Evidence map›Paper›PMID 30737307›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Cell Kinetics in the Adult Neurogenic Niche and Impact of Diet-Induced Accelerated Aging.

Alexander J Stankiewicz, Farzad Mortazavi, Peter V Kharchenko, Erin M McGowan, Vasili Kharchenko, Irina V Zhdanova

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. 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
0.6field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Aqueous Extract ofAntioxidants (Basel, Switzerland) · 2022
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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 2 institutions in 2 countries.

Alexander J StankiewiczDepartment of Preclinical Research, BioChron LLC, Worcester, Massachusetts 01605.ORCID 0000-0001-5298-955X
Farzad MortazaviDepartment of Anatomy and Neurobiology, Boston University School of Medicine, Boston, Massachusetts 02118.
Peter V KharchenkoDepartment of BioMedical Informatics, Harvard Medical School, Boston, Massachusetts 02115.
Erin M McGowanDepartment of Anatomy and Neurobiology, Boston University School of Medicine, Boston, Massachusetts 02118.
Vasili KharchenkoInstitute for Theoretical Atomic, Molecular & Optical Physics, Harvard University, Cambridge, Massachusetts 02138, and irina.zhdanova@bio-chron.com vasili.kharchenko@uconn.edu.
Irina V ZhdanovaDepartment of Preclinical Research, BioChron LLC, Worcester, Massachusetts 01605, irina.zhdanova@bio-chron.com vasili.kharchenko@uconn.edu.
Boston University · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurogenesis in the adult brain, a powerful mechanism for neuronal plasticity and brain repair, is altered by aging and pathological conditions, including metabolic disorders. The search for mechanisms and therapeutic solutions to alter neurogenesis requires understanding of cell kinetics within neurogenic niches using a high-throughput quantitative approach. The challenge is in the dynamic nature of the process and multiple cell types involved, each having several potential modes of division or cell fate. Here we show that cell kinetics can be revealed through a combination of the BrdU/EdU pulse-chase, based on the circadian pattern of DNA replication, and a differential equations model that describes time-dependent cell densities. The model is validated through the analysis of cell kinetics in the cerebellar neurogenic niche of normal young adult male zebrafish, with cells quantified in 2D (sections), and with neuronal fate and reactivation of stem cells confirmed in 3D whole-brain images (CLARITY). We then reveal complex alterations in cell kinetics associated with accelerated aging due to chronic high caloric intake. Low activity of neuronal stem cells in this condition persists 2 months after reverting to normal diet, and is accompanied by overproduction of transient amplifying cells, their accelerated cell death, and slow migration of postmitotic progeny. This combined experimental and mathematical approach should allow for relatively high-throughput analysis of early signs of pathological and age-related changes in neurogenesis, evaluation of specific therapeutic targets, and drug efficacy.

Indexed as

Energy IntakeAging, PrematureAnimalsBrainCell DivisionCircadian RhythmDietDNA ReplicationHyperphagiaKineticsMagnetic Resonance ImagingMaleMitosisModels, TheoreticalNeural Stem CellsNeurogenesisadult neurogenesisagingcell kineticsmathematical modelingneurogenesiszebrafish

Identifiers

PMID30737307
PMCPMC6462444
OpenAlexW2912629789

What OpenQuestion 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 OpenQuestion graph.