Neurogenesis impairment: An early developmental defect in Down syndrome

Stagni, Fiorenza; Giacomini, Andrea; Emili, Marco; Guidi, Sandra; Bartesaghi, Renata

doi:10.1016/j.freeradbiomed.2017.07.026

Cited by 81 publications

(104 citation statements)

References 168 publications

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“…The brain growth spurt of rodents occurs at postnatal day 7 to postnatal day 10, which is comparable to a term human infant of 36 to 40 weeks postmenstrual age . Alterations at both embryonic and postnatal ages have been reported in Ts65Dn and Ts1Cje mice and reviewed in several recent publications . More recently, the Dp16 strain did not show any forebrain defects embryonically (embryonic day 13.5–18.5), but did show delayed growth, and delayed acquisition of milestones postnatally and a decrease in cortical excitatory and interneuron populations were observed at postnatal day 15, but were not evaluated at earlier postnatal ages .…”

Section: Mouse Models Of Down Syndromementioning

confidence: 83%

“…). Importantly, as in human postmortem studies, an imbalance of excitatory and inhibitory neurons, impaired neurogenesis, synaptogenesis, and altered dendritic development are also observed in mouse models of Down syndrome (detailed reviews are available elsewhere) …”

Section: Mouse Models Of Down Syndromementioning

confidence: 99%

“…Therefore magnetic resonance imaging (MRI) is an attractive alternative which is safe, does not use ionizing radiation, and can provide more extensive, detailed biometric data across gestation including information about both brain macro‐ and microstructure . Although there are MRI studies which have assessed structural brain volume in early childhood, very little work has been done with infants younger than 2 years of age with Down syndrome. Quantitative early MRI data could be related to data derived from clinical, cognitive, and behavioural assessments, as well as genetic information, thus allowing a comprehensive understanding of the complex relationships which underpin the Down syndrome phenotype.…”

Section: Advances In Fetal and Neonatal Magnetic Resonance Imagingmentioning

confidence: 99%

“…Importantly, as in human postmortem studies, an imbalance of excitatory and inhibitory neurons, impaired neurogenesis, synaptogenesis, and altered dendritic development are also observed in mouse models of Down syndrome (detailed reviews are available elsewhere). 9,[17][18][19]41,56,58,59 The Ts65Dn mouse (B6EiC3Sn a/A-Ts [17 16 ]65Dn/J) has historically been very important in the study of Down syndrome as it is trisomic for 90 protein coding genes on Mmu16 (approximately 55% of orthologous genes to Hsa21). However, Ts65Dn mice contain an extra copy of 60 genes (35 protein coding) located on Mmu17 (orthologous to Hsa6) that are not triplicated in people with Down syndrome and the resultant Ts65Dn phenotypes may be more severe than those seen in the human condition or possess spurious phenotypes not relevant to Down syndrome.…”

Section: Mouse Models Of Down Syndromementioning

confidence: 99%

“…56,71 Alterations at both embryonic and postnatal ages have been reported in Ts65Dn and Ts1Cje mice 72 and reviewed in several recent publications. 9,41,59 More recently, the Dp16 strain did not show any forebrain defects embryonically (embryonic day 13.5-18.5), but did show delayed growth, and delayed acquisition of milestones postnatally and a decrease in cortical excitatory and interneuron populations were observed at postnatal day 15, but were not evaluated at earlier postnatal ages. 73,74 Comparisons of embryonic and adult gene expression, brain development, and mouse behaviour have recently been done in the Ts65Dn, Ts1Cje, and Dp16 mouse strains and suggest widespread differences between models.…”

Section: Mouse Models Of Down Syndromementioning

confidence: 99%

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New approaches to studying early brain development in Down syndrome

Baburamani

Patkee

Arichi

et al. 2019

Develop Med Child Neuro

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Down syndrome is the most common genetic developmental disorder in humans and is caused by partial or complete triplication of human chromosome 21 (trisomy 21). It is a complex condition which results in multiple lifelong health problems, including varying degrees of intellectual disability and delays in speech, memory, and learning. As both length and quality of life are improving for individuals with Down syndrome, attention is now being directed to understanding and potentially treating the associated cognitive difficulties and their underlying biological substrates. These have included imaging and postmortem studies which have identified decreased regional brain volumes and histological anomalies that accompany early onset dementia. In addition, advances in genome‐wide analysis and Down syndrome mouse models are providing valuable insight into potential targets for intervention that could improve neurogenesis and long‐term cognition. As little is known about early brain development in human Down syndrome, we review recent advances in magnetic resonance imaging that allow non‐invasive visualization of brain macro‐ and microstructure, even in utero. It is hoped that together these advances may enable Down syndrome to become one of the first genetic disorders to be targeted by antenatal treatments designed to ‘normalize’ brain development. What this paper adds Magnetic resonance imaging can provide non‐invasive characterization of early brain development in Down syndrome. Down syndrome mouse models enable study of underlying pathology and potential intervention strategies. Potential therapies could modify brain structure and improve early cognitive levels. Down syndrome may be the first genetic disorder to have targeted therapies which alter antenatal brain development.

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Section: Mouse Models Of Down Syndromementioning

confidence: 83%

Section: Mouse Models Of Down Syndromementioning

confidence: 99%

Section: Advances In Fetal and Neonatal Magnetic Resonance Imagingmentioning

confidence: 99%

Section: Mouse Models Of Down Syndromementioning

confidence: 99%

Section: Mouse Models Of Down Syndromementioning

confidence: 99%

See 3 more Smart Citations

New approaches to studying early brain development in Down syndrome

Baburamani

Patkee

Arichi

et al. 2019

Develop Med Child Neuro

View full text Add to dashboard Cite

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Development of Cortical Neuron Heterogeneity and Impact of Neurodevelopmental Disorders

Li,,

Tylerand,

Haydar

2023

Neocortical Neurogenesis in Development and Evolution

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Growth curves for French people with Down syndrome from birth to 20 years of age

Mircher

Briceño

Toulas

et al. 2018

American J of Med Genetics Pt A

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We present new and complete growth charts for 2,598 healthy French children and adolescents with Down syndrome (DS) from 0 to 20 years old, obtained with highly reliable statistical methods. This study is retrospective and addresses data collected over a period of 12 years, monocentric and with a satisfactory representation of the population nationwide. Final occipito‐frontal circumference (OFC) is at the fifth percentile compared to WHO charts, with a drop between 12 and 18 months. Final height is at the first percentile compared to WHO charts for girls and boys with two periods of reduced growth velocity: before 36 months and around puberty. We observed no pubertal growth peak for girls. For boys, pubertal growth peak showed to happen earlier and to be less significant than in the general population. When compared to a previous French study with people affected with DS, pubertal growth acceleration begins at a later age for girls and boys; girls in our study are taller at age 15 (+5 cm), but there is no difference for boys at this age. Overweight is more frequent compared to the typical French population. Mean body mass index (BMI) rises rapidly above the 75th percentile of typical French children as early as age 4, with an earlier age for precocious adiposity rebound. The second period for rapid increase of BMI is around 14 years old. When compared to a previous French study with DS, we did not observe any BMI increase, at least up to the age of 14.

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Neurogenesis impairment: An early developmental defect in Down syndrome

Cited by 81 publications

References 168 publications

New approaches to studying early brain development in Down syndrome

New approaches to studying early brain development in Down syndrome

Development of Cortical Neuron Heterogeneity and Impact of Neurodevelopmental Disorders

Growth curves for French people with Down syndrome from birth to 20 years of age

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