Evidence map›Paper›PMID 26854932›Full record

ArticleExperimental neurology2016

Longitudinal measures of cognition in the Ts65Dn mouse: Refining windows and defining modalities for therapeutic intervention in Down syndrome.

J Luis Olmos-Serrano, William A Tyler, Howard J Cabral, Tarik F Haydar

Abstract read
In one paragraph

Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Sex-specific developmental phenotypes and their response to neonatalbioRxiv : the preprint server for biology · 2026
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  13. Behavioral Phenotyping for Down Syndrome in Mice.Current protocols in mouse biology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

J Luis Olmos-SerranoDepartment of Anatomy and Neurobiology, Boston University School of Medicine, 72 East Concord Street, L-1004, Boston, MA 02118, United States. Electronic address: lolmos@bu.edu.
William A TylerDepartment of Anatomy and Neurobiology, Boston University School of Medicine, 72 East Concord Street, L-1004, Boston, MA 02118, United States. Electronic address: wtyler@bu.edu.
Howard J CabralDepartment of Biostatistics, Boston University School of Public Health, 801 Massachusetts Avenue, Boston, MA 02118, United States. Electronic address: hjcab@bu.edu.
Tarik F HaydarDepartment of Anatomy and Neurobiology, Boston University School of Medicine, 72 East Concord Street, L-1004, Boston, MA 02118, United States. Electronic address: thaydar@bu.edu.
Boston University · US

Funding

Rescue of Forebrain Defects in Mouse Models of Down syndromeR01NS076503 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GALDZICKI, ZYGMUNT, HAYDAR, TARIK F · 2011 to 2015
$2.2M
Forebrain Development in Down Syndrome and in Ts65Dn model miceR01HD057580 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI HAYDAR, TARIK F · 2009 to 2010
$1.1M
NICHD NIH HHS R01 HD057580NINDS NIH HHS R01 NS076503NINDS NIH HHS R01NS076503
6 · The paper itself

Abstract

Mouse models have provided insights into adult changes in learning and memory in Down syndrome, but an in-depth assessment of how these abnormalities develop over time has never been conducted. To address this shortcoming, we conducted a longitudinal behavioral study from birth until late adulthood in the Ts65Dn mouse model to measure the emergence and continuity of learning and memory deficits in individuals with a broad array of tests. Our results demonstrate for the first time that the pace at which neonatal and perinatal milestones are acquired is correlated with later cognitive performance as an adult. In addition, we find that life-long behavioral indexing stratifies mice within each genotype. Our expanded assessment reveals that diminished cognitive flexibility, as measured by reversal learning, is the most robust learning and memory impairment in both young and old Ts65Dn mice. Moreover, we find that reversal learning degrades with age and is therefore a useful biomarker for studying age-related decline in cognitive ability. Altogether, our results indicate that preclinical studies aiming to restore cognitive function in Ts65Dn should target both neonatal milestones and reversal learning in adulthood. Here we provide the quantitative framework for this type of approach.

Indexed as

AgingAnimalsBiomarkersCognitionCognition DisordersDown SyndromeFemaleGenotypeInstinctLearning DisabilitiesMaleMaze LearningMemory DisordersMiceNesting BehaviorReversal LearningBiomarkersAgingAlzheimer DiseaseCognitionDevelopmental disorderDevelopmental milestonesDown syndromeMouse behaviorMouse modelReversal learningTs65Dn

Identifiers

PMID26854932
PMCPMC5716476
OpenAlexW2262837973

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.