ArticleCurrent psychosis & therapeutics reports2006
Emerging Novel Treatments for Severe Mood Disorders Involving Cellular Plasticity Cascades.
Article in Current psychosis & therapeutics reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Transcriptomic Studies of Antidepressant Action in Rodent Models of Depression: A First Meta-Analysis.International journal of molecular sciences · 2022Pooled it
- Article
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 at 1 institution in 1 country.
Funding
Abstract
Mood disorders are the most prevalent psychiatric disorders. Despite recent advances in the understanding of therapeutically relevant biochemical pathways associated with mood regulation, patients with bipolar disorder and major depression present high rates of recurrences, residual symptoms, and pharmacologic refractoriness. Increasing evidence supports the observations that mood disorders are accompanied by regional brain volumetric reductions accompanied by cellular atrophy/loss. In this paper, we review and critique the data suggesting that neurotrophic signaling cascades may play a role in the pathophysiology and treatment of mood disorders. This suggests that effective treatments will need to provide both trophic and neurochemical support, which serves to enhance and maintain normal synaptic connectivity, thereby allowing the chemical signal to reinstate optimal functioning of critical circuits necessary for normal affective functioning. For many refractory patients, drugs mimicking "traditional" strategies, which directly or indirectly alter monoaminergic levels, may be of limited benefit. Newer "plasticity enhancing" strategies that may have utility in the treatment of mood disorders include inhibitors of glutamate release, NMDA antagonists, AMPA potentiators, cAMP phosphodiesterase inhibitors, and glucocorticoid receptor antagonists.
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.