ArticleFrontiers in molecular neuroscience2022
Potential biomarkers of Alzheimer's disease and cerebral small vessel disease.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 13 citations in OpenAlex.
- Sex differences in neuromodulatory subcortical systems and their implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- The value of machine learning models in differentiating alzheimer's disease from Moderate-to-Severe cerebral small vessel disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Bioinformatics identification and experimental validation of hub genes associated with narcolepsy type 1.Journal of clinical and translational science · 2026Article
- Single-Nucleus Landscape of Glial Cells and Neurons in Alzheimer's Disease.Molecular neurobiology · 2025Article
- The Role of Changes in the Expression of Inflammation-Associated Genes in the Variants of Cerebral Small Vessel Disease.International journal of molecular sciences · 2024Article
- Downregulation of miR-181c-5p in Alzheimer's disease weakens the response of microglia to Aβ phagocytosis.Scientific reports · 2024Article
- Identification of altered immune cell types and molecular mechanisms in Alzheimer's disease progression by single-cell RNA sequencing.Frontiers in aging neuroscience · 2024Article
- Transcriptional patterns of brain structural abnormalities in CSVD-related cognitive impairment.Frontiers in aging neuroscience · 2024Article
- The Role of Oxytocin in Alzheimer's Disease and Its Relationship with Social Interaction.Cells · 2023Review
- Exploration of novel biomarkers in Alzheimer's disease based on four diagnostic models.Frontiers in aging neuroscience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cerebral small vessel disease (CSVD) is associated with the pathogenesis of Alzheimer's disease (AD). Effective treatments to alleviate AD are still not currently available. Hence, we explored markers and underlying molecular mechanisms associated with AD by utilizing gene expression profiles of AD and CSVD patients from public databases, providing more options for early diagnosis and its treatment. Methods: Gene expression profiles were collected from GSE63060 (for AD) and GSE162790 (for CSVD). Differential analysis was performed between AD and mild cognitive impairment (MCI) or CSVD progression and CSVD no-progression. In both datasets, differentially expressed genes (DEGs) with the same expression direction were identified as common DEGs. Then protein-protein interaction (PPI) network was constructed for common DEGs. Differential immune cells and checkpoints were calculated between AD and MCI. Results: A total of 146 common DEGs were identified. Common DEGs were mainly enriched in endocytosis and oxytocin signaling pathways. Interestingly, endocytosis and metabolic pathways were shown both from MCI to AD and from CSVD no-progression to CSVD progression. Moreover, SIRT1 was identified as a key gene by ranking degree of connectivity in the PPI network. SIRT1 was associated with obesity-related genes and metabolic disorders. Additionally, SIRT1 showed correlations with CD8 T cells, NK CD56 bright cells, and checkpoints in AD. Conclusion: The study revealed that the progression of AD is associated with abnormalities in gene expression and metabolism and that the SIRT1 gene may serve as a promising therapeutic target for the treatment of AD.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.