ReviewFrontiers in pharmacology2025
Current insights and prospects for the pathogenesis and treatment of clinical manifestations associated with Down syndrome through neurotransmitter, inflammatory, and oxidative stress pathways.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndrome.Brain research bulletin · 2026Article
- Harnessing the microbiota-gut-brain axis to prevent and treat pediatric neurodevelopmental disorders: translational insights and strategies.Journal of translational medicine · 2025Review
- Pro-Inflammatory Protein PSCA Is Upregulated in Neurological Diseases and Targets β2-Subunit-Containing nAChRs.Biomolecules · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Individuals with Down syndrome exhibit various changes in the human body systems, including alterations in the ocular, neurological, and dermatological systems. Especially, preclinical and clinical studies have determined Down syndrome patients to possess reduced intellectual and cognition abilities, which neurobehavioral effects are associated with altered molecular markers in the brain. For instance, neuroinflammation and increased brain oxidative stress are reported in animals models of Down syndrome, and the reversal of those markers lead to positive effects. Dopaminergic and serotonergic neurons are altered in individuals with Down syndrome, with dopamine and serotonin secretion reduced and their transporters upregulated. Hence, blocking reuptake of dopamine and serotonin might improve Down syndrome behavioral impairments. Norepinephrine loss was observed in a mouse model of Down syndrome, and treatment with a β2 adrenergic receptor agonist improved behavioral symptoms. Moreover, targeting certain glutamatergic receptors, particularly in the hippocampus, might correct the glutamatergic dysfunction and altered behaviors. Inverse agonists or antagonists of GABAergic receptors suppress GABA's inhibitory role, an effect associated with improved cognition behaviors in models of Down syndrome. Reports also suggest partial involvement of the histaminergic system in the impairment of memory function observed in Down syndrome. Finally, cholinergic system alteration has been reported, but the therapeutic role of its modulation needs further investigation. This review collects and reports multi-Omics Studies on Down syndrome, the crucial roles of inflammation, oxidative stress independently as well as role of oxidative stress in pregnancies with Down Syndrome and biomarkers of maternal diagnosis of Down syndrome. This review further explained the role of neurotransmitter pathways in Down syndrome pathogenesis, prognosis and therapeutic intervention for Down syndrome and future directions for interventions.
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.