSD at 46%, suggesting that the combined effects of significant functional impairment and metabolic dysregulation create a particularly vulnerable psychological state.

The metabolic susceptibility subtype demonstrated unique risk features. Despite exhibiting relatively preserved functional status, this subtype showed a markedly elevated metabolic burden alongside a PSD incidence of 32.08%. These findings suggest that even in the absence of overt functional impairments, underlying inflammatory and oxidative stress may increase vulnerability to post-stroke depression. Previous research has reported strong associations between TyG and increased white blood cell counts or high-sensitivity C-reactive protein levels, suggesting a potential inflammatory pathway linking metabolic dysregulation to PSD risk.

Inflammatory mechanisms are central to ischemic brain injury, and an imbalance between pro- and anti-inflammatory mediators can worsen neurological outcomes. Such dysregulation has been implicated in both PSD and primary major depressive disorder, suggesting potentially shared biological pathways. Recent animal studies further support this pathological pathway: following stroke, alleviating hippocampal inflammation promotes neuronal repair and significantly improves depressive-like symptoms in post-stroke mouse models. Metabolic dysregulation further amplifies this cascade by provoking oxidative stress, compromising blood–brain barrier integrity, and exacerbating neuro-inflammation.

The dual-impaired subtype was characterized by severe dysfunction and pronounced metabolic abnormalities. Patients in this group may be particularly susceptible to psychological distress due to the combined effects of significant functional impairment—which fosters dependency and social isolation—and metabolic dysregulation such as insulin resistance and dyslipidemia. These coexisting conditions can jointly disrupt emotional regulation, resulting in heightened psychophysiological vulnerability. Previous research has demonstrated that impairments in activities of daily living not only reflect substantial neurological damage but also indicate the need for considerable assistance with basic life tasks, often leading to negative emotional states including feelings of helplessness and social withdrawal.

This study is the first to apply PLS-K-means clustering to categorize stroke patients based on integrated functional and metabolic indicators, revealing substantial heterogeneity across patients. The findings underscore the importance of simultaneously assessing functional status and metabolic phenotype in the early stages following stroke. Incorporating both functional and metabolic assessments into early screening strategies may support the development of more targeted psychological interventions tailored to specific patient phenotypes, thereby reducing PSD incidence and improving long-term outcomes. However, the researchers acknowledge several limitations, including the cross-sectional nature of the study, the relatively limited sample size, and the single assessment window within the first month after stroke, which precludes inference of causal relationships and may not capture the temporal evolution of depressive symptoms.

Subject of Research: Combined effect of functional impairment and metabolic dysregulation on post-stroke depression risk

Article Title: Combined effect of functional impairment and metabolic dysregulation on post-stroke depression risk

Article References: Zhang, T., Shi, W., Chi, Q., Qian, J., Wang, T., Zhu, L., Ding, W., & Chen, Z. (2026). Combined effect of functional impairment and metabolic dysregulation on post-stroke depression risk. Frontiers in Psychiatry, 17, Article 1843802. https://doi.org/10.3389/fpsyt.2026.1843802

Image Credits: AI Generated

DOI: 10.3389/fpsyt.2026.1843802

Keywords: Combined, effect, functional, impairment, metabolic, dysregulation, post-stroke, depression, risk, scientific research

The clinical picture of DACI most often resembles vascular cognitive impairment, with executive function and processing speed taking the earliest hits, although memory deficits are also common. Diabetes raises the risk of vascular dementia by about 58 percent and Alzheimer’s disease by about 30 percent, and even prediabetes has been linked to elevated dementia risk. Notably, cognitive deficits and brain atrophy can be detected in young and middle-aged adults with diabetes long before any dementia diagnosis would be made. Each 1 percent increase in HbA1c is associated with an 8 percent higher risk of developing dementia, yet intensive glucose-lowering strategies targeting HbA1c below 6 or 6.5 percent have not conferred significant cognitive benefit compared with standard approaches, suggesting that hyperglycemia alone does not fully explain the brain changes.

On brain imaging, the most consistent findings are cerebral atrophy, cerebral small vessel disease, and glucose hypometabolism. Diabetes increases the burden of silent brain infarcts and white matter hyperintensities, and the severity of small vessel disease is an important predictor of future cognitive decline. Diffusion tensor imaging reveals lower fractional anisotropy and higher mean diffusivity in diabetic patients with mild cognitive impairment compared with diabetic patients whose cognition remains normal. Resting-state functional MRI studies show reduced connectivity within the default mode network, a pattern also observed in aging and dementia, while fluorodeoxyglucose PET demonstrates cerebral glucose hypometabolism whose regional distribution varies considerably across studies.

Mechanistically, the review frames DACI as a neurovascular-metabolic disorder. Vascular injury begins with endothelial dysfunction: endothelial cells rely on insulin-independent GLUT1 and GLUT3 glucose transport, which can expose them to excess intracellular glucose during hyperglycemic episodes. Hyperglycemia then induces oxidative stress through mitochondrial dysfunction, activates chronic inflammatory pathways including nuclear factor-κB, reduces nitric oxide bioavailability, and promotes endothelial-to-mesenchymal transition via TGF-β signaling. Persistent endothelial damage accelerates atherosclerosis through advanced glycation end products and inflammatory mediators that upregulate adhesion molecules, promoting monocyte and macrophage infiltration into the subendothelial space, while glycation of LDL particles increases their atherogenicity. The risk of ischemic stroke is more than twofold higher in individuals with diabetes even after adjusting for smoking, BMI, systolic blood pressure, and dyslipidemia.

Neurovascular coupling, the dynamic adjustment of cerebral blood flow to neuronal activity, is also disrupted in diabetes, reflecting impaired coordination between neuronal demand and perfusion within the neurovascular unit of neurons, astrocytes, endothelial cells, smooth muscle cells, and pericytes. Orthostatic hypotension, a manifestation of autonomic neuropathy that is nearly twice as common in diabetes at approximately 25 percent, further compounds the problem and has been associated with increased risk of dementia, Alzheimer’s disease, and vascular dementia. The blood-brain barrier itself shows disruption, evidenced by basement membrane thickening, endothelial dysfunction, and pericyte degeneration, an early feature that may precede both brain atrophy and cognitive symptoms.

Brain insulin resistance emerges as a shared feature of type 2 diabetes and Alzheimer’s disease. Insulin crosses the blood-brain barrier through a saturable transporter whose efficiency is modulated by obesity, aging, and neurodegeneration, and in humans the CSF-to-serum insulin ratio correlates positively with peripheral insulin sensitivity, suggesting reduced transport with greater resistance. Within the CNS, insulin signaling through IRS-AKT and IRS-MAPK cascades supports neurite outgrowth, inhibits apoptosis, enhances mitochondrial function, and modulates synaptic plasticity. Postmortem studies in Alzheimer’s and diabetic brains reveal abnormalities in IRS1-AKT-mTOR and GSK3 pathways, and postmortem measures of central insulin resistance correlate positively with amyloid-β and tau pathology and inversely with cognitive performance.

Perhaps the most intriguing finding concerns amyloid and tau. Most neuropathological studies have found no association between diabetes and classic Alzheimer’s changes such as neuritic plaques or neurofibrillary tangles, and cross-sectional PET studies have not identified significant differences in amyloid deposition between diabetic and non-diabetic individuals. Instead, diabetes may preferentially modify tau pathology. Insulin resistance may leave GSK-3β active to phosphorylate tau through impaired PI3K/Akt pathway activation. An exploratory multicohort analysis suggested enrichment of amyloid-negative, tau-positive CSF profiles in individuals with diabetes, and in a PET imaging study of diabetes-related dementia, 11 of 21 participants showed a tau-positive but amyloid-negative pattern. In the Framingham Heart Study subgroup, higher fasting plasma glucose predicted increased temporal tau deposition 14 years later without any significant association with amyloid-β. The review raises the question of whether diabetes promotes an earlier, pre-tangle form of tauopathy rather than the mature tangle burden of advanced Alzheimer’s disease.

Oxidative stress and neuroinflammation complete the pathological profile. The brain is highly vulnerable to oxidative injury given its high energy demands and lipid content, and diabetes contributes through excessive reactive oxygen species generation and mitochondrial dysfunction. AGE-RAGE signaling activates NF-κB, MAPK, PI3K/AKT, and GSK-3β pathways, driving microglial activation, proinflammatory cytokine release, and increased amyloid-β and tau hyperphosphorylation in experimental models. Higher insulin resistance and BMI have been associated with increased cortical TSPO-PET signal indicative of microglial activation in cognitively unimpaired older adults. Ferroptosis, a non-apoptotic iron-dependent form of cell death, has been implicated in both conditions, with patients showing higher brain iron levels on MRI-based methods. The glymphatic system, which clears neurotoxic proteins including amyloid and tau, also shows impairment, with human studies reporting decreased ALPS index, an indirect marker of glymphatic activity, in individuals with diabetes.

On the therapeutic front, GLP-1 receptor agonists have generated the most excitement. A recent large meta-analysis of 23 clinical trials of cardioprotective glucose-lowering agents reported a statistically significant reduction in dementia risk among individuals receiving GLP-1 receptor agonists, with an odds ratio of 0.55, though sodium-glucose cotransporter 2 inhibitors did not show a significant change in the same analysis. Animal models of Alzheimer’s disease have shown that GLP-1 receptor agonists reduce amyloid and tau pathology and attenuate central insulin resistance. However, a recent Phase 3 trial of oral semaglutide in early Alzheimer’s failed to show slowing of clinical progression, and a Phase 2b trial of daily liraglutide showed no changes in cerebral glucose metabolism as the primary outcome, with only a modest improvement in executive function as a secondary outcome. Intranasal insulin, which efficiently reaches the brain and modulates regional cerebral blood flow, showed no cognitive improvement in diabetic patients in a Phase 2 randomized trial of 223 participants, though it did improve gait speed and medial prefrontal cortex blood flow.

Vascular risk factor management remains essential, with blood pressure control slowing progression of white matter hyperintensities and stroke risk, while antiplatelet therapy has not demonstrated primary cognitive benefit in diabetic patients without established cardiovascular disease. The AGE-RAGE antagonist azeliragon failed to show cognitive benefit in a Phase 3 trial in mild Alzheimer’s disease. Nasal anti-CD3, developed as Foralumab, is currently under investigation in Phase 2a trials for mild Alzheimer’s disease and non-active secondary progressive multiple sclerosis, with preliminary evidence of reduced microglial activation on TSPO-PET. Gut-brain axis interventions including probiotics show mixed cognitive effects, while intermittent fasting and caloric restriction may modulate shared metabolic and neuroinflammatory pathways, though human data remain limited to small studies. The review concludes that prospective trials specifically powered to assess cognitive outcomes in diabetes are needed, and that the cognitive benefits of pleiotropic agents may be most apparent when initiated early, before irreversible neurodegeneration has occurred, highlighting the importance of optimizing diabetes management at the earliest signs of cognitive impairment.

Subject of Research: Diabetes‐Associated Cognitive Impairment: Pathophysiology and Emerging Therapies

Article Title: Diabetes‐Associated Cognitive Impairment: Pathophysiology and Emerging Therapies

Article References: Corbali, O., Menon, P., Corbali, H. I., Jagannathan, R., & Levey, A. I. (2026). Diabetes‐Associated Cognitive Impairment: Pathophysiology and Emerging Therapies. Annals of Clinical and Translational Neurology, Article acn3.70487. https://doi.org/10.1002/acn3.70487

Image Credits: AI Generated

DOI: 10.1002/acn3.70487

Keywords: Diabetes, Associated, Cognitive, Impairment, Pathophysiology, Emerging, Therapies, scientific research

Myelodysplastic syndromes are a family of clonal disorders of the hematopoietic stem cell, characterized by ineffective blood formation, cytopenias, and a variable risk of transformation to acute myeloid leukemia. Patients classified as higher-risk, typically by a Revised International Prognostic Scoring System score of 4 or above, face a median overall survival of roughly 16 to 21 months. Although leukemic progression remains the dominant lethal force, infectious complications account for a substantial share of deaths in this population, a fact that has traditionally been attributed to neutropenia, transfusion-related iron overload, and treatment-related immunosuppression. What has remained largely unexplored is whether specific molecular lesions shape infectious vulnerability independently of these conventional hematologic factors.

TP53, the guardian of the genome, is among the most adverse molecular lesions in myeloid malignancy. Biallelic inactivation, meaning loss of normal TP53 function through combined mutational, cytogenetic, or copy-number mechanisms, is strongly associated with genomic instability, complex karyotype, treatment resistance, and rapid disease progression. Previous work had already hinted at a connection between TP53-altered myeloid disease and infectious complications, including pulmonary infection, invasive fungal disease, and infection-related mortality. But the infectious burden specifically tied to biallelic TP53 in strictly defined higher-risk myelodysplastic syndromes had never been systematically characterized.

The Ningbo team, led by Binbin Lai and Guifang Ouyang, retrospectively analyzed 97 hospitalized patients with higher-risk myelodysplastic syndromes identified through hospitalizations between June 2023 and April 2026. Thirty-one of these patients carried biallelic TP53 alterations. Clinically significant infections were defined as suspected or documented events requiring inpatient management or intravenous anti-infective therapy, a deliberately conservative threshold that excluded mild outpatient episodes. Infection events were adjudicated using inpatient clinical notes, imaging, microbiologic evidence, anti-infective treatment records, and discharge diagnoses, and severity was graded retrospectively according to the National Cancer Institute Common Terminology Criteria for Adverse Events, version 6.0.

The numbers are striking. During a median follow-up of just 0.8 years, 59 patients, or 60.8 percent of the cohort, developed clinically significant infections, and 27 patients, or 27.8 percent, died from infection. Among patients with biallelic TP53 alterations, the infection rate reached 87.1 percent, compared with 48.5 percent in those without. Recurrent infection, defined as two or more episodes, occurred in 54.8 percent of the biallelic group versus 30.3 percent of the non-biallelic group. Infection within 100 days of diagnosis struck 77.4 percent of biallelic patients versus 28.8 percent of others, and within one year, 83.9 percent versus 39.4 percent. Infection incidence density, measured in episodes per person-year, was dramatically higher in the biallelic group, with a median of 7.93 episodes per person-year compared with 0.00 in the non-biallelic group.

Once infected, patients with biallelic TP53 alterations fared far worse. Among infected patients, 85.2 percent of the biallelic group experienced infection-related death, compared with 12.5 percent of the non-biallelic group. Most infections in the biallelic group were graded as CTCAE grade 5, meaning fatal, while most in the non-biallelic group were grade 3, severe but survivable. Anti-infective treatment escalation, meaning upgrade to advanced or combination intravenous antibiotics, was required in 85.2 percent of infected biallelic patients versus 31.3 percent of infected non-biallelic patients. Antifungal therapy was added in 74.1 percent of infected biallelic patients versus 15.6 percent of infected non-biallelic patients, a pattern consistent with the elevated risk of invasive fungal disease previously reported in TP53-mutated myeloid malignancy.

Perhaps the most intriguing technical finding concerns the cellular immune profile. Baseline neutrophil counts, hemoglobin levels, and platelet counts were comparable between the two groups, yet patients with biallelic TP53 alterations had significantly lower circulating counts of CD3-positive T cells, CD4-positive helper T cells, CD8-positive cytotoxic T cells, and natural killer cells. The median CD4-positive T-cell count in the biallelic group was 193 cells per microliter, less than half the 398.5 cells per microliter observed in the non-biallelic group. Natural killer cell counts showed a similar pattern, with a median of 54 cells per microliter versus 101. These measurements, obtained at diagnosis before any documented infection, suggest that the immune deficit in biallelic TP53 disease extends beyond neutropenia into the adaptive and innate cellular arms of immunity.

The association persisted in multivariable analysis. Using Cox proportional hazards regression, the team found that biallelic TP53 alterations remained associated with shorter composite event-free survival, a prespecified endpoint combining infection-related death and transformation to acute myeloid leukemia, with a hazard ratio of 7.56 and a 95 percent confidence interval of 2.79 to 20.46. Very-high-risk status on the Molecular International Prognostic Scoring System, which integrates clinical, cytogenetic, and molecular abnormalities, also remained significant with a hazard ratio of 3.51. Among infected patients, Firth penalized logistic regression, a technique designed for situations with limited events, showed that biallelic TP53 alterations remained associated with infection-related death with an odds ratio of 7.52 and a 95 percent confidence interval of 1.15 to 49.37.

The authors are careful to frame these findings as hypothesis-generating rather than causal. This was a single-center retrospective study of hospitalized patients, and hospital-based inclusion may introduce selection bias. Retrospective ascertainment of infections, antimicrobial exposure, and causes of death may introduce information bias, and limited microbiological confirmation restricted pathogen-specific analyses. Moreover, IPSS-R, IPSS-M, cytogenetic risk, and biallelic TP53 status share substantial prognostic information, making it difficult to disentangle the independent contribution of any single variable. All 31 patients with biallelic TP53 alterations were classified as IPSS-M very high risk, meaning the two categories overlap almost completely. The authors also note that baseline measurements describe cell abundance but do not directly measure immune function, and that the absence of longitudinal immune profiling limits mechanistic interpretation.

Nevertheless, the practical implications are considerable. If infection risk in higher-risk myelodysplastic syndromes is shaped by molecular disease architecture, then risk stratification may need to incorporate TP53 allelic status and cellular immune profiling alongside conventional neutrophil counts. Such an approach could help identify patients who require closer infection surveillance, earlier diagnostic evaluation for occult infection, and more individualized supportive-care strategies. The early and often fatal infectious burden observed in biallelic TP53 patients also raises the question of whether timely transplant referral, before severe infectious complications occur, might improve outcomes in carefully selected transplant-eligible patients. Universal antibacterial or antifungal prophylaxis cannot be recommended based on these retrospective data, but prospective multicenter studies should evaluate whether TP53 allelic status and immune-cell measurements improve infection risk assessment beyond established clinical factors. For a disease whose molecular signature has long been synonymous with treatment resistance and rapid progression, the possibility that the same signature also renders patients defenseless against ordinary pathogens adds a new and urgent dimension to the clinical management of higher-risk myelodysplastic syndromes.

Subject of Research: Infectious burden and cellular immune impairment in higher-risk myelodysplastic syndromes with biallelic TP53 alterations

Article Title: Infectious burden and cellular immune impairment in higher-risk myelodysplastic syndromes with biallelic TP53 alterations

Article References: Lai, B., Yan, X., Chen, L., Wang, Y., Sheng, L., & Ouyang, G. (2026). Infectious burden and cellular immune impairment in higher-risk myelodysplastic syndromes with biallelic TP53 alterations. Frontiers in Cellular and Infection Microbiology, 16, Article 1908881. https://doi.org/10.3389/fcimb.2026.1908881

Image Credits: AI Generated

DOI: 10.3389/fcimb.2026.1908881

Keywords: Infectious, burden, cellular, immune, impairment, higher-risk, myelodysplastic, syndromes, biallelic, TP53, alterations, scientific research

The research team, led by investigators at the Tri-institutional Center for Translational Research in Neuroimaging and Data Science and Georgia State University, analyzed complete data from 2,187 older adults, including 963 non-Hispanic White, 277 Black, and 947 Hispanic participants. Cognitive impairment was defined as a diagnosis of either mild cognitive impairment or dementia, compared against cognitively unimpaired status. Using logistic regression, the researchers tested whether higher concentrations of plasma IL-6, measured with ultrasensitive Simoa assays and log-transformed to correct for the right-skewed distribution typical of circulating cytokines, predicted greater odds of impairment after adjusting for age, education, sex, depressive symptoms, ethnoracial group, and APOE ε4 carrier status, the strongest known genetic risk factor for late-onset Alzheimer’s disease.

The results were unambiguous. Each tenfold increase in plasma IL-6 was associated with 87 percent greater odds of cognitive impairment in the full sample, with an odds ratio of 1.87 and a 95 percent confidence interval of 1.31 to 2.68, a statistically robust effect. Critically, formal interaction testing revealed no significant difference in this association across ethnoracial groups, with the likelihood-ratio test yielding a p-value of 0.172. In other words, the inflammatory signal appeared to operate similarly regardless of group membership, pointing toward a shared biological pathway rather than one specific to any single population.

Because demographic imbalance between groups can distort associations in multi-ethnic cohorts, the team conducted rigorous sensitivity analyses using propensity score matching. They created 1:1 matched subsamples in which White participants were matched exactly to Black or Hispanic participants on sex and cognitive status, and balanced on age and education. The Black/White matched sample included 554 participants and the Hispanic/White matched sample included 794, later reduced to 788 for adjusted analyses because six participants lacked APOE ε4 data. Within these carefully balanced subsamples, the IL-6 association not only persisted but strengthened, with odds ratios of 2.62 in the Black/White matched sample and 2.24 in the Hispanic/White matched sample, both statistically significant, and again with no significant IL-6-by-ethnoracial-group interactions.

The study also examined depressive symptoms, measured with the 15-item Geriatric Depression Scale, which have long been recognized as a robust predictor of late-life cognitive decline. Meta-analytic evidence indicates that late-life depression is associated with roughly 1.85-fold higher risk of all-cause dementia. In this cohort, each additional point on the depression scale was independently associated with approximately 6 percent greater odds of cognitive impairment, an effect that held in both the full sample and the matched subsamples. The convergence of depression and inflammation as independent correlates of impairment raises the question of whether one might statistically transduce the other.

Mediation analyses provided modest but intriguing support for that hypothesis. Higher depression scores were significantly associated with higher IL-6 concentrations, and IL-6 remained significantly associated with cognitive impairment after adjustment for depressive symptoms. The indirect effect of depression on cognitive impairment through IL-6 was statistically significant in the full sample, with a Sobel test p-value of 0.014, though the researchers emphasize that IL-6 accounted for only a small proportion of the total association. In the Hispanic/White matched sample, the indirect effect approached significance, while in the Black/White matched sample the depression-to-IL-6 path was not significant, resulting in a nonsignificant indirect effect. These patterns suggest possible ethnoracial variation in how inflammation links mood to cognition, though the authors caution that subgroup differences in statistical significance do not establish significant between-group differences.

Secondary analyses of the broader cytokine panel revealed a more selective inflammatory profile than a generalized elevation across all immune markers. Plasma IL-10 and TNF-α showed no significant associations with cognitive impairment in fully adjusted models, despite their frequent discussion in the Alzheimer’s neuroinflammation literature. Notably, IL-5 showed an inverse association, such that higher concentrations corresponded to lower odds of impairment, an exploratory signal that may reflect a distinct type 2 immune-regulatory pathway whose relationship to cognition differs from canonical pro-inflammatory markers. The selectivity of the IL-6 finding strengthens the interpretation that this particular cytokine captures a chronic inflammatory pathway most relevant to cognitive aging in this cohort.

Mechanistically, IL-6 occupies a unique position at the intersection of immune signaling and neurodegeneration. The cytokine coordinates both innate and adaptive immune responses, and while transient IL-6 activity can be protective, sustained IL-6 trans-signaling is predominantly proinflammatory and can perpetuate chronic immune activation. In the brain, IL-6 signaling promotes activation of microglia and astrocytes, the resident immune cells that release further pro-inflammatory mediators capable of impairing synaptic function and accelerating neuronal loss. IL-6 has been linked to amyloid-β deposition, tau hyperphosphorylation, reduced hippocampal and cortical volumes, and poorer cognitive performance in prior research. Psychological stress may upregulate IL-6 through repeated activation of the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis, and over time altered β-adrenergic signaling and reduced glucocorticoid sensitivity can weaken normal anti-inflammatory feedback, providing a plausible route by which chronic stress and depression translate into systemic inflammation.

The researchers also explored whether chronic stress might account for the IL-6 association, given that social determinants of health such as discrimination, ongoing stressors, and inequities in healthcare access are linked to Alzheimer’s risk. In an exploratory sensitivity analysis with data from 2,168 participants, higher chronic stress was associated with higher IL-6 concentrations, but chronic stress was not independently associated with cognitive impairment after adjustment for IL-6 and remaining covariates. The IL-6 association remained significant and materially unchanged when chronic stress was added to the model, suggesting that stress did not explain away the inflammatory signal. This finding points toward IL-6 as a potential convergence point where multiple upstream exposures, from vascular and metabolic burden to psychosocial adversity, may jointly shape vulnerability to cognitive decline.

The implications for equitable biomarker development are significant. Black older adults face approximately twice the risk, and Hispanic older adults about 1.5 times the risk, of developing Alzheimer’s disease and related dementias compared with non-Hispanic White adults, yet these groups remain persistently underrepresented in dementia research. If interventions targeting IL-6, whether through lifestyle modification, anti-inflammatory therapies, or depression management, could benefit diverse populations without requiring race or ethnicity-specific tailoring, the pathway toward precision prevention becomes more scalable and more just. The authors emphasize, however, that the cross-sectional design of this study precludes conclusions about temporal ordering, and longitudinal analyses within HABS-HD and other diverse cohorts will be needed to determine whether baseline IL-6 predicts incident cognitive decline, whether changes in IL-6 mediate treatment effects on cognition, and whether IL-6 represents a causal contributor to neurodegeneration or a downstream marker of an already active disease process. As the scientific community increasingly recognizes brain health as a modifiable construct, IL-6 shows promise as a scalable, generalizable biomarker for identifying midlife adults with inflammation-related concerns about cognitive aging, and future work will be critical for translating these biomarker associations into actionable strategies to reduce dementia burden across all racial and ethnic groups.

Subject of Research: Plasma IL-6 as a shared inflammatory marker of cognitive impairment across racially and ethnically diverse older adults: matched analyses from the HABS-HD study

Article Title: Plasma IL-6 as a shared inflammatory marker of cognitive impairment across racially and ethnically diverse older adults: matched analyses from the HABS-HD study

Article References: Misiura, M. B., Joseph, T. O., Cooper, J. A., Champion, G., Burnette, J., Bartlett, A., Thatcher, K., Austin, N. C., & Dotson, V. M. (2026). Plasma IL-6 as a shared inflammatory marker of cognitive impairment across racially and ethnically diverse older adults: matched analyses from the HABS-HD study. Frontiers in Dementia, 5, Article 1930196. https://doi.org/10.3389/frdem.2026.1930196

Image Credits: AI Generated

DOI: 10.3389/frdem.2026.1930196

Keywords: Plasma, IL-6, shared, inflammatory, marker, cognitive, impairment, across, racially, ethnically, diverse, older

The review, led by Barbara Johanne Thomas Nordhjem and colleagues at Copenhagen University Hospital Rigshospitalet, followed PRISMA-ScR guidance and searched MEDLINE, PsycINFO, and Web of Science from database inception to February 2025. After screening 3,577 records, the team included 60 articles published between 1981 and 2025. Most were small and cross-sectional, with publication output increasing markedly after 2015. The registered protocol is available on PROSPERO under identifier CRD420251084951.

EEG records cortical electrophysiological activity with millisecond temporal resolution, offering a complementary approach to MRI-based neuroimaging. Although scalp EEG has less anatomical specificity than MRI, it can characterize the timing and coordination of neural activity at rest and during cognitive processing. The information obtained depends strongly on the recording condition, paradigm, and analytic approach. Task-based EEG typically yields event-related potentials, or ERPs — time-locked voltage responses to discrete stimuli — while resting-state recordings are analyzed using quantitative EEG, or qEEG, methods applied to spectral power, functional connectivity, and network organization.

Among the 60 included articles, 35 reported ERP measures only, 19 reported qEEG measures only, and 6 included both. Task-based paradigms were used in 47 articles, resting-state in 18, and sleep EEG in just one. Oddball and deviance paradigms, which present rare stimuli among frequent ones to elicit the P300 component, and attention or executive control tasks were the most frequently used. The P300 component is commonly interpreted in relation to attentional-resource allocation and context updating, whereas P300 latency provides an index of stimulus-evaluation speed.

In populations with cancers outside the central nervous system, longer P300 latency and lower amplitude were the most recurrent findings, reported across childhood cancer, breast cancer, radiotherapy, and acute treatment studies. However, opposite and null findings also occurred. Some studies reported stable P300 measures, shorter latencies, or no group differences at all. Differences in stimulus modality, target probability, electrode selection, peak definition, age, and treatment timing further limit cross-study comparison, making it difficult to interpret longer P300 latency as a reliable cognitive marker of cancer-related cognitive impairment.

The evidence from primary CNS and other intracranial tumor populations was sparse, with only 9 articles addressing these groups. All 9 included fewer than 50 cancer participants. In these studies, EEG findings were more often examined in relation to tumor-related neurological factors, including focal or diffuse slowing, altered phase synchrony, and differences in network organization. Two reports from one glioma cohort found that greater theta activity and theta-band network organization were related to poorer language performance, offering the clearest preliminary candidate for a reproducible EEG-cognition relationship in this population.

Quantitative EEG findings showed limited convergence across articles. Spectral power was the most frequently reported analysis family in 19 articles, connectivity or phase-based measures in 5, and aperiodic 1/f measures in just 1. In one longitudinal breast cancer cohort, aperiodic slopes became flatter from before to after treatment in patients relative to controls, which the authors interpreted as increased neural noise. Flatter slopes were also associated with poorer executive control and alerting performance. This aperiodic finding is a specific candidate, but it has not been independently replicated.

A central finding of the review is the gap between detecting an EEG abnormality and validating an EEG marker of cognition. Overall, only 21 of 60 articles reported at least one direct EEG-outcome association that met the statistical significance threshold used in the original article. Many articles instead reported task-related EEG modulation, group differences, or parallel longitudinal changes without testing whether individual differences in EEG measures were associated with cognitive outcomes. Associations involving standardized cognitive tests administered independently of the EEG task were less common.

Cancer populations were also unevenly represented. Breast cancer was the most frequently studied diagnosis, accounting for 21 of the 60 articles. Hematologic malignancies and primary CNS tumors followed with 8 articles each. Only 9 articles included children or adolescents, and 5 of these included mixed pediatric and adult samples. Geographically, 29 articles were conducted in Europe, 22 in North America, and 9 in Asia, with no eligible articles exclusively from other world regions.

The authors conclude that EEG provides a complementary approach to investigating cognition in people with cancer, but the evidence remains methodologically heterogeneous. Larger longitudinal studies, more consistent cognitive outcome selection, and closer integration of neural and cognitive measures are needed to establish reproducible findings. The potential of EEG for risk stratification and prediction remains largely unexplored, and the current evidence is insufficient to support biomarker or clinical applications. The findings should be viewed as hypothesis-generating rather than as evidence for established EEG markers of cancer-related cognitive impairment.

Subject of Research: Functional brain activity in cancer-related cognitive impairment: a scoping review of EEG studies

Article Title: Functional brain activity in cancer-related cognitive impairment: a scoping review of EEG studies

Article References: Nordhjem, B. J. T., Rothschild, L. M. T., Honoré, C. R., Larsen, A. T. S., Fridh, M. K., & Hjalgrim, L. L. (2026). Functional brain activity in cancer-related cognitive impairment: a scoping review of EEG studies. Frontiers in Human Neuroscience, 20, Article 1851560. https://doi.org/10.3389/fnhum.2026.1851560

Image Credits: AI Generated

DOI: 10.3389/fnhum.2026.1851560

Keywords: Functional, brain, activity, cancer-related, cognitive, impairment, scoping, review, studies, scientific research

A new mixed-methods study published in the Journal of Eating Disorders by Josefa Ilg, Anne-Katrin Merz, Lena Kramer, Alexander Nettlau, Anja Hilbert, and Ricarda Schmidt offers one of the most detailed portraits to date of what it actually means to live with ARFID as an adult in the community. Drawing on data from 97 adults with an interview-based diagnosis of ARFID, the research team combined qualitative accounts of personal impairment with quantitative measures of symptoms, temperament, and personality traits, providing an unusually granular view of both the burden of the disorder and the remarkably varied paths it can take over time.

The methodological design was deliberately two-pronged. Participants, recruited through an online study on ARFID, answered open-ended questions asking them to describe in their own words what they struggle with most because of their avoidant or restrictive eating and how their symptoms have changed since onset. The researchers then applied a qualitative content-thematic analysis to these free-text responses, a technique that allows themes to emerge from the data rather than imposing pre-existing categories. In parallel, established questionnaires assessed ARFID symptom severity, obsessive-compulsive personality traits, temperament, and sensory sensitivity, and statistical comparisons were run across groups defined by different symptom trajectories.

What emerged from the thematic analysis was a taxonomy of suffering that extends far beyond the dinner table. Seven main themes of impairment were identified. Health-related impairment was by far the most commonly reported, cited by 68.8 percent of participants, encompassing concerns about nutritional deficiencies, medical consequences, and the physical toll of a restricted diet. Impairment of lifestyle followed at 39.6 percent, capturing restrictions on everyday activities such as travel, dining out, work events, and social gatherings that revolve around food. Notably, 34.4 percent of participants described the eating behavior itself as a burden, pointing to the exhausting, distressing nature of the avoidance and restriction rather than only its downstream consequences.

The social dimension of ARFID proved equally consequential. Nearly a quarter of respondents, 24.0 percent, reported impairment stemming from their social relationships, including negative or dismissive responses from the social environment. Within this broader social theme, 13.5 percent specifically described difficulties in romantic partnerships, where shared meals are a cornerstone of intimacy and everyday routine, and 8.3 percent described challenges in family life and parenthood, including worries about modeling eating behavior for children or navigating mealtimes as a parent with a severely restricted diet. Perhaps most sobering for the healthcare system, 2.1 percent of participants reported impairment directly attributable to their experiences with practitioners, suggesting that even clinical encounters can become a source of burden for adults whose disorder is frequently misunderstood or overlooked.

Equally significant were the findings on symptom progression. Rather than following a single course, ARFID in this community sample displayed striking heterogeneity, falling into four distinct trajectory groups. The largest group, 41.3 percent of participants, reported improved symptoms over time. A further 32.6 percent described consistent symptoms that neither improved nor worsened, 18.5 percent reported worsened symptoms, and 7.6 percent described a varying course marked by fluctuations. For a disorder often assumed to be either a transient phase of childhood or a lifelong fixed condition, this variability is a finding with real clinical weight.

The quantitative comparisons between progression groups sharpened the picture. Adults whose symptoms had improved were older and more highly educated than those whose symptoms had deteriorated, suggesting that age and educational attainment may serve as markers, or perhaps even enablers, of recovery or adaptation. Conversely, greater fear of aversive consequences, one of the three core maintaining mechanisms of ARFID alongside sensory sensitivity and low interest in eating, was associated with a deteriorated course. This aligns with the mechanistic model of ARFID as a disorder maintained by negative reinforcement: individuals who dread choking, vomiting, or other frightening consequences of eating may progressively narrow their food repertoire, entrenching the restriction and its consequences in a self-perpetuating loop. The association between worsening symptoms and this specific fear profile offers a potential target for early identification and intervention.

The study’s authors are careful to frame these findings as exploratory. Because the data are cross-sectional and retrospective, based on participants’ own accounts of how their symptoms have changed, they cannot establish causality or prospectively track the disorder’s course. Higher education and age might correlate with improvement for reasons ranging from greater access to information and healthcare to cognitive resources for developing coping strategies, and the fear-of-aversive-consequences association could reflect either a driver of deterioration or a feature of more entrenched cases. The researchers explicitly call for longitudinal studies that can prospectively identify the risk and protective factors governing ARFID’s progression and persistence across adulthood.

Even so, the implications of the work are considerable. For clinicians, the seven impairment themes provide a practical map of the domains worth assessing and addressing in adult patients, from medical monitoring and nutritional rehabilitation to couple and family counseling and even the quality of the therapeutic encounter itself. The finding that nearly four in ten participants reported lifestyle-wide restrictions underscores that ARFID in adulthood is not a quirk of picky eating but a condition with pervasive functional impact. The public health significance is equally clear: if a substantial fraction of adults with ARFID report worsening symptoms while the majority remain stable or improve, then understanding what distinguishes these trajectories could redirect scarce treatment resources toward those most at risk.

The study also carries a message for primary care and mental health services, where adult ARFID frequently goes unrecognized precisely because screening and awareness are calibrated to childhood presentations and to better-known eating disorders such as anorexia nervosa and bulimia nervosa. Adults whose restrictive eating is driven by sensory aversion or fear rather than body image concerns may never see themselves reflected in standard eating disorder screening, and their reports of practitioner-related burden in this study hint at the cost of that invisibility. By centering the lived experience of adults with interview-confirmed diagnoses, the Leipzig-based research team has produced evidence that ARFID is a genuine adult mental health concern, one whose heterogeneous course demands the same longitudinal scientific scrutiny long afforded to other eating disorders.

Beyond its headline findings, the study illustrates the value of mixed-methods designs in eating disorder research, where standardized symptom scores alone can miss the texture of daily struggle. By pairing closed-ended questionnaire data with open-ended narratives, the researchers allowed participants to name burdens that might otherwise never appear in clinical inventories, such as the strain of explaining one’s eating at work functions or the anxiety of feeding children while maintaining a narrow diet oneself. This approach is particularly suited to ARFID, a diagnosis whose presentation varies widely depending on which of its maintaining mechanisms dominates in a given individual.

The community-based recruitment also matters scientifically. Much of the existing ARFID literature draws on treatment-seeking samples, which risk overrepresenting severe or medically complicated cases and underrepresenting adults who have never been diagnosed. By studying individuals in the general population with interview-confirmed diagnoses, the Leipzig team captured a broader spectrum of severity, including people who may have developed informal coping strategies over years of living with the condition. This may partly explain why the largest trajectory group reported improvement rather than deterioration, a pattern that could look different in clinical cohorts.

The measurement of obsessive-compulsive personality traits, temperament, and sensory sensitivity alongside symptom severity reflects the growing recognition that ARFID sits at the intersection of eating pathology and broader neurodevelopmental and personality characteristics. Elevated sensory sensitivity, for instance, is frequently reported in ARFID and overlaps with profiles seen in autism spectrum conditions, while perfectionism and rigidity may sustain restriction through inflexible food rules. Including these constructs in a single adult sample helps lay groundwork for identifying which psychological profiles predict which courses, an essential step toward personalized intervention.

Practically, the trajectory findings suggest that clinicians should not assume stability in adult ARFID. A substantial minority of participants described worsening symptoms, and the association with heightened fear of aversive consequences points to a specific, assessable risk marker that could be screened for during routine evaluation. Conversely, the link between improvement and higher age or education hints that accumulated life experience, resources, or self-directed learning about the condition may support adaptation, hypotheses that future longitudinal work can test directly.

As an open-access publication supported by Leipzig University’s Behavioral Medicine Research Unit, the study also lowers barriers for clinicians and researchers worldwide to build on its findings, an important consideration for a disorder whose adult presentation remains under-recognized across healthcare systems.

Subject of Research: Adult community-dwelling individuals with avoidant/restrictive food intake disorder (ARFID), examining their experienced impairments and symptom progression patterns

Article Title: Avoidant/Restrictive food intake disorder in adults within the community: A mixed-method study on individual impairment and progression

Article References: Ilg, J., Merz, A.-K., Kramer, L., Nettlau, A., Hilbert, A., & Schmidt, R. (2026). Avoidant/Restrictive food intake disorder in adults within the community: A mixed-method study on individual impairment and progression. Journal of Eating Disorders, 14(1), Article 218. https://doi.org/10.1186/s40337-026-01765-w

Image Credits: AI Generated

DOI: 10.1186/s40337-026-01765-w

Keywords: ARFID, avoidant/restrictive food intake disorder, eating disorders, adult mental health, impairment, symptom progression, mixed-methods research, sensory sensitivity, lived experience, psychopathology, Journal of Eating Disorders, longitudinal research