Evidence map›Paper›PMID 25204496›Full record

ReviewMolecular neurobiology2015

Beta-Amyloid Precursor Protein (βAPP) Processing in Alzheimer's Disease (AD) and Age-Related Macular Degeneration (AMD).

Yuhai Zhao, Surjyadipta Bhattacharjee, Brandon M Jones, James M Hill, Christian Clement, Kumar Sambamurti, Prerna Dua, Walter J Lukiw

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
  2. Review
  3. Journal of pharmacopuncture · 2025
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Potential Retinal Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Salivary Exosomes in Health and Disease: Future Prospects in the Eye.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 1 country.

Yuhai ZhaoLSU Neuroscience Center, Louisiana State University Health Sciences Center, 2020 Gravier Street, Suite 904, New Orleans, LA, 70112, USA.
Surjyadipta Bhattacharjee
Brandon M Jones
James M Hill
Christian Clement
Kumar Sambamurti
Prerna Dua
Walter J Lukiw
Louisiana State University Health Sciences Center New Orleans · USLouisiana State University · USMedical University of South Carolina · USSouthern University at New Orleans · US

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
OCULAR HSV: LATENCY, REACTIVATION, &RECURRENCER01EY006311 · NEI · LSU HEALTH SCIENCES CENTER · PI HILL, JAMES M · 1985 to 2012
$5.3M
Multiphoton ConfocalP30GM103340 · NIGMS · LSU HEALTH SCIENCES CENTER · PI BAZAN, NICOLAS G. · 2012 to 2016
$5.1M
microRNA (miRNA) signaling in Alzheimer's disease(AD)R01AG038834 · NIA · LSU HEALTH SCIENCES CENTER · PI BAZAN, NICOLAS G. · 2011 to 2020
$3.3M
Gene Expression in Alzheimer's DiseaseR01AG018031 · NIA · LSU HEALTH SCIENCES CENTER · PI LUKIW, WALTER J · 2001 to 2006
$1.4M
Understanding the Neuroprotective Activities of PosiphenR21AG046200 · NIA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SAMBAMURTI, KUMAR · 2013 to 2014
$411k
NEI NIH HHS NEI EY006311NEI NIH HHS R01 EY006311NIA NIH HHS NIA AG038834NIA NIH HHS NIA AG18031NIA NIH HHS NIA P50AG16573NIA NIH HHS NIH NIA AG046200NIA NIH HHS P50 AG016573NIA NIH HHS R01 AG018031NIA NIH HHS R01 AG038834NIA NIH HHS R21 AG046200NIGMS NIH HHS P30 GM103340NIGMS NIH HHS P30-GM103340
6 · The paper itself

Abstract

Amyloid is a generic term for insoluble, often intensely hydrophobic, fibrous protein aggregates that arise from inappropriately folded versions of naturally-occurring polypeptides. The abnormal generation and accumulation of amyloid, often referred to as amyloidogenesis, has been associated with the immune and pro-inflammatory pathology of several progressive age-related diseases of the human central nervous system (CNS) including Alzheimer's disease (AD) and age-related macular degeneration (AMD). This 'research perspective' paper reviews some of the research history, biophysics, molecular-genetics and environmental factors concerning the contribution of amyloid beta (Aβ) peptides, derived from beta-amyloid precursor protein (βAPP), to AD and AMD that suggests an extensive similarity in immune and inflammatory degenerative mechanisms between these two CNS diseases.

Indexed as

Protein Processing, Post-TranslationalAlzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalEpigenesis, GeneticHumansMacular DegenerationAmyloid beta-Peptides

Identifiers

PMID25204496
PMCPMC4362880
OpenAlexW2009744995

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.