Evidence map›Paper›PMID 20725513›Full record

ArticleFrontiers in aging neuroscience2010

Do different neurons age differently? Direct genome-wide analysis of aging in single identified cholinergic neurons.

Leonid L Moroz, Andrea B Kohn

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
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  3. Age-related degradation of behavioral and network features ofbioRxiv : the preprint server for biology · 2025
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  7. RNA Isolation from Ctenophores.Methods in molecular biology (Clifton, N.J.) · 2024
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  17. Multiple Origins of Neurons From Secretory Cells.Frontiers in cell and developmental biology · 2021
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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

2 authors at 1 institution in 1 country.

Leonid L MorozDepartment of Neuroscience, Evelyn F and William L. McKnight Brain Institute, University of Florida Gainesville, FL, USA.
Andrea B Kohn
Whitney Museum of American Art · US

Funding

Molecular Engineering Approach to Study Long Term Synaptic PlasticityR01NS060762 · NINDS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI JU, JINGYUE · 2008 to 2011
$2.3M
Genomic Bases of Behavioral Learning: Single Cell ApproachesR01GM097502 · NIGMS · UNIVERSITY OF FLORIDA · PI HAWKINS, ROBERT D, MOROZ, LEONID L · 2011 to 2014
$1.6M
Genomic Dissection of Circuit DynamicsR21RR025699 · NCRR · UNIVERSITY OF FLORIDA · PI BUCHER, DIRK MARTIN, MOROZ, LEONID L · 2009 to 2010
$408k
NCRR NIH HHS R21 RR025699NIGMS NIH HHS R01 GM097502NINDS NIH HHS R01 NS060762
6 · The paper itself

Abstract

Aplysia californica is a powerful experimental system to study the entire scope of genomic and epigenomic regulation at the resolution of single functionally characterized neurons and is an emerging model in the neurobiology of aging. First, we have identified and cloned a number of evolutionarily conserved genes that are age-related, including components of apoptosis and chromatin remodeling. Second, we performed gene expression profiling of different identified cholinergic neurons between young and aged animals. Our initial analysis indicates that two cholinergic neurons (R2 and LPl1) revealed highly differential genome-wide changes following aging suggesting that on the molecular scale different neurons indeed age differently. Each of the neurons tested has a unique subset of genes differentially expressed in older animals, and the majority of differently expressed genes (including those related to apoptosis and Alzheimer's disease) are found in aging neurons of one but not another type. The performed analysis allows us to implicate (i) cell specific changes in histones, (ii) DNA methylation and (iii) regional relocation of RNAs as key processes underlying age-related changes in neuronal functions and synaptic plasticity. These mechanisms can fine-tune the dynamics of long-term chromatin remodeling, or control weakening and the loss of synaptic connections in aging. At the same time our genomic tests revealed evolutionarily conserved gene clusters associated with aging (e.g., apoptosis-, telomere- and redox-dependent processes, insulin and estrogen signaling and water channels).

Indexed as

Alzheimer's diseaseAplysiaepigenetics of aginghistonessingle neuron transcriptome

Identifiers

PMID20725513
PMCPMC2910937
OpenAlexW2055122816

What OpenQuestion holds

Textmetadata
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.