Evidence map›Paper›PMID 26651341›Full record

ReviewCurrent Alzheimer research2016

Aging in Down Syndrome and the Development of Alzheimer's Disease Neuropathology.

Elizabeth Head, Ira T Lott, Donna M Wilcock, Cynthia A Lemere

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 157 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

157 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Article
  18. U1-70K and U1A and tau pathogenesis in demented and non-demented individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  19. Alzheimer's Disease Research Center Down Syndrome Cores: Experience from two sites.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  20. Longitudinal diffusion tensor imaging correlates with amyloid burden in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article

97 more citing papers are in PubMed but not listed here.

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.

Elizabeth HeadSanders Brown Center on Aging, University of Kentucky, 800 South Limestone Street, Lexington, KY, 40536, USA. elizabeth.head@uky.edu.
Ira T Lott
Donna M Wilcock
Cynthia A Lemere

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
Aging of Frontal Structure and Function in Down Syndrome and DementiaR01HD064993 · NICHD · UNIVERSITY OF KENTUCKY · PI HEAD, ELIZABETH, SCHMITT, FREDERICK · 2009 to 2019
$5.1M
Understanding and Mitigating Vascular Side-Effects Associated with Anti-Amyloid ImmunotherapyR01NS136122 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI CYNTHIA A LEMERE · 2024 to 2026
$2.5M
Predicting Cognitive Decline in Adults with Down SyndromeR01HD065160 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI LOTT, IRA T. · 2009 to 2013
$2.3M
Vascular breakdown in Alzheimers Disease with cerebrovascular diseaseR01NS079637 · NINDS · UNIVERSITY OF KENTUCKY · PI WILCOCK, DONNA M · 2012 to 2016
$1.6M
Pyroglutamate Amyloid-beta as an Immunotherapeutic Target for Alzheimer's DiseaseR01AG040092 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LEMERE, CYNTHIA A · 2012 to 2015
$1.5M
NIA NIH HHS P50 AG016573NIA NIH HHS R01 AG040092NIA NIH HHS R01AG16573NICHD NIH HHS R01 HD064993NICHD NIH HHS R01HD064993NICHD NIH HHS R01 HD065160NICHD NIH HHS R01HD065160NINDS NIH HHS NS079637NINDS NIH HHS R01 NS079637NINDS NIH HHS R01 NS136122
6 · The paper itself

Abstract

Chromosome 21, triplicated in Down Syndrome, contains several genes that are thought to play a critical role in the development of AD neuropathology. The overexpression of the gene for the amyloid precursor protein (APP), on chromosome 21, leads to early onset beta-amyloid (Aβ) plaques in DS. In addition to Aβ accumulation, middle-aged people with DS develop neurofibrillary tangles, cerebrovascular pathology, white matter pathology, oxidative damage, neuroinflammation and neuron loss. There is also evidence of potential compensatory responses in DS that benefit the brain and delay the onset of dementia after there is sufficient neuropathology for a diagnosis of AD. This review describes some of the existing literature and also highlights gaps in our knowledge regarding AD neuropathology in DS. It will be critical in the future to develop networked brain banks with standardized collection procedures to fully characterize the regional and temporal pathological events associated with aging in DS. As more information is acquired regarding AD evolution in DS, there will be opportunities to develop interventions that are age-appropriate to delay AD in DS.

Indexed as

NeuropathologyAge FactorsAgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsDown SyndromeHumansNeurofibrillary Tanglestau ProteinsAmyloid beta-Protein Precursortau Proteins

Identifiers

PMID26651341
PMCPMC4948181

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.