Evidence map›Paper›PMID 41723778›Full record

ArticleCellular and molecular neurobiology2026

Unravelling Synaptic and Metabolic Mechanisms of Cognitive Resilience in Asymptomatic Alzheimer's Disease Across Two Alzheimer's Disease Cohorts.

Rümeysa Aksu, Hatice Büşra Lüleci, Tunahan Çakır

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Article in Cellular and molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Rümeysa AksuDepartment of Bioengineering, Gebze Technical University, 41400, Kocaeli, Turkey.ORCID http://orcid.org/0009-0005-6462-743X
Hatice Büşra LüleciDepartment of Bioengineering, Gebze Technical University, 41400, Kocaeli, Turkey.ORCID http://orcid.org/0000-0002-7115-7211
Tunahan ÇakırDepartment of Bioengineering, Gebze Technical University, 41400, Kocaeli, Turkey. tcakir@gtu.edu.tr.ORCID http://orcid.org/0000-0001-8262-4420

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asymptomatic Alzheimer's Disease (AsymAD) is a preclinical stage of Alzheimer's Disease (AD) identified by amyloid plaques and neurofibrillary tangles in cognitively normal individuals and offers essential understanding for early diagnosis and treatment of AD. To uncover molecular insights into AsymAD, RNA sequencing (RNA-seq) datasets from two different consortia, ROSMAP (Religious Orders Study and Memory and Aging Project) and MSBB (Mount Sinai Brain Bank), were investigated. The individuals in the datasets were grouped into AD and AsymAD based on clinical and neuropathological criteria. Differentially expressed genes (DEGs), differentially expressed transcripts (DETs), and differentially used transcripts (DUTs) were identified between AD and AsymAD samples. The results were interpreted through functional enrichment analysis and compared with the predefined lists of AD-related and learning-memory-cognition-related genes, and genes from an independent mouse dataset. The genes from the list of DEGs, DETs and DUTs were mapped onto a human protein-protein interaction network, revealing subnetworks associated with AsymAD. This led to the discovery of biomarker candidate genes: NRXN3, DGKB, ADAMTS2, GNG4, ENPP5, PCOLCE, COL25A1, COL26A1, MRPL1, and MRPL30. This study introduces an innovative approach by including DETs and DUTs in the analyses, beyond the standard focus on DEGs, pointing out comprehensive insights into the molecular mechanisms of AsymAD. In addition, combining the results of the subnetwork analysis from DEGs, DETs, and DUTs provided a new perspective to AsymAD and resulted in the discovery of further important genes, which can pave the way for early detection and intervention of AD.

Indexed as

Alzheimer DiseaseAsymptomatic DiseasesCognitionSynapsesAgedAnimalsCohort StudiesFemaleGene Expression ProfilingGene Regulatory NetworksHumansMaleProtein Interaction MapsAsymptomatic Alzheimer’s diseaseBiomarker candidate genesDifferentially expressed genesDifferentially expressed transcriptsDifferentially used transcriptsSubnetwork analysis

Identifiers

PMID41723778
PMCPMC12996523

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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 OpenQuestion graph.