ReviewDevelopmental neuroscience2011
On the promise of pharmacotherapies targeted at cognitive and neurodegenerative components of Down syndrome.
Review in Developmental neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Pharmacological interventions for cognitive decline in people with Down syndrome.The Cochrane database of systematic reviews · 2015Pooled it
- Antagonism of NMDA receptors as a potential treatment for Down syndrome: a pilot randomized controlled trial.Translational psychiatry · 2012Trial
- Profiling hippocampal neuronal populations reveals unique gene expression mosaics reflective of connectivity-based degeneration in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease.Frontiers in molecular neuroscience · 2025Article
- Breathing and Oxygen Carrying Capacity in Ts65Dn and Down Syndrome.Function (Oxford, England) · 2023Article
- Computerized physical and cognitive training improves the functional architecture of the brain in adults with Down syndrome: A network science EEG study.Network neuroscience (Cambridge, Mass.) · 2021Article
- On the Design of Broad-Based Neuropsychological Test Batteries to Assess the Cognitive Abilities of Individuals with Down Syndrome in the Context of Clinical Trials.Brain sciences · 2018Review
- Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome.Neurobiology of disease · 2017Article
- Early neurotrophic pharmacotherapy rescues developmental delay and Alzheimer's-like memory deficits in the Ts65Dn mouse model of Down syndrome.Scientific reports · 2017Article
- SHH desmoplastic/nodular medulloblastoma and Gorlin syndrome in the setting of Down syndrome: case report, molecular profiling, and review of the literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2016Review
- Article
- Cardiac autonomic modulation of children with Down syndrome.Pediatric cardiology · 2015Article
- A new cognitive evaluation battery for Down syndrome and its relevance for clinical trials.Frontiers in psychology · 2015Article
- Review
- Global DNA hypermethylation in down syndrome placenta.PLoS genetics · 2013Article
- Alzheimer disease: Treatment of Alzheimer disease in Down syndrome.Nature reviews. Neurology · 2012Article
- From abnormal hippocampal synaptic plasticity in down syndrome mouse models to cognitive disability in down syndrome.Neural plasticity · 2012Review
- Age-related neurodegeneration and memory loss in down syndrome.Current gerontology and geriatrics research · 2012Article
- Neurological phenotypes for Down syndrome across the life span.Progress in brain research · 2012Review
- Exaggerated NMDA mediated LTD in a mouse model of Down syndrome and pharmacological rescuing by memantine.Learning & memory (Cold Spring Harbor, N.Y.) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Down syndrome (DS) is the phenotypic consequence of trisomy 21 and is the most common genetically defined cause of intellectual disability. The most complete, widely available, and well-studied animal model of DS is the Ts65Dn mouse. Recent preclinical successes in rescuing learning and memory deficits in Ts65Dn mice are legitimate causes for optimism that pharmacotherapies for cognitive deficits in DS might be within reach. This article provides a snapshot of potential pharmacotherapies for DS, with emphasis on our recent results showing that the N-methyl-D-aspartate receptor antagonist memantine can reverse learning and memory deficits in Ts65Dn mice. Because memantine has already been approved for the therapy of Alzheimer's dementia, we have been able to very rapidly translate these results into human research and are currently conducting a 16-week, randomized, double-blind, placebo-controlled evaluation of the efficacy, tolerability and safety of memantine hydrochloride on enhancing the cognitive abilities of young adults with DS. The design and current status of this clinical trial will be discussed, which will be followed by some speculation on the potential impact of this and future clinical trials in the field of DS.
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.