Evidence map›Paper›PMID 36768896›Full record

ReviewInternational journal of molecular sciences2023

Aging Effects on Optic Nerve Neurodegeneration.

Janet Coleman-Belin, Alon Harris, Bo Chen, Jing Zhou, Thomas Ciulla, Alice Verticchio, Gal Antman, Michael Chang, Brent Siesky

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

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  20. Natural Compounds for Preventing Age-Related Diseases and Cancers.International journal of molecular sciences · 2024
    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

9 authors.

Janet Coleman-BelinDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0002-5148-0214
Alon HarrisDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Bo ChenDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Jing ZhouDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Thomas CiullaVitreoretinal Medicine and Surgery, Midwest Eye Institute, Indianapolis, IN 46290, USA.ORCID 0000-0001-5557-6777
Alice VerticchioDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Gal AntmanDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Michael ChangDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Brent SieskyDepartment of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

Funding

Integration of clinical measures and theoretical modeling to quantify sectorial specific changes in ocular structure, function, and hemodynamicsR01EY030851 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ARCIERO, JULIA, HARRIS, ALON · 2020 to 2023
$1.3M
NEI NIH HHS R01 EY030851
6 · The paper itself

Abstract

Common risk factors for many ocular pathologies involve non-pathologic, age-related damage to the optic nerve. Understanding the mechanisms of age-related changes can facilitate targeted treatments for ocular pathologies that arise at any point in life. In this review, we examine these age-related, neurodegenerative changes in the optic nerve, contextualize these changes from the anatomic to the molecular level, and appreciate their relationship with ocular pathophysiology. From simple structural and mechanical changes at the optic nerve head (ONH), to epigenetic and biochemical alterations of tissue and the environment, multiple age-dependent mechanisms drive extracellular matrix (ECM) remodeling, retinal ganglion cell (RGC) loss, and lowered regenerative ability of respective axons. In conjunction, aging decreases the ability of myelin to preserve maximal conductivity, even with "successfully" regenerated axons. Glial cells, however, regeneratively overcompensate and result in a microenvironment that promotes RGC axonal death. Better elucidating optic nerve neurodegeneration remains of interest, specifically investigating human ECM, RGCs, axons, oligodendrocytes, and astrocytes; clarifying the exact processes of aged ocular connective tissue alterations and their ultrastructural impacts; and developing novel technologies and pharmacotherapies that target known genetic, biochemical, matrisome, and neuroinflammatory markers. Management models should account for age-related changes when addressing glaucoma, diabetic retinopathy, and other blinding diseases.

Indexed as

GlaucomaOptic DiskAgedAgingAnimalsAxonsDisease Models, AnimalHumansOptic NerveRetinal Ganglion Cellsactive agingdiabetic retinopathyembryologyglaucomainflammationneurodegenerationneuroregenerationoptic nerveoxidative stresssenescence

Identifiers

PMID36768896
PMCPMC9917079

What Socratic holds

Textmetadata
LicenceCC BY
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.