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[Independence of the slowly progressive form of schizophrenia].

The development stereotype of slowly progressive schizophrenia is determined by a long subclinical course (latent period), a protracted stage of florid psychopathological signs (active period) and an eventual stabilization seen in the late phases of the process. The clinical picture of the active period and the defect structure is characterized by axial symptoms, the typology of which is considered as a basis of the following systematics of slowly progressive schizophrenia: 1) latent schizophrenia; 2) slowly progressive schizophrenia with obsessions; 3) slowly progressive schizophrenia with hysterical symptoms; 4)slowly progressive schizophrenia with depersonalization; 5) hypochondriacal schizophrenia (non-delusional hypochondria); 6) slowly progressive delusional schizophrenia; 7) slowly progressive schizophrenia with a prevalence of affective disturbances; 8) schizophrenia with poor symptoms.

Affective Symptoms↗

The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the diabetes control and complications trial.

The Diabetes Control and Complications Trial (DCCT) demonstrated that a regimen of intensive therapy aimed at maintaining near-normal blood glucose values markedly reduces the risks of development or progression of retinopathy and other complications of insulin-dependent diabetes mellitus (IDDM) when compared with a conventional treatment regimen. This report presents an epidemiological assessment of the association between levels of glycemic exposure (HbA1c) before and during the DCCT with the risk of retinopathy progression within each treatment group. The initial level of HbA1c observed at eligibility screening as an index of pre-DCCT glycemia and the duration of IDDM on entry were the dominant baseline predictors of the risk of progression. The shorter the duration of IDDM on entry, the greater were the benefits of intensive therapy. In each treatment group, the mean HbA1c during the trial was the dominant predictor of retinopathy progression, and the risk gradients were similar in the two groups; a 10% lower HbA1c (e.g., 8 vs. 7.2%) is associated with a 43% lower risk in the intensive group and a 45% lower risk in the conventional group. These risk gradients applied over the observed range of HbA1c values and were unaffected by adjustment for other covariates. Over the range of HbA1c achieved by DCCT intensive therapy, there does not appear to be a level of glycemia below which the risks of retinopathy progression are eliminated. The change in risk over time, however, differed significantly between the treatment groups, the risk increasing with time in the study in the conventional group but remaining relatively constant in the intensive group. The risks were compounded by a multiplicative effect of the level of HbA1c with the duration of exposure (time in study). Total glycemic exposure was the dominant factor associated with the risk of retinopathy progression. When examined simultaneously within each treatment group, each of the components of pre-DCCT glycemic exposure (screening HbA1c value and IDDM duration) and glycemic exposure during the DCCT (mean HbA1c, time in study, and their interaction) were significantly associated with risk of retinopathy progression. Similar results also apply to other retinopathic, nephropathic, and neuropathic outcomes. The recommendation of the DCCT remains that intensive therapy with the goal of achieving near-normal glycemia should be implemented as early as possible in as many IDDM patients as is safely possible.

Biomarkers↗

Nonrandom cytogenetic changes accompany malignant progression in clonal lines abelson virus-infected lymphocytes.

Initially, lymphoid cells transformed by v-abl or BCR/ABL oncogenes are poorly oncogenic but progress to full transformation over time. Although expression of the oncogene is necessary to initiate and maintain transformation, other molecular mechanisms are thought to be required for full transformation. To determine whether tumor progression in ABL oncogene-transformed lymphoid cells has a genetic basis, we examined whether progression of the malignant phenotype of transformed clones correlates with particular cytogenetic abnormalities. A modified in vitro bone marrow transformation model was used to obtain clonal Abelson murine leukemia virus-transformed B lymphoid cells that were poorly oncogenic. Multiple subclones were then derived from each clone and maintained over a marrow-derived stromal cell line for several weeks. Over time, clonally related Abelson murine leukemia virus-transformed subclones progressed asynchronously to full transformation. The data show that tumor progression can occur in the absence of detectable cytogenetic changes but, more importantly, that certain cytogenetic abnormalities appear reproducibly in highly malignant subclones. Therefore, three independent subclones showed deletion in a common region of chromosome 13. Other highly malignant cells carried a common breakpoint in the X chromosome, and, finally, two subclones carried an additional chromosome 5. These results are consistent with the hypothesis that ABL oncogenes are sufficient for the initial transformation of cells but that additional genetic events can drive oncogenic progression. These observations further suggest that diverse genetic mechanisms may be able to drive tumor progression in cells transformed with ABL oncogenes.

Abelson murine leukemia virus↗

[Progression to 2d and 3d grade atrioventricular block in patients after electrostimulation for bundle-branch block and syncope: a long-term study].

BACKGROUND: Patients with bundle branch block and syncope, especially those with abnormal electrophysiologic study, are at high risk of progression to second-or third-degree atrioventricular block and therefore they often receive a permanent back-up pacemaker. The aim of this study was to evaluate of the incidence of bundle branch block progression to second or third-degree atrioventricular block during long-term follow-up. METHODS: A retrospective study was performed on 60 patients (49 males, age 77 +/- 9 years) with bundle branch block and permanent back-up pacemaker. The patients were subdivided into 3 groups: 13 patients, at pre-implant electrophysiologic study had HV interval > or = 100 msec and/or second- or third-degree atrioventricular block induced by ajmaline i.v. administration (Group 1); 20 patients with HV interval of 70-100 msec and/or HV > or = 120 msec after ajmaline administration (Group 2); 27 patients who had received a permanent pacemaker because of carotid sinus syndrome or sick sinus syndrome (22 patients) or because of recurrent syncopes and negative electrophysiologic study (5 patients) (Group 3). RESULTS: During a mean follow-up of 62 +/- 41 months, 17/60 patients (28%) had progression to second- (n = 4) or third-degree (n = 13) atrioventricular block: atrioventricular block occurred in 54% of Group 1 patients in 25% of Group 2 patients and in 19% of Group 3 patients. The actuarial rate of progression to atrioventricular block for the overall population was, at 5 and 10 years, 25% and 58% respectively; in Group 1 it was 46% and 62%; in Group 2 it was 22% and 55% and in Group 3 it was 21% and 59% (p = 0.06). The patients with right bundle branch block and left anterior hemiblock were at higher risk of progression to atrioventricular block than those with right bundle branch block or left bundle branch block (risk 42% vs 14%, p = 0.06). The presence of an abnormal electrophysiologic study did not increase the progression rate either in the patients with right bundle branch block and left anterior hemiblock (risk of 43%), nor did it in those patients with other types of bundle branch block (risk of 18%). Moreover, the induction of second- or third-degree atrioventricular block during ajmaline administration was associated with a higher risk of block during the follow-up (60% vs 25%, p = 0.06). CONCLUSIONS: Patients treated with pacemaker because of symptomatic bundle branch block have a high risk of progression to second- or third-degree atrioventricular block in the long-term follow-up. The results argue against the practical usefulness of electrophysiological study since a risk stratification could be obtained by the simpler surface electrocardiogram; moreover, risk of block was also present in the patients affected by carotid sinus syndrome or sick sinus syndrome, and in those affected by unexplained syncope with negative electrophysiologic study.

Age Factors↗

A cyclin-dependent kinase inhibitor, butyrolactone I, inhibits phosphorylation of RB protein and cell cycle progression.

Butyrolactone I is a selective inhibitor of the cyclin-dependent kinase (cdk) family. It inhibits both cdk2 and cdc2 kinase, but scarcely affects C-kinase, A-kinase, casein kinases, MAP kinase or EGF receptor-tyrosine kinase (Kitagawa et al., 1993, Oncogene, 8, 2425-2432). We studied the effects of butyrolactone I on the cell cycle as well as on phosphorylation of retinoblastoma protein (pRB). Butyrolactone I inhibited phosphorylation of pRB catalyzed by cyclin A-cdk2 produced by baculovirus in vitro. Furthermore, it inhibited phosphorylation of pRB and cell cycle progression from G1 to S phase in WI38 cell cultures. WI38 cells arrested at the G0 phase by serum starvation progressed in the cell cycle after serum stimulation. pRB was phosphorylated after 10 h serum stimulation. Incorporation of [3H]thymidine into the cells began to increase after 16 h serum stimulation. These processes were inhibited by butyrolactone I. Flow cytometric analysis showed that exposure to butyrolactone I inhibited progression of the cell cycle from G1 to S phase. These data suggested that initiation of DNA synthesis was inhibited by butyrolactone I and that the cell cycle was arrested in the G1 phase. Butyrolactone I also inhibited H1 histone phosphorylation in human WI38 cells and their G2/M progression. tsFT210 cells, a temperature-sensitive cdc2 mutant cell line, were synchronized at G2/M at a nonpermissive temperature, butyrolactone I inhibited the cell cycle progression of these cells at G2/M at the permissive temperature. Thus butyrolactone I, a cyclin-dependent kinase family inhibitor, which prevented the phosphorylations of the cell cycle-regulating proteins pRB and H1 histone, inhibited the cell cycle at G1/S and G2/M, respectively. These results suggest that the phosphorylations of pRB and H1 histone may play crucial roles in G1/S and G2/M progression, respectively, although it is possible that phosphorylations of other proteins by cdks are involved in G1/S and G2/M progression.

4-Butyrolactone↗

Progression of aortic stenosis in adults: new insights provided by Doppler echocardiography.

Aortic stenosis is a progressive disease. The mechanisms and patterns of progression have been studied over the years using clinical assessment, cardiac catheterization, and more recently, Doppler echocardiography. Doppler is the ideal tool with which to study the progression of aortic stenosis since it provides accurate hemodynamic data non-invasively and, hence, can be repeated serially over long follow up periods. Recent Doppler echocardiographic studies have shown that the progression of aortic stenosis occurs with a wide range of individual variations, and that its rate and pattern cannot be predicted at the time of initial evaluation. However, it does follow a linear pattern, and individual trends can therefore be determined in a given patient. Symptoms lack specificity and, at a given point in time, do not predict progression. However, new and/or worsening symptoms are a mark of significant hemodynamic progression. The relationship between the cause of aortic stenosis and its progression remains imperfectly documented, and further longitudinal studies should focus on this question.

Aortic Valve↗

Zidovudine resistance, syncytium-inducing phenotype, and HIV disease progression in a case-control study. The VA Cooperative Study Group.

A case-control study of patients with progressive (cases) or nonprogressive (controls) disease was designed to determine the association among disease progression, zidovudine sensitivity, and syncytium-inducing phenotype. Viral isolates were screened for sensitivity to zidovudine using a peripheral blood mononuclear cell-based assay and for syncytium-inducing (SI) phenotype in MT2 cell culture. Thirty-four patients, whose disease progressed to AIDS or whose CD4 cell numbers fell < 200 cells/mm3, were matched with 34 patients whose conditions had not progressed or whose CD4 cell numbers remained > 200 cells/mm3. Virus was successfully cultured from both the progressor and the nonprogressor in 17 of these 34 matched case-control pairs. In six of the 17 pairs, virus isolated from the progressor had an IC50 (50% inhibitory concentration) for zidovudine > 1 microM and at least threefold greater than the IC50 of virus isolated from the matched nonprogressor (p = 0.04). In 16 of these 17 pairs the virus isolated from the progressor had the SI phenotype, indicative of high cytopathogenicity, while the virus from the matched nonprogressor had a non-syncytium-inducing phenotype (p < 0.0001). Zidovudine therapy did not appear to select for the SI phenotype in this patient population. A statistically significant association between high-level zidovudine resistance and clinical disease progression was demonstrated. A statistically significant association between the SI phenotype and disease progression was demonstrated. The results suggest that disease progression while being treated with zidovudine therapy may be more closely associated with the SI phenotype than with zidovudine resistance.

Acquired Immunodeficiency Syndrome↗

Contralateral disease progression after carotid endarterectomy.

BACKGROUND: We report the natural history of the carotid artery contralateral to the ipsilateral endarterectomized carotid artery. METHODS: The incidence of new symptoms and disease progression of the patient contralateral side after unilateral carotid endarterectomy (CE) was studied by clinical follow-up and serial duplex scanning in 127 patients. RESULTS: During a mean follow-up of 44 months, new hemispheric events occurred in nine (7%) and significant progression was recorded in 27 (21%) patients. In 97 patients with initial stenosis of less than 50% (group I), contralateral progression to greater than 50% was noted in 22% and new symptoms (one transient ischemic attack and one cerebrovascular accident) in 2% of patients; three patients underwent CE. In 30 patients with initial stenosis between 50% and 99% (group II), new symptoms (all transient ischemic attacks) occurred in seven (23%) (group II vs group I; p < 0.003) and nine underwent CE (group II vs group I; p < 0.001). Progression in 26 patients with 50% to 79% stenosis within group II to greater than 80% was noted in 19% of patients (difference not significant compared with group I). CONCLUSIONS: Overall, new symptoms occurred in 7% and significant contralateral disease progression in 21% of patients; subsequent CE was performed in 9.4% of patients. Initial presence of greater than 50% contralateral stenosis is a predictor of future hemispheric symptoms, which are likely to be transient ischemic attacks. New symptoms did not necessarily correlate with disease progression. Because disease progression was observed in patients with varying degrees of initial contralateral stenosis, serial clinical and duplex scanning in all patients undergoing unilateral CE is recommended.

Aged↗

Shope papilloma cell and leukocyte proliferation in regressing and progressing lesions.

Lesions generated by infection with cottontail rabbit papillomavirus frequently undergo spontaneous regression. The purpose of this immunohistochemical study was to compare leukocyte and papilloma cell proliferation in progressing and regressing papillomas and to test the hypothesis that regression was associated with an inhibition of papilloma cell proliferation. The monoclonal antibodies (MAbs) MAb-019 (specific for DNA/bromodeoxyuridine [BrdU] complexes), Ki-67 (specific for actively proliferating cells), L11/135 (specific for rabbit T cells), and 2C4 (specific for rabbit class II antigen) were used for this purpose. In progressing papillomas, there were few leukocytes (< 1%) in the dermis that stained with MAb-019 and Ki-67, whereas these antibodies stained 4.5% and 6.8% of the intraepidermal leukocytes, respectively. Regressing papillomas contained conspicuous leukocytic infiltrates in the dermis, of which 76.9% were L11/135-positive T cells. However, few intradermal leukocytes (< 3%) stained positively with MAb-019 and Ki-67 MAbs, despite expressing rabbit class II antigen. The epidermis of regressing papillomas contained a higher percentage of MAb-019- and Ki-67-positive leukocytes than the epidermis of progressing papillomas. Intraepidermal leukocytes in progressing and regressing papillomas consisted mainly of T cells stained by L11/135. It appeared that many dermal leukocytes (mainly T cells) form a non-cycling T cell population in both progressing and regressing papillomas, whereas intraepidermal T cells in regressing papillomas were effectively activated and represented a cycling T cell population. MAb-019 and Ki-67 MAbs demonstrated similar staining patterns in papilloma and normal tissues. However, in both progressing and regressing papillomas, the Ki-67 MAb usually stained a larger percentage of cells than the MAb-019 MAb. MAb-019 and Ki-67 MAbs showed a homogeneous distribution of positive cells from basal layer to the upper layer in progressing papillomas. On the other hand, in regressing papillomas, cell staining with the two antibodies was concentrated in the basal and lower layers, but not in the upper layers. This result indicates that cell proliferation in the upper epidermal layers is suppressed in regressing papillomas. Our present data show that intraepidermal T- cell activation and suppression of tumor proliferation might play a crucial role in papilloma regression.

Animals↗

[Does parenteral gold inhibit roentgen progression of chronic polyarthritis?].

The retardation of radiological progression is one of the most important characteristics of a disease-modifying effect of an antirheumatic drug. For the following overview 10 trials were identified dealing with x-ray progression under treatment with parenteral gold. Nine of these trials were randomised parallel studies, one was a retrospective long-term observational study, all had a control group, in five this control group was treated with placebo, in two trials parenteral gold was compared with another DMARD (auranofin and methotrexate, respectively), in two trials different doses of gold were compared and in two trials the radiological progression during the first 6 months was compared with the following treatment period (in one of these trials gold was compared with methotrexate as well). The duration of treatment and follow-up was up to 1 year in two trials, up to 2 years in six, and over 2 years in only two studies. There is a great number of limitations in these studies: for instance, there was a large number of withdrawals who were not followed, x-rays were available for evaluation only in a relatively small proportion of treated patients in five studies, in six studies the disease duration was over 2 years at baseline, which limits the evaluability of x-ray progression for technical reasons. In one study juxta articular osteoporosis and joint swelling were evaluated; but these parameters are very difficult to evaluate in a multicenter study because of the different quality of the films. In spite of all limitations and reservations with the studies reviewed the published results indicate a reduction of radiological progression with parenteral gold treatment of rheumatoid arthritis patients: in the placebo-controlled studies outcome in the gold group was significantly better than in the placebo group. The study of the Empire Rheumatism Council failed to show a significant difference compared to the control group after 30 months, but the patients had been treated sufficiently only for 5 months. The study of Cats indicated a better outcome in the group of patients with a high gold dose, which is confirmed by the retrospective analysis of Luukkainen. In a comparison between 113 patients treated with parenteral gold and 119 patients treated with auranofin for 1 year Larsen found a significantly smaller progression in the patients treated with parenteral gold. In a patient population of 73 and 53 the difference between methotrexate and parenteral gold was too small to be detectable, but the progression curve was significantly flattened after the first 6 months, indicating a treatment effect. In a macroradiographic study the erosion surface area increased during the first 6 months of gold treatment, it did not change during the second 6 months, and decreased during the third 6 months together with healing of erosions. In conclusion, the studies reviewed in this paper indicate a disease-modifying potency of parenteral gold treatment, especially when the treatment is started early and sufficiently dosed.

Animals↗

[The effect of complete thymic extract on motility and progressive motility of spermatozoa in asthenozoospermia].

The thymic gland is involved in immunologic and endocrinologic heomostasis of the body. Neonatal thymectomy of experimental animals leads to gonadal dysgenesis. Both eostrogen and androgen receptors have been identified in thymic epitelial cells, and sex steroids can be modulated by secretion of thymosin. High levels of thymosin alpha-1 in seminal plasma are correlated with sperm count, viability and motility in fertile males as compared to infertile ones. In this study we examined the effects of complete thymic extract on motility and progressive motility of spermatozoa obtained from asthenozoospermic men. In the first part of experiment, we studied the influence of complete thymic extract, as a bioactive medium component, on movement of spermatozoa samples with initial motility lower than 30%, in vitro. The study was carried out on two groups of sperm samples, 40 samples each, obtained by masturbation after a 72-hour-abstinence. After completed liquefaction at room temperature (30-40 min.), we determined the usual parameters of sperm quality. Total motility (M%) and progressive motility (PM%) of spermatozoa were analyzed in 10 microscopic view fields. Each group of sperm samples was prepared by swim-up and swim-down method. Then, we estimated the total motility and progressive motility of "washed" spermatozoa in every sample. In addition, every sample was divided in two equal parts. One part was immediately left in thermostat (control). To the second part we added 0.2 mg of complete thymic extract before incubation (experimental group). Total and progressive motilities were analyzed after 1, 4, 12 and 24 hours of incubation. The t-test was used for statistical analysis of results. The second part of the study was carried out on a group of 10 asthenozoospermic men (volunteers). We examined the influence of complete thymic extract, as intra-muscular injection, in a doze of 150 mg daily, during seven days, on motility and progressive motility of spermatozoa. Sperm samples were obtained by masturbation after four days of abstinence. We compared the parameters before and after the therapy. They were statistically processed by a method of difference. The results showed that the complete thymic extract increased the total and progressive motilities of spermatozoa separated by swim-down method (p < 0.001), in vitro (Table 1-4). The parenteral application of complete thymic extract, statistically significantly increased motility and progressive motility of spermatozoa in asthenozoospermic men (p < 0.05) (Table 5). These findings could be useful in assisted reproductive technology.

Adult↗

Tumor heterogeneity and progression: conceptual foundations for modeling.

A conceptual foundation for modeling tumor progression, growth, and heterogeneity is presented. The purpose of such models is to aid understanding, test ideas, formulate experiments, and to model cancer 'in machina' to address the dynamic features of tumor cell heterogeneity, progression, and growth. The descriptive capabilities of such an approach provides a consistent language for qualitatively reasoning about tumor behavior. This approach provides a schema for building conceptual models that combine three key phenomenological driving elements: growth, progression, and genetic instability. The growth element encompasses processes contributing to changes in tumor bulk and is distinct from progression per se. The progression element subsumes a broad collection of processes underlying phenotypic progression. The genetics elements represents heritable changes which potentially affect tumor character and behavior. Models, conceptual and mathematical, can be built for different tumor situations by drawing upon the interaction of these three distinct driving elements. These models can be used as tools to explore a diversity of hypotheses concerning dynamic changes in cellular populations during tumor progression, including the generation of intratumor heterogeneity. Such models can also serve to guide experimentation and to gain insight into dynamic aspects of complex tumor behavior.

Animals↗

[No evidence for hearing aid-induced progressive pediatric hearing loss in the Cologne region].

Progressive hearing loss during childhood caused by a hearing-aid induced deterioration has been discussed controversely since 1939. However, it is unchallenged that in cases of profound sensorineural hearing loss in infancy and early childhood powerful hearing aids are necessary for auditory and speech development. Due to an increase of progressive hearing losses during the last 4 years, we discussed the possible causes and the probability of hearing aid induced progressions once more. Our study consists of two investigations: First, all patients since 1993 suffering from progressive hearing loss among all hearing impaired children in the department of Audiology and Pedaudiology of the ENT-Hospital of Cologne were taken into account. Second, all children of the Rheinische school for hearing impaired children were investigated. The evaluated data included the degree of severity and etiology of the hearing loss, the duration of the hearing aids use and the amplification of the hearing aid. 23 children were diagnosed with a progressive hearing loss in the period. We observed a massive increase over these years. No correlation between the duration of the hearing aid usage and the maximum output level was found. Furthermore, there was no difference between the causes of the hearing losses between the children of the school and the children with progressive hearing loss. At the moment, we do not see any reason to change our strategy for fitting hearing aids. The increase of progressive cases in the last 2 years should be the reason for further investigations in this field.

Adolescent↗

Can strategies used by statewide tobacco control programs help smokers make progress in quitting?

Many states have recently adopted programs to encourage smokers to quit. Here, we seek evidence that strategies generally used by these programs have the potential to influence smoking cessation. In California, 1,736 smokers from a population-based telephone survey were interviewed in 1990 and 1992. We examined the association of demographic and program-related variables (reporting of work area smoking bans; belief in the harmfulness of environmental tobacco smoke, including in-home smoking restrictions; and quitting assistance) with quitting progress. Smokers were categorized into levels in a previously developed Quitting Continuum, which considers their addiction level and quitting history. Smokers in each higher continuum category had an increased likelihood of future successful cessation. Smokers progressed if they were at a higher continuum level in 1992 than in 1990. College graduates showed 2.3 times more progress than did high school dropouts. Smokers reporting work area smoking bans showed 1.6 times more progress than did workers not reporting such restrictions. Smokers with the strongest beliefs (home smoking restrictions) regarding the harmfulness of environmental tobacco smoke showed 3.4 times more progress than smokers with no belief. Smokers who reported having some form of cessation assistance showed 3.0 times more progress. The more program-related factors were reported, the higher the rate of progress was: 13.1% for those reporting no factors, 23.4% for one factor, and 40.6% for two or more. These results suggest but do not prove that strategies promoted by statewide tobacco control programs can potentially be effective and that these efforts should be continued and expanded.

Adult↗

NeuroOmics-Net: An interpretable multimodal deep learning framework for Alzheimer's disease diagnosis and progression prediction using neuroimaging, EEG, and genomic data.

Accurate diagnosis and progression prediction of Alzheimer's disease (AD) remain challenging due to the heterogeneous nature of the disease, which involves structural brain degeneration, electrophysiological dysfunction, and molecular dysregulation. Most existing deep learning approaches rely on a single modality or limited multimodal combinations, thereby failing to capture the complex cross-domain interactions underlying AD progression. Furthermore, the scarcity of large-scale datasets containing synchronized neuroimaging, electrophysiological, and genomic measurements restricts the development of comprehensive multimodal diagnostic systems. To address these challenges, this study proposes NeuroOmics-Net, a multimodal deep learning framework for Alzheimer's disease analysis that integrates structural magnetic resonance imaging (sMRI), electroencephalography (EEG), and gene expression data. The proposed framework combines a Hierarchical Multi-View Encoder (HME) for modality-specific feature extraction, a Cross-Omics Attention Fusion (CAF) module for adaptive integration of complementary biomarkers, and a Disease Progression Graph Learning (DPGL) module for modeling progression-related relationships across biological domains. To facilitate cross-modal integration from independent cohorts, Regularized Canonical Correlation Analysis (RCCA) is employed to align heterogeneous feature representations within a shared latent space. Experiments were conducted using publicly available datasets from ADNI, PhysioNet, and GEO repositories comprising 1120 diagnosis-aligned samples. The proposed framework achieved 94.3% classification accuracy and an AUC of 0.975 for distinguishing normal controls (NC), mild cognitive impairment (MCI), and Alzheimer's disease subjects, while attaining 93.7% accuracy for predicting conversion from stable mild cognitive impairment (sMCI) to progressive mild cognitive impairment (pMCI). However, a fairness sensitivity analysis using stratified demographic reweighting revealed accuracy ranging from 90.8% (low-education, high-comorbidity proxy subgroup) to 96.1% (low-risk, high-reserve proxy subgroup), a demographic parity gap of 5.3 percentage points, indicating that overall accuracy reflects a performance ceiling in a relatively homogeneous research cohort rather than a realistic estimate for demographically diverse clinical populations. Comparative evaluations demonstrated consistent improvements over state-of-the-art unimodal and multimodal deep learning models. Interpretability analysis further identified clinically relevant biomarkers, including hippocampal and entorhinal atrophy, theta-alpha EEG alterations, and APOE-associated molecular pathways. Because sMRI, EEG, and gene expression data were sourced from separate, unpaired cohorts with no subjects possessing all three synchronized measurements, all reported cross-modal associations reflect population-level statistical correspondence across diagnosis-matched groups rather than within-subject physiological coupling; no claim of intra-individual causal cross-modal interaction is made. These findings demonstrate that NeuroOmics-Net provides an effective computer-aided framework for multimodal biomedical data processing and Alzheimer's disease analysis. By integrating neuroimaging, electrophysiological, and genomic information, the proposed approach enables accurate diagnosis, progression prediction, and biologically interpretable decision support for clinical and translational applications.

Humans↗

Prognostic effect of serum glial fibrillary acidic protein and neurofilament light chain for predicting progression independent of relapse activity in multiple sclerosis: A systematic review.

BACKGROUND: Progression independent of relapse activity (PIRA) is increasingly appreciated as one of the important factors contributing to disability accumulation in MS. sGFAP and sNfL could represent markers reflecting two separate biological processes related to relapse-independent progression in MS. OBJECTIVE: To perform a systematic review of the literature on blood GFAP and/or NfL measured in relation to PIRA or other similar relapse-independent progression endpoints in people with MS. METHODS: PubMed, Scopus, and Web of Science databases were searched from inception to 1 June 2026. The eligible studies were original human studies measuring blood GFAP and/or NfL concentrations in serum, plasma, or any other type of blood-derived material and assessing PIRA, PIRMA, CDP/CDW without relapses, relapse-free EDSS progression, non-inflammatory progression, or comparable relapse-independent disability worsening outcomes. Methodological quality was assessed according to the Newcastle-Ottawa scale and the QUIPS instrument for bias detection in the body of evidence on prognostic factors. Due to heterogeneity of outcomes, biomarker measurements and effect estimates, results were synthesized qualitatively rather than quantitatively. RESULTS: After removing duplicates, 1206 records were screened, followed by full-text review of 120 reports. A total of 18 reports were included. Overall, sGFAP was associated more frequently with PIRA or PIRA-like disability progression, particularly in cohorts with suppressed or limited overt inflammatory activity. Evidence for sNfL was more variable and context-dependent: several studies reported associations with PIRA-like or relapse-independent disability worsening when acute inflammatory activity was absent, suppressed, or analytically separated, whereas other studies reported negative or inconclusive findings. Negative or inconclusive results were reported by several articles, particularly when broad outcomes were evaluated or the study population was small. CONCLUSION: Blood GFAP and NfL give complementary but non-interchangeable information concerning PIRA in MS patients. The existing evidence base does not allow us to perform meta-analysis because of heterogeneity in terms of outcomes, standardization of biomarkers, and treatment context. Further prospective investigations with uniform criteria will be necessary for their use as biomarkers of PIRA in clinical settings.

Humans↗

Short-term accrual of gray matter pathology in patients with progressive multiple sclerosis: an in vivo study using diffusion tensor MRI.

The mechanisms underlying the progressive course of multiple sclerosis (MS) are not fully understood yet. Since diffusion tensor (DT) MRI can provide quantitative estimates of both MRI-visible and MRI-occult brain damage related to MS, the present study investigated the value of DT MRI-derived measures for the assessment of the short-term accumulation of white and gray matter (GM) pathology in patients with primary progressive (PP) and secondary progressive (SP) MS. Fifty-four patients with PPMS and 22 with SPMS were studied at baseline and after a mean follow-up of 15 months. Dual-echo, T1-weighted, and DT MRI scans of the brain were acquired on both occasions. Total lesion volumes (TLV) and percentage brain volume changes (PBVC) were computed. Mean diffusivity (MD) and fractional anisotropy (FA) maps of the normal-appearing white (NAWM) and gray matter (NAGM) were produced, and histogram analysis was performed. In both patient groups, a significant increase of average lesion MD (P = 0.01) and of average NAGM MD (P = 0.007) was found at follow-up. No significant differences between PPMS and SPMS patient groups were found for the on-study changes of any MRI-derived measure. No significant correlations were found between the percentage changes of DT MRI-derived measures and those of TLV and PBVC. No significant changes of DT MRI-derived measures were observed in age-matched healthy controls over the same study period. Over a 1-year period of follow-up, DT MRI can detect tissue changes beyond the resolution of conventional MRI in the NAGM of patients with progressive MS. The accumulation of DT MRI-detectable gray matter damage does not seem to merely depend upon the concomitant increase of T2-visible lesion load and the reduction of brain volume. These observations suggest that progressive NAGM damage might yet be an additional factor leading to the accumulation of disability in progressive MS.

Adult↗

Progressive myoclonic ataxia and JC virus encephalitis in an AIDS patient.

A case of progressive myoclonic ataxia in an AIDS patient is described, which evolved over a 13 month period. The ataxia persisted as the only clinical finding for several months before the appearance of a severe tetraparesis and cachexia. Throughout the clinical progression, magnetic resonance imaging (MRI) revealed the presence of bilateral, progressive, isolated, and symmetrical lesions involving the red nuclei, subthalami, thalami, lenticular nuclei, and primary motor cortices. Neuropathological examination, supplemented by in situ hybridisation for JC virus DNA, confirmed that the lesions were those of progressive multifocal leucoencephalopathy (PML). The exceptional clinical presentation of PML in this case is the first report of progressive myoclonic ataxia caused by PML. The selective nature of the lesions confirms the role of the dentato-rubral-thalamo-cortical tract in the pathogenesis of progressive myoclonic ataxia. The atypical MRI findings further emphasise the need for expanded diagnostic criteria for PML in AIDS patients and support the use of more aggressive diagnostic methods as new treatments become available.

Acquired Immunodeficiency Syndrome↗