Statin is associated with higher cortical thickness in early Alzheimer's disease
Bibliographic record
Abstract
BACKGROUND: The brain is the most cholesterol-rich organ, essential for myelination and neuronal function. Statins, widely used to lower cholesterol, cross the blood-brain barrier and may impact brain cholesterol synthesis. Despite their widespread use, the effects of statins on cortical regions relevant to Alzheimer's disease (AD) are not well understood. This study aimed to compare cortical thickness between statin-exposed and statin-unexposed older adults and evaluate the potential neuroprotective effects of statins. METHODS: Data were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI). The sample included 193 healthy controls (HC), 485 individuals with mild cognitive impairment (MCI), and 169 individuals with Alzheimer's disease (AD). Participants were categorized as statin users if they had used statins for at least two years. MRI data were processed using FreeSurfer software to estimate cortical thickness in 64 regions of interest. ANCOVA models assessed the association between statin use and cortical thickness at baseline, and linear mixed models evaluated longitudinal changes. RESULTS: Statin use was associated with increased cortical thickness in multiple brain regions across HC, MCI, and AD participants. In HC, statin users had greater thickness in the right lateral occipital, left middle temporal, and left parahippocampal regions. MCI participants exhibited additional increases in the right cuneus, right posterior cingulate, and left superior temporal cortex. In AD, statin users had higher thickness in the right cuneus and right superior parietal lobule. Longitudinal analysis revealed no statin-related differences in cortical thickness changes among HC and AD groups, but in MCI, statins slowed cortical thinning in the left medial orbitofrontal cortex. CONCLUSION: Statin use is associated with greater cortical thickness in older adults, particularly in those with MCI. These findings suggest that statins may have neuroprotective effects, potentially mitigating neurodegenerative changes in early cognitive decline. Further research with larger cohorts and longer follow-up periods is needed to confirm these findings and understand the mechanisms involved.
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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 | 0.000 | 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".