Evidence map›Paper›PMID 41494407›Full record

ArticleNeurobiology of aging2026

A timeline of structural and functional consequences to ipRGCs in a mouse model of Alzheimer's disease.

Brandy S Recio, William A Pérez, Ruth Tjondropurnomo, Jenibelle Hsu, Simrah Ahmed, Sachin Parikh, Jake Sun, Sreya Mitra, Rajesh Kumar Goit, Nicholas C Brecha and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

13 authors.

Brandy S RecioDepartment of Neurobiology, David Geffen School of Medicine at Los Angeles, University of California, Los Angeles, Los Angeles, CA, USA.
William A PérezCollege of Optometry, University of Houston, Houston, TX, USA.
Ruth TjondropurnomoDepartment of Ophthalmology, Jules Stein Eye Institute, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA; Brain Research Institute, UCLA, Los Angeles, CA, USA.
Jenibelle HsuDepartment of Ophthalmology, Jules Stein Eye Institute, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA; Brain Research Institute, UCLA, Los Angeles, CA, USA.
Simrah AhmedDepartment of Ophthalmology, Jules Stein Eye Institute, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA; Brain Research Institute, UCLA, Los Angeles, CA, USA.
Sachin ParikhDepartment of Ophthalmology, Jules Stein Eye Institute, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA; Brain Research Institute, UCLA, Los Angeles, CA, USA.
Jake SunDepartment of Neurobiology, David Geffen School of Medicine at Los Angeles, University of California, Los Angeles, Los Angeles, CA, USA.
Sreya MitraCollege of Optometry, University of Houston, Houston, TX, USA.
Rajesh Kumar GoitDepartment of Ophthalmology, Jules Stein Eye Institute, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA; Brain Research Institute, UCLA, Los Angeles, CA, USA.
Nicholas C BrechaDepartment of Neurobiology, David Geffen School of Medicine at Los Angeles, University of California, Los Angeles, Los Angeles, CA, USA; Department of Ophthalmology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA, USA; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Nimesh PatelCollege of Optometry, University of Houston, Houston, TX, USA.
Anna MatyniaCollege of Optometry, University of Houston, Houston, TX, USA. Electronic address: amatynia@Central.UH.EDU.
Luis Pérez de Sevilla MüllerDepartment of Neurobiology, David Geffen School of Medicine at Los Angeles, University of California, Los Angeles, Los Angeles, CA, USA. Electronic address: luis@biocent.com.

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Molecular, cellular, anatomical and neurobiological investigation of melanopsin-expressing corneal innervation, and its role in pain and photophobiaR01EY030864 · NEI · UNIVERSITY OF HOUSTON · PI MATYNIA, ANNA · 2020 to 2024
$1.9M
VRC: Reduction of Vision Loss with Early Interventions After Optic Nerve InjuryR01EY034715 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRECHA, NICHOLAS C. · 2022 to 2023
$406k
BLRD VA I01 BX005926BLRD VA IK6 BX005230NEI NIH HHS R01 EY030864NEI NIH HHS R01 EY034715NIDDK NIH HHS P30 DK041301
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects cognitive, sensory and motor systems, including the visual system and has a significant impact on autonomy and quality of life. Emerging evidence suggests that visual system abnormalities may enable early detection and monitoring for AD, appearing before cognitive symptoms. Intrinsically photosensitive retinal ganglion cells (ipRGCs or mRGCs) are among the first neurons affected in AD. This study investigates the structural and functional changes in ipRGCs during aging. ipRGC and retinal ganglion cell (RGC) degeneration were assessed using immunohistological analyses of retinal wholemounts of the 3xTg-AD mouse model. Behavioral changes were analyzed using light aversion with and without pupil dilation, contrast sensitivity function across five spatial frequencies, and pupillary light reflex (PLR) at three light levels. Changes in ipRGC dendritic varicosities begin between 4-8 months followed by degeneration of other RGC types by 12-16 months of age. Alterations in light aversion were observed at both 6 and 12 months with no alterations in contrast sensitivity function or PLR. Sex-specific differences in disease progression were detected in RGC degeneration. Our findings support the hypothesis that ipRGC dysfunction occurs early in AD and precedes cognitive decline. These findings are similar to ipRGC degeneration previously observed in postmortem human AD retinas, and thus provides a valuable model for studying the mechanism of degeneration and identifying potential behavior changes that might serve as early biomarkers in AD.

Indexed as

AgingAlzheimer DiseaseRetinal Ganglion CellsAnimalsContrast SensitivityDisease Models, AnimalDisease ProgressionFemaleMaleMiceMice, Inbred C57BLMice, TransgenicReflex, PupillaryTime FactorsAlzheimer’sBiomarkerContrast sensitivityIpRGCLight aversionMelanopsinPupillometryRetinaStructure-function

Identifiers

PMID41494407
PMCPMC13283469

What Socratic 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 Socratic graph.