Enhanced expression of autophagy‐related p62 without increased deposits of neurodegeneration‐associated proteins in glioblastoma and surrounding tissue – An autopsy‐based study
Bibliographic record
Abstract
Neurodegenerative diseases are a major health burden. The underlying causes are not yet fully understood, but different mechanisms such as cell stress and chronic inflammation have been described as contributing factors. Neurodegenerative changes have been observed in the vicinity of brain tumors, typically around slowly growing benign lesions. Moreover, in-vitro data suggest a potential induction of pathological tau deposits also in glioblastoma, a highly malignant and proliferative brain cancer. The aim of this study was to evaluate neurodegeneration-associated protein deposition and autophagy as well as microglial activation within and surrounding glioblastoma. Post-mortem brain tissue of 22 patients with glioblastoma was evaluated immunohistochemically for phosphorylated tau, beta-amyloid, alpha-synuclein and phosphorylated TDP-43. Additionally, the autophagy marker p62 and the microglial marker HLA-DR were investigated. The data was compared to 22 control cases and ten cases with other space occupying brain lesions. An increase of p62-immunoreactivity was observed within and adjacent to the glioblastoma tumor tissue. Moreover, dense microglial infiltration in the tumor tissue and the immediate surrounding brain tissue was a constant feature. Deposition of neurodegeneration-associated proteins was found in the majority of cases (86.4%) but in distant sites. These findings suggested a preexisting neurodegenerative pathology, which followed a typical distributional pattern: ten cases with Alzheimer disease neuropathological changes, including two severe cases, eight cases with primary age-related tauopathy, six cases with aging-related tau astrogliopathy and one case with progressive supranuclear palsy. Collectively, our data suggests enhanced autophagy in glioblastoma tumor cells and the surrounding brain. The variety and distribution of distant neurodegeneration-associated protein aggregates observed in the majority of cases, suggest a preexisting rather than a tumor-induced neurodegenerative condition.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".