Evidence map›Paper›PMID 42712109›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Tau-associated neuronal loss in the intermediate nucleus of the human hypothalamus, a putative VLPO analog, in progressive supranuclear palsy and Alzheimer's disease.

Shima Rastegar-Pouyani, Caroline Lew, Felipe L Pereira, Abhijit Satpati, Ana Moreno Arnas, Vitor Paes, Renata Elaine Paraízo Leite, Claudia Kimie Suemoto, Salvatore Spina, Gowoon Son and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Shima Rastegar-PouyaniFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Caroline LewFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Felipe L PereiraDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Abhijit SatpatiFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Ana Moreno ArnasDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Vitor PaesPhysiopathology in Aging Laboratory (LIM-22), Department of Pathology, University of São Paulo Medical School, Sao Paulo, Brazil.
Renata Elaine Paraízo LeitePhysiopathology in Aging Laboratory (LIM-22), Department of Pathology, University of São Paulo Medical School, Sao Paulo, Brazil.
Claudia Kimie SuemotoDivision of Geriatrics, Department of Internal Medicine, University of São Paulo Medical School, Sao Paulo, Brazil.
Salvatore SpinaFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Gowoon SonDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Helmut HeinsenUniversity of Wuerzburg, Würzburg, Bavaria, Germany.
William W SeeleyFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Christine M WalshFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Thomas C NeylanDepartments of Psychiatry and Neurology, University of California San Francisco, San Francisco, California, USA.
Lea T GrinbergFein Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.ORCID https://orcid.org/0000-0002-6809-0618

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Katherine P Rankin · 2019 to 2026
$36.9M
Investigating regional and cellular vulnerabilities to tau pathology in young-onset Alzheimer's diseaseR01AG075802 · NIA · MAYO CLINIC JACKSONVILLE · PI BERNARDINO Francesco GHETTI, Lea Tenenholz Grinberg · 2022 to 2026
$15.5M
Clinical Features and Neuropathological Basis of Sleep Wake Behavior in Alzheimer's and PSPR01AG060477 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Lea Tenenholz Grinberg, Thomas C Neylan · 2019 to 2026
$8.2M
Linking Sleep Dysfunction to Tau-related Degeneration across AD ProgressionR01AG064314 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRINBERG, LEA TENENHOLZ, NEYLAN, THOMAS C · 2019 to 2023
$4.0M
Neuropathological changes underlying clinical heterogeneity in Alzheimer diseaseK24AG053435 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRINBERG, LEA TENENHOLZ · 2016 to 2025
$1.8M
NIA NIH HHS K24 AG053435NIA NIH HHS P01 AG019724NIA NIH HHS P30 AG062422NIA NIH HHS R01 AG060477NIA NIH HHS R01 AG064314NIA NIH HHS R01 AG075802NIH HHS NIA K24 AG053435NIH HHS P01AG019724NIH HHS P30 ADRC AG062422NIH HHS R01 AG060477NIH HHS R01AG064314NIH HHS R01AG075802Rainwater Charitable Foundation
6 · The paper itself

Abstract

backgroundSleep phenotypes differ in progressive supranuclear palsy (PSP) and Alzheimer's disease (AD). The human intermediate nucleus (IntN), a putative ventrolateral preoptic analog, promotes non-rapid eye movement (NREM) sleep, but its disease-specific vulnerability is unclear.

methodsPost mortem hypothalami (n = 30; baseline [Braak stage I-II] n = 6; PSP n = 9; Braak III-IV n = 4; Braak V-VI n = 11) underwent marker-guided IntN delineation, galanin/phospho-tau (T231) immunohistochemistry, and stereology.

resultsAdvanced PSP showed profound IntN degeneration (84% neuron reduction vs baseline). In AD neuropathologic change, IntN neuronal loss and phospho-tau burden were greater in higher Braak stages and preferentially affected galanin-positive neurons (≈77% reduction in late AD); phospho-tau burden was higher in galanin-positive neurons.

conclusionsThe IntN is a disease-sensitive node, with near-ablation in PSP and progressive, preferential loss of detectable galaninergic neurons in AD. Although longitudinal observations and premortem sleep/wake measurements were not available for this sample, these findings are consistent with disease-level differences in NREM/ slow-wave sleep disturbance reported in PSP and AD.

Indexed as

Alzheimer DiseaseHypothalamusNeuronsSupranuclear Palsy, Progressivetau ProteinsAgedAged, 80 and overFemaleGalaninHumansMalePhosphorylationGalanintau Proteinsautopsyhumanintermediate nucleus of the hypothalamusneuronal vulnerabilityprogressive supranuclear palsyslow wave sleepstereologytautypical and atypical Alzheimer's disease

Identifiers

PMID42712109
PMCPMC13554983

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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.