Article in Journal of Alzheimer's disease : JAD, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
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
1 citing paper in PubMed, 4 citations in OpenAlex.
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
4 authors at 3 institutions in 2 countries.
Pasquale MoneDepartment of Molecular Pharmacology, Einstein Institute for Neuroimmunology and Inflammation, Albert Einstein College of Medicine, New York, NY, USA.
Antonio De LucaDepartment of Mental and Physical Health and Preventive Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.
Urna KansakarDepartment of Molecular Pharmacology, Einstein Institute for Neuroimmunology and Inflammation, Albert Einstein College of Medicine, New York, NY, USA.
Gaetano SantulliDepartment of Molecular Pharmacology, Einstein Institute for Neuroimmunology and Inflammation, Albert Einstein College of Medicine, New York, NY, USA.
Albert Einstein College of Medicine · USUniversity of Campania "Luigi Vanvitelli" · ITUniversity of Molise · IT
Funding
CTSA Administrative Supplement for Informatics Core: A novel AI/ML system to predict respiratory failure and ARDS in Covid-19 patientsUL1TR002556 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI KELLER, MARLA J, KIM, MIMI Y · 2018 to 2022
$26.7M
Einstein-Montefiore Clinical and Translational Science Award HubUM1TR004400 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Jessica Kahn, Mimi Y Kim · 2023 to 2026
$17.3M
REGULATION OF THE INSULIN RECEPTOR KINASER01DK033823 · NIDDK · UNIVERSITY OF IOWA · PI KURLAND, IRWIN JACK, PESSIN, JEFFREY E. · 1986 to 2022
$6.7M
Modulation of Mitofusin Activity to Treat Heart DiseaseR01HL159062 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI KITSIS, RICHARD N · 2021 to 2024
$2.6M
Caspase-9 as a nodal point connecting necrotic and apoptotic cell death in myocardial infarctionR01HL164772 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI KITSIS, RICHARD N · 2022 to 2025
$2.5M
Functional role of IP3 receptors in the regulation of cardiac myofibroblastsR01HL146691 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SANTULLI, GAETANO · 2019 to 2023
$2.1M
Mechanisms of cardiovascular diseaseT32HL144456 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Carlos Jose Rodriguez, Nicholas E Sibinga · 2019 to 2026
$1.9M
Beta Cell Intracellular Calcium and DiabetesR01DK123259 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI SANTULLI, GAETANO · 2020 to 2023
Alzheimer's disease (AD) is a neurodegenerative disorder marked by amyloid-β accumulation, tau dysfunction, and neuroinflammation, involving endothelial cells and leukocytes. The breakdown of the blood-brain barrier allows immune cell infiltration, intensifying inflammation. A decreased ratio of Connexin-37 (Cx37, also known as GJA4: Gap Junction Protein Alpha 4) and Prolyl Hydroxylase Domain-Containing Protein 3 (PHD3, also known as EGLN3: Egl-9 Family Hypoxia Inducible Factor 3), Cx37/PHD3, consistently observed in different AD-related models, may represent a novel potential biomarker of AD, albeit the exact mechanisms underlying this phenomenon, most likely based on gap junction-mediated cellular interaction that modulate the cellular metabolite status, remain to be fully elucidated.
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.
Leukocytes and Endothelial Cells Participate in the Pathogenesis of Alzheimer's Disease: Identifying New Biomarkers Mirroring Metabolic Alterations. · full record | OpenQuestion