Evidence map›Paper›PMID 28450267›Full record

ArticleNeuroscience2017

Retinal changes in the Tg-SwDI mouse model of Alzheimer's disease.

Fred G Oliveira-Souza, Marci L DeRamus, Thomas van Groen, Alexis E Lambert, Mark S Bolding, Christianne E Strang

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Alzheimer's disease pathophysiology in the Retina.Progress in retinal and eye research · 2024
    Review
  2. Potential Retinal Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2023
    Review
  3. Article
  4. Article
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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

6 authors at 1 institution in 1 country.

Fred G Oliveira-SouzaOptometry and Vision Science, University of Alabama at Birmingham, Birmingham, AL, United States.
Marci L DeRamusOptometry and Vision Science, University of Alabama at Birmingham, Birmingham, AL, United States.
Thomas van GroenCell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States.
Alexis E LambertPsychology, University of Alabama at Birmingham, Birmingham, AL, United States.
Mark S BoldingRadiology, University of Alabama at Birmingham, Birmingham, AL, United States.
Christianne E StrangPsychology, University of Alabama at Birmingham, Birmingham, AL, United States. Electronic address: cstrang@uab.edu.
University of Alabama at Birmingham · US

Funding

Visual Phenotyping CoreP30EY003039 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Paul Douglas Gamlin · 1985 to 2026
$16.9M
UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRITT, WILLIAM JARVIS · 2005 to 2019
$8.5M
NEI NIH HHS P30 EY003039NINDS NIH HHS P30 NS047466
6 · The paper itself

Abstract

Alzheimer's disease (AD), a debilitating neurodegenerative illness, is characterized by neuronal cell loss, mental deficits, and abnormalities in several neurotransmitter and protein systems. AD is also associated with visual disturbances, but their causes remain unidentified. We hypothesize that the visual disturbances stem from retinal changes, particularly changes in the retinal cholinergic system, and that the etiology in the retina parallels the etiology in the rest of the brain. To test our hypothesis, quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC) were employed to assess changes in acetylcholine receptor (AChR) gene expression, number of retinal cells, and astrocytic gliosis in the Transgenic Swedish, Dutch and Iowa (Tg-SwDI) mouse model as compared to age-matched wild-type (WT). We observed that Tg-SwDI mice showed an initial upregulation of AChR gene expression early on (young adults and middle-aged adults), but a downregulation later on (old adults). Furthermore, transgenic animals displayed significant cell loss in the photoreceptor layer and inner retina of the young adult animals, as well as specific cholinergic cell loss, and increased astrocytic gliosis in the middle-aged adult and old adult groups. Our results suggest that the changes observed in AD cerebrum are also present in the retina and may be, at least in part, responsible for the visual deficits associated with the disease.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCerebellumCholine O-AcetyltransferaseDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsHumansMiceMice, TransgenicMutationPresenilin-1Receptors, CholinergicAmyloid beta-Protein PrecursorCholine O-AcetyltransferaseGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsPresenilin-1PSEN1 protein, humanReceptors, CholinergicRNA, MessengerAlzheimer’s diseaseamyloid precursor protein mutationhistologyqPCRretinal cholinergic systemvision

Identifiers

PMID28450267
PMCPMC5495115
OpenAlexW2608304269

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.