ArticleNeurology2020
Effect of escitalopram on Aβ levels and plaque load in an Alzheimer mouse model.
Article in Neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Efficacy of selective serotonin reuptake inhibitors-related antidepressants in Alzheimer's disease: a meta-analysis.European journal of medical research · 2024Pooled it
- Effect of escitalopram dose and treatment duration on CSF Aβ levels in healthy older adults: A controlled clinical trial.Neurology · 2020Trial
- Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026Review
- Lower Plasma Serotonin is Associated with Higher Amyloid Burden, Hippocampal Atrophy, and Cognitive decline in Alzheimer's Disease: A 24-Month Longitudinal Study.Journal of molecular neuroscience : MN · 2026Article
- Galantamine as add-on therapy to escitalopram: enhancing antidepressant therapeutic potential via. Targeting α7nAChR/BDNF/KYN signalling.Psychopharmacology · 2026Article
- Prioritizing repurposable drugs for Alzheimer's disease using network-based analysis with concurrent assessment of Long QT syndrome risk.Biotechnology reports (Amsterdam, Netherlands) · 2025Article
- Targeting the serotonergic system in the treatment of neurodegenerative diseases-emerging therapies and unmet challenges.Pharmacological reviews · 2025Review
- Fecal Microbiota Transplantation in Alzheimer's Disease: Mechanistic Insights Through the Microbiota-Gut-Brain Axis and Therapeutic Prospects.Microorganisms · 2025Review
- Anxious-depressive symptoms and sleep disturbances across the Alzheimer disease spectrum.Nature. Mental health · 2025Article
- Repurposing Sigma-1 Receptor-Targeting Drugs for Therapeutic Advances in Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Therapeutic modulation of neurogenesis to improve hippocampal plasticity and cognition in aging and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Deciphering the Functions of Raphe-Hippocampal Serotonergic and Glutamatergic Circuits and Their Deficits in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Neurobiological and therapeutic landmarks of depression associated with Alzheimer's disease dementia.Frontiers in aging neuroscience · 2025Review
- Systemic Modulators: Potential Mechanism for the 5-HT System to Mediate Exercise Amelioration in Alzheimer's Disease.Aging and disease · 2024Review
- Microbiota-gut-brain axis and its therapeutic applications in neurodegenerative diseases.Signal transduction and targeted therapy · 2024Review
- Potential drugs for the treatment of Alzheimer's disease.Pharmacological reports : PR · 2023Review
- Metabolomic and lipidomic signatures in autosomal dominant and late-onset Alzheimer's disease brains.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Beyond "Psychotropic": Repurposing Psychiatric Drugs for COVID-19, Alzheimer's Disease, and Cancer.The Journal of clinical psychiatry · 2023Review
- The Role of α-Synuclein in the Regulation of Serotonin System: Physiological and Pathological Features.Biomedicines · 2023Review
- Differences in pharmacologic and demographic factors in male and female patients with vascular dementia, Alzheimer's disease, and mixed vascular dementia.Frontiers in dementia · 2023Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSeveral neurotransmitter receptors activate signaling pathways that alter processing of the amyloid precursor protein (APP) into β-amyloid (Aβ). Serotonin signaling through a subset of serotonin receptors suppresses Aβ generation. We proposed that escitalopram, the most specific selective serotonin reuptake inhibitor (SSRI) that inhibits the serotonin transporter SERT, would suppress Aβ levels in mice.
objectivesWe hypothesized that acute treatment with escitalopram would reduce Aβ generation, which would be reflected chronically with a significant reduction in Aβ plaque load.
methodsWe performed in vivo microdialysis and in vivo 2-photon imaging to assess changes in brain interstitial fluid (ISF) Aβ and Aβ plaque size over time, respectively, in the APP/presenilin 1 mouse model of Alzheimer disease treated with vehicle or escitalopram. We also chronically treated mice with escitalopram to determine the effect on plaques histologically.
resultsEscitalopram acutely reduced ISF Aβ by 25% by increasing α-secretase cleavage of APP. Chronic administration of escitalopram significantly reduced plaque load by 28% and 34% at 2.5 and 5 mg/d, respectively. Escitalopram at 5 mg/kg did not remove existing plaques, but completely arrested individual plaque growth over time.
conclusionsEscitalopram significantly reduced Aβ in mice, similar to previous findings in humans treated with acute dosing of an SSRI.
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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.