Evidence map›Paper›PMID 26391050›Full record

ReviewCurrent Alzheimer research2016

Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome.

Eric D Hamlett, Heather A Boger, Aurélie Ledreux, Christy M Kelley, Elliott J Mufson, Maria F Falangola, David N Guilfoyle, Ralph A Nixon, David Patterson, Nathan Duval and 1 more

Abstract readReview
In one paragraph

Review in Current Alzheimer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Targeting dysregulated CB1 receptors in a Down syndrome mouse model improves neurological outcomes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

11 authors at 1 institution in 1 country.

Eric D Hamlett
Heather A Boger
Aurélie Ledreux
Christy M Kelley
Elliott J Mufson
Maria F Falangola
David N Guilfoyle
Ralph A Nixon
David Patterson
Nathan Duval
Ann-Charlotte E GranholmDepartment Neurosciences, Director, Center on Aging, Medical Univ. South Carolina, Basic Science Bldg, Room 403, 173 Ashley Avenue, Charleston, SC 29425, USA. Granholm@musc.edu.
Medical University of South Carolina · US

Funding

Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0M
An animal model for age-related degenerationR01AG012122 · NIA · UNIVERSITY OF COLORADO DENVER · PI GRANHOLM-BENTLEY, ANN-CHARLOTTE ESTHER · 1994 to 2010
$2.8M
NIA NIH HHS AG012122NIA NIH HHS P01 AG017617NIA NIH HHS R01 AG012122
6 · The paper itself

Abstract

Down syndrome (DS) is the most common non-lethal genetic condition that affects approximately 1 in 700 births in the United States of America. DS is characterized by complete or segmental chromosome 21 trisomy, which leads to variable intellectual disabilities, progressive memory loss, and accelerated neurodegeneration with age. During the last three decades, people with DS have experienced a doubling of life expectancy due to progress in treatment of medical comorbidities, which has allowed this population to reach the age when they develop early onset Alzheimer's disease (AD). Individuals with DS develop cognitive and pathological hallmarks of AD in their fourth or fifth decade, and are currently lacking successful prevention or treatment options for dementia. The profound memory deficits associated with DS-related AD (DS-AD) have been associated with degeneration of several neuronal populations, but mechanisms of neurodegeneration are largely unexplored. The most successful animal model for DS is the Ts65Dn mouse, but several new models have also been developed. In the current review, we discuss recent findings and potential treatment options for the management of memory loss and AD neuropathology in DS mouse models. We also review agerelated neuropathology, and recent findings from neuroimaging studies. The validation of appropriate DS mouse models that mimic neurodegeneration and memory loss in humans with DS can be valuable in the study of novel preventative and treatment interventions, and may be helpful in pinpointing gene-gene interactions as well as specific gene segments involved in neurodegeneration.

Indexed as

NeuroimagingAlzheimer DiseaseAnimalsCognition DisordersDisease Models, AnimalDown SyndromeHumansMiceNeuropathology

Identifiers

PMID26391050
PMCPMC5034871
OpenAlexW2296860665

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.