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Cited by 49Neurogenesis and neuroplasticity mechanismsDevelopmental Biology and Gene RegulationNeural dynamics and brain function

Computational Models of Neocortical Neuronogenesis and Programmed Cell Death in the Developing Mouse, Monkey, and Human

Gohlke, Julia M., Griffith, William C., Faustman, Elaine M.·2007·Cerebral Cortex
DOI 10.1093/cercor/bhl151
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Abstract

This paper presents a computational model allowing quantitative simulations of acquisition of neocortical neuronal number across mammalian species. When extrapolating scientific findings from rodents to humans, it is particularly pertinent to acknowledge the importance of the accelerated enlargement of the neocortex during human evolution. Neocortex development is marked by discrete stages of neural progenitor cell proliferation and death, neuronal differentiation, and neuronal programmed cell death. We have developed computational models of human and rhesus monkey neocortical neuronal cell acquisition based on experimentally derived parameters of cell cycle length, commitment to cell cycle exit, and cell death. Our model results agree with independent stereological studies estimating neocortical neuron number in adult and developing rhesus monkey and human. Comparisons of our primate models with previously developed rodent models suggest correlations between the lengthening of the duration of the neuronogenesis period and a lengthening of the cellular processes of cell cycle progression and death can account for the vast increase in size of the primate neocortex. Furthermore, when compared with rodents, we predict that cell death may play a larger role in shaping the primate neocortex. Our mathematical models of the development and evolution of the neocortex provide a quantitative, biologically based construct for extrapolation between rodent and humans. These models can assist in focusing future experimental research on the differing mechanisms of rodent versus human neocortical development.

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Crossref · 10.1093/cercor/bhl151

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  • Because proliferation of cortical neurons is exponential between 10 and 20 weeks of gestation and does not occur postnatally, pathological neuron excess cannot be caused by post-natal events and instead indicates neural disorder in ASD has a prenatal origin, likely by the first and/or second trimester.

    “Because proliferation of cortical neurons is exponential between 10 and 20 weeks of gestation [43, 44] and does not occur postnatally, pathological neuron excess cannot be caused by post-natal events and instead indicates neural disorder in ASD has a prenatal origin, likely by the first and/or second trimester.”

    From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [44]

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Related

Authors
Gohlke, J. M., Griffith, W. C., & Faustman, E. M.
Affiliations
University of Washington (US)
ORCID
Venue
Cerebral Cortex
Publisher
Oxford University Press (OUP)
Published
2007-01-04
Volume
17
Issue
10
Pages
2433-2442
ISSN
  • 1047-3211 (ISSN-L)
  • 1460-2199
DOI
10.1093/cercor/bhl151
OpenAlex
W2172176015
Cited by
49
References
101
Citations by year
2021: 2 · 2020: 2 · 2019: 5 · 2018: 15 · 2017: 4 · 2016: 3 · 2014: 4 · 2013: 2 · 2012: 1
FWCI
0.82
Type
journal article
Language
en
Open access
closed
Locations
  • Cerebral Cortex (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Environmental Health Sciences (R01-ES10613, P01ES009601, 2P01 ES 09601, R01ES010613)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD02274, P30HD002274)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
programmed cell death, neural progenitor proliferation, cell cycle duration, cell cycle exit, neuronal differentiation, human neocortex, rhesus monkeys, rodent-to-human extrapolation, stereology, computational model
MeSH terms
Aging, Animals, Animals, Newborn, Cell Cycle, Humans, Infant, Newborn, Macaca mulatta, Models, Neurological, Neurons, Apoptosis, Neocortex, Mice

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