Modeling transformations of neurodevelopmental sequences across mammalian species
Open accessAbstract
A general model of neural development is derived to fit 18 mammalian species, including humans, macaques, several rodent species, and six metatherian (marsupial) mammals. The goal of this work is to describe heterochronic changes in brain evolution within its basic developmental allometry, and provide an empirical basis to recognize equivalent maturational states across animals. The empirical data generating the model comprises 271 developmental events, including measures of initial neurogenesis, axon extension, establishment, and refinement of connectivity, as well as later events such as myelin formation, growth of brain volume, and early behavioral milestones, to the third year of human postnatal life. The progress of neural events across species is sufficiently predictable that a single model can be used to predict the timing of all events in all species, with a correlation of modeled values to empirical data of 0.9929. Each species' rate of progress through the event scale, described by a regression equation predicting duration of development in days, is highly correlated with adult brain size. Neural heterochrony can be seen in selective delay of retinogenesis in the cat, associated with greater numbers of rods in its retina, and delay of corticogenesis in all species but rodents and the rabbit, associated with relatively larger cortices in species with delay. Unexpectedly, precocial mammals (those unusually mature at birth) delay the onset of first neurogenesis but then progress rapidly through remaining developmental events.
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A study of protein expression in human female fetuses with and without trisomy (n = 4 each) at gestational week 18-19 found no differences in protein expression.
“Notably, a study of protein expression in human female fetuses with and without trisomy (n = 4 each) at gestational week 18–19, a stage of human brain development that is roughly equivalent to the late fetal period in mouse brain development (Workman et al., 2013), found no differences in protein expression (Cheon et al., 2003).”
From Sex-specific developmental alterations in DYRK1A expression in the brain of a Down syndrome mouse model (2024) · cites this paper as Workman et al., 2013
The Workman citation is attached to the human–mouse developmental-stage comparison, not to the protein-expression finding, which the sentence cites to Cheon et al. In “Slope and onset of progression through neural events” (page unavailable), Workman et al. compare the timing of neural milestones across species, but the passages found do not establish that human gestational weeks 18–19 specifically correspond to the late fetal period in mice. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThese significant and large increases in DYRK1A expression suggest that P6 may be a time of excessive DYRK1A kinase activity that alters the trajectory of the trisomic brain at a critical period of its development.
“These significant and large increases in DYRK1A expression suggest that P6—roughly equivalent to the period of human brain development in the early third trimester (Workman et al., 2013)— may be a time of excessive DYRK1A kinase activity that alters the trajectory of the trisomic brain at a critical period of its development.”
From Sex-specific developmental alterations in DYRK1A expression in the brain of a Down syndrome mouse model (2024) · cites this paper as Workman et al., 2013
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“…in human female fetuses with and without trisomy ( n = 4 each) at gestational week 18 – 19, a stage of human brain development that is roughly equivalent to the late fetal period in mouse brain development (Workman et al., 2013), found no differences in protein expression (Cheon et al., 2003).”
- Authors
- Workman, A. D., Charvet, C. J., Clancy, B., Darlington, R. B., & Finlay, B. L.
- Affiliations
- Cornell University (US)
- University of Central Arkansas (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2013-04-24
- Volume
- 33
- Issue
- 17
- Pages
- 7368-7383
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3928428
- OpenAlex
- W2022567100
- Cited by
- 833
- References
- 5
- Citations by year
- 2026: 48 · 2025: 82 · 2024: 46 · 2023: 59 · 2022: 65 · 2021: 76 · 2020: 76 · 2019: 68 · 2018: 74 · 2017: 60 · 2016: 76 · 2015: 48 · 2014: 34 · 2013: 21
- FWCI
- 22.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (0849627, 0849612)
- National Institutes of Health
- U.S. Public Health Service (NIH CHHD 1F32HD067011-01A1)
- National Center for Research Resources (P20RR016460, P20 RR 16460)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (F32HD067011, U10 HD-500009)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Social Sciences › Psychology › Social Psychology › Primate Behavior and Ecology
- Keywords
- neural development, brain evolution, heterochrony, developmental timing, neurogenesis, axon growth, myelination, brain growth, retinal development, cortical development, marsupials, rodents, macaque, human development
- MeSH terms
- Animals, Brain, Cats, Biological Evolution, Ferrets, Gerbillinae, Guinea Pigs, Cricetinae, Humans, Macropodidae, Macaca, Models, Neurological, Rabbits, Sheep, Species Specificity, Trichosurus, Mice, Rats, Neurogenesis
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