ReviewCellular and molecular neurobiology2025
Targeting Neuronal Alpha7 Nicotinic Acetylcholine Receptor Upregulation in Age-Related Neurological Disorders.
Review in Cellular and molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Nicotine in Neurodegenerative and Neuropsychiatric Disorders: Mechanisms and Clinical Evidence.Neurochemical research · 2026Review
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- Common metabolic, environmental, and molecular mechanisms underlying neurodevelopmental and neurodegenerative disorders.Frontiers in neurology · 2026Review
- Functional deletion of α7 nicotinic acetylcholine receptor impairs CaFrontiers in physiology · 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
3 authors.
Funding
Abstract
The multifunctional roles of alpha7 nicotinic acetylcholine receptors (α7nAChRs), ranging from cognitive enhancement, neuroprotection, and anti-inflammatory action, credit tagging this receptor as "unique" among the cholinergic receptor family. The uniqueness of α7nAChRs in neuronal function and communication lies in their high calcium permeability among the cholinergic receptor family. The ionotropic function of α7nAChRs is governed by protein kinases' post-translational modification (PTMs), which alter their expression and function, affecting neuronal communication. A decrease in the ionotropic function of α7nAChRs and its downstream signaling pathways is observed across many neurologic disorders. The loss of α7nAChRs, decreased cholinergic function, and increased acetylcholinesterase levels are commonly associated with neuronal degeneration, cognitive impairment, and decreased memory function. An extensive body of evidence suggests the cognitive benefits of simple nutraceutical supplementation, Vitamin D3 (VD), in many neurologic disorders (Skv et al. in Mol Neurobiol 61:7211-7238, 2024). The present review will, however, focus on recent and past evidence deciphering the unique properties of α7nAChRs crucial for brain function. We have also emphasized on the therapeutic benefits of VD supplementation in restoring cholinergic neurotransmission and α7nAChRs expression in various neuropsychiatric and neurologic disorders.
Indexed as
Identifiers
What Socratic 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 Socratic graph.