ArticleNeurobiology of aging2014
Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amyloid beta production.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- The aging epigenome: integrative analyses reveal intersection with Alzheimer's disease.GeroScience · 2026Pooled it
- Pooled it
- Calmodulin controls spatial and temporal specificity of calcium-induced calcium release.PLoS computational biology · 2026Article
- No-observed-adverse-effect-level (NOAEL) clothianidin, a neonicotinoid pesticide, impairs hippocampal memory and motor learning associated with alteration of gene expression in cerebellum.The Journal of veterinary medical science · 2024Article
- Exploring the role of mitochondrial uncoupling protein 4 in brain metabolism: implications for Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Chronic Administration of Ion Channel Blockers Impact Microglia Morphology and Function in a Murine Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- CaNeuropharmacology · 2023Article
- Systemic Inflammation Causes Microglial Dysfunction With a Vascular AD phenotype.Brain, behavior, & immunity - health · 2023Article
- Age-dependent expression of ion channel genes in rat.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- CaInternational journal of molecular sciences · 2022Review
- Vascular calcium signalling and ageing.The Journal of physiology · 2021Review
- Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model.Current medical science · 2021Article
- Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability.Frontiers in neural circuits · 2021Article
- Advances in transcriptome analysis of human brain aging.Experimental & molecular medicine · 2020Review
- Aging, calcium channel signaling and vascular tone.Mechanisms of ageing and development · 2020Review
- SAK3 Administration Improves Spine Abnormalities and Cognitive Deficits in AppInternational journal of molecular sciences · 2020Article
- Verapamil and Alzheimer's Disease: Past, Present, and Future.Frontiers in pharmacology · 2020Review
- Folate-Dependent Cognitive Impairment Associated With Specific Gene Networks in the Adult Mouse Hippocampus.Frontiers in nutrition · 2020Article
- The Puzzling Role of Neuron-Specific PMCA Isoforms in the Aging Process.International journal of molecular sciences · 2019Review
- CaAging cell · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's is a crippling neurodegenerative disease that largely affects aged individuals. Decades of research have highlighted age-related changes in calcium homeostasis that occur before and throughout the duration of the disease, and the contributions of such dysregulation to Alzheimer's disease pathogenesis. We report an age-related decrease in expression of the CaV3.1 T-type calcium channel at the level of messenger RNA and protein in both humans and mice that is exacerbated with the presence of Alzheimer's disease. Downregulating T-type calcium channels in N2a cells and the 3xTg-AD mouse model of Alzheimer's disease, by way of pharmacologic inhibition with NNC-55-0396, results in a rapid increase in amyloid beta production via reductions in non-amyloidogenic processing, whereas genetic overexpression of the channel in human embryonic kidney cells expressing amyloid precursor protein produces complementary effects. The age-related decline in CaV3.1 expression may therefore contribute to a pro-amyloidogenic environment in the aging brain and represents a novel opportunity to intervene in the course of Alzheimer's disease pathogenesis.
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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.