ReviewIntractable & rare diseases research2026
The skin as a sentinel organ for neurodegeneration: An underrecognized target for dementia prevention.
Review in Intractable & rare diseases research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dementia prevention increasingly requires attention to modifiable systemic inflammatory stressors. In older adults, bullous pemphigoid (BP), herpes zoster (HZ), psoriasis, atopic dermatitis (AD), rosacea, prurigo nodularis (PN), and chronic pruritus are not merely disorders limited to the skin; they may signal or amplify neuroimmune vulnerability. Observational studies link BP with dementia and Alzheimer's disease, HZ with incident dementia and vascular cognitive injury, and psoriasis, AD, rosacea, or PN with smaller but biologically plausible cognitive risks. The proposed skin-brain axis integrates cytokine spillover, endothelial activation, blood-brain barrier dysfunction, BP180/ BP230 autoantigen sharing, varicellazoster virus neurotropism and vasculopathy, barrier failure, dysbiosis, itching-induced fragmented sleep, and medication or frailty-related cognitive toxicity. Clinically, cognitive impairment also worsens skin surveillance, hygiene, topical adherence, and recognition of pain, itching, infection, or blistering. Although causality and dementia prevention remain unproven, the evidence justifies proactive dermatological care in older adults and greater cognitive vigilance in older patients with severe inflammatory or pruritic dermatoses. Recombinant zoster vaccination, prompt antiviral therapy, steroid-sparing BP strategies, modern anti-inflammatory treatment for AD, psoriasis, and PN, and systematic attention to sleep, itching, caregiver capacity, and the medication burden are practical, low-regret steps while prospective brain-relevant trials are developed. This translational framework highlights mechanisms clinicians can now interrupt and endpoints investigators can soon measure. We propose that the skin should be recognized as a sentinel organ for neurodegeneration and that dermatological disease represents a potentially modifiable contributor to cognitive decline.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.