Evidence map›Paper›PMID 41978790›Full record

ArticleBrain communications2026

Plasma p-tau217 and glucose metabolism correlate in neocortical association areas in Alzheimer's disease.

Lauren N Koenig, Hanna Huber, Anjalika Chongtham, Guglielmo Di Molfetta, Randolph D Andrews, Ana Lukic, Neeva Shafiian, Howard M Fillit, Kaj Blennow, Nicholas J Ashton and 3 more

Abstract read
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In one paragraph

Article in Brain communications, 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

13 authors.

Lauren N KoenigADM Diagnostics, Inc., Northbrook, IL 60062, USA.ORCID https://orcid.org/0000-0003-2279-4510
Hanna HuberDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, 43180 Mölndal, Sweden.
Anjalika ChongthamDepartment of Neurology, Icahn School of Medicine at Mount Sinai, NewYork, NY 10029, USA.ORCID https://orcid.org/0000-0001-8437-3899
Guglielmo Di MolfettaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, 43180 Mölndal, Sweden.ORCID https://orcid.org/0009-0001-5339-933X
Randolph D AndrewsADM Diagnostics, Inc., Northbrook, IL 60062, USA.ORCID https://orcid.org/0000-0002-1712-1920
Ana LukicADM Diagnostics, Inc., Northbrook, IL 60062, USA.
Neeva ShafiianDepartment of Neurology, Icahn School of Medicine at Mount Sinai, NewYork, NY 10029, USA.ORCID https://orcid.org/0009-0009-5683-1026
Howard M FillitThe Alzheimer's Drug Discovery Foundation, NewYork, NY 10019, USA.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, 43180 Mölndal, Sweden.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, 43180 Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, 43180 Mölndal, Sweden.ORCID https://orcid.org/0000-0003-3930-4354
Dawn C MatthewsADM Diagnostics, Inc., Northbrook, IL 60062, USA.ORCID https://orcid.org/0000-0002-0516-7470
Ana C PereiraDepartment of Neurology, Icahn School of Medicine at Mount Sinai, NewYork, NY 10029, USA.

Funding

Mechanisms of Susceptibility of Excitatory Neurons to Tau Pathology and Neurodegeneration in Alzheimer's diseaseR01AG063819 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PEREIRA, ANA C. · 2020 to 2024
$3.9M
Mechanisms of Obstructive Sleep Apnea in Tau Pathophysiology, Risk and Progression of Alzheimer's DiseaseR01AG064020 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PEREIRA, ANA C. · 2019 to 2023
$2.9M
NIA NIH HHS R01 AG063819NIA NIH HHS R01 AG064020
6 · The paper itself

Abstract

While the biomarkers available for Alzheimer's disease are continually expanding, including clinically approved blood tests, not all of the relationships between various biomarkers have been fully elucidated. In this study, we explore how regional brain metabolism, as measured by fludeoxyglucose-18 (FDG)-PET, relates to plasma biomarkers such as p-tau217, Glial fibrillary acidic protein (GFAP), phosphorylated-tau (p-tau)217/beta-amyloid (Aβ) 42, and Aβ42/40 in a cohort of participants with early symptomatic Alzheimer's disease. P-tau217 showed a consistent pattern of participants with higher p-tau217 levels having increased hypometabolism in Alzheimer's disease-related regions in neocortical association areas such as the lateral temporal cortex, the precuneus and inferior parietal cortex and atrophy accompanied by greater cognitive impairment. GFAP also related to regional hypometabolism and atrophy in regions known to be affected in Alzheimer's disease, though with a slightly different regional pattern. We additionally observed that participants with equivalent biomarker levels still exhibited diverse patterns of FDG-PET and atrophy. This suggests that, despite the above correlations, imaging provides additional information. These findings support and extend our knowledge of how plasma p-tau217 relates to other Alzheimer's disease biomarkers and cerebral metabolism, helping to contextualize both the benefits and limitations of these plasma biomarkers.

Indexed as

Alzheimer’s diseaseFDG-PETplasmap-tau217tau protein

Identifiers

PMID41978790
PMCPMC13070614

What Socratic holds

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Registered trials

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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 Socratic graph.