ArticleCell press blue2026
Tanycytic degeneration impairs tau clearance and contributes to Alzheimer's disease pathology.
Article in Cell press blue, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- A synaptoid connectome differentiates tanycytic subpopulations and underlies neuroglial communication and neuroendocrine regulation.Nature communications · 2026Article
- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Metabolic and renal factors associated with plasma phosphorylated tau analytes used to detect Alzheimer's disease pathology.Alzheimer's & dementia (Amsterdam, Netherlands)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors.
Funding
Abstract
Alzheimer's disease (AD) is characterized by pathological Tau protein accumulation in the brain and cerebrospinal fluid (CSF), instead of timely efflux into the blood. However, the underlying mechanisms are unclear. We show, using animal and cellular models and patient tissues, that tanycytes of the hypothalamic median eminence, which bridge the blood and CSF, are involved in Tau transport and AD pathogenesis. In mice, tanycytes take up CSF-borne Tau and release it into pituitary portal capillaries, whence it enters the systemic circulation. Blocking tanycytic vesicular transport blunts CSF-to-blood Tau efflux and potentiates Tau pathology. In AD patients, plasma-to-CSF ratios of total and p181 Tau are decreased. Tanycytes from postmortem AD patient brains display dramatically fragmented processes and significant transcriptomic alterations by single-nucleus RNA sequencing, notably in vesicular-transport-related genes, explaining this clearance deficit. The involvement of tanycytic dysfunction in human pathophysiology and evidence for a brain-to-blood tanycytic shuttle has far-reaching implications.
Identifiers
What 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.