ReviewInflammopharmacology2025
Impact of corticoid receptors on Alzheimer's disease: a neuroendocrine perspective.
Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Higher baseline CSF cortisol is associated with adverse 24-month tau-related, neuroimaging, and cognitive outcomes across the Alzheimer's disease continuum.European geriatric medicine · 2026Article
- A multi-omic atlas in the African turquoise killifish reveals increased glucocorticoid signaling as a hallmark of brain aging.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that has been strongly associated with changes in corticoid receptor function and HPA axis dysregulation. This review gives an overview of the complex role of GC and MC receptors in AD, especially how chronic exposure to elevated cortisol contributes to hippocampal degeneration, oxidative stress, and cognitive decline. Specific emphasis lies with cortisol, brought to the attention of neurotoxicity, and relates it to Cushing syndrome with chronic hyper-cortisolism simulating cognitive and structural impairments seen in AD. The impact of HPA axis over-activity in AD pathology is presented, demonstrating its contribution to neuro-inflammation and possible utilization as a biomarker for disease progression. This review further includes pharmacological strategies that modulate corticoid receptors for the reduction of GC-induced neurotoxicity and includes selective GR antagonists and MR agonists. Lifestyle modifications, which modulate HPA activity, are the other non-pharmacological approach to managing AD. Finally, novel drugs and interventions targeting the regulation of GC, anti-inflammatory pathways, as well as attenuation of oxidative stress are emerging strategies. Such a strategy implies that it is possible that receptor activity balance can delay or arrest AD progression.
Indexed as
Identifiers
40249479What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.