Welcome to The Visible Embryo
The Visible Embryo Birth Spiral Navigation
Fetal Timeline--- -Maternal Timeline-----News-----Prescription Drugs in Pregnancy---- Pregnancy Calculator----Female Reproductive System

WHO International Clinical Trials Registry Platform

The World Health Organization (WHO) has a Web site to help researchers, doctors and patients obtain information on clinical trials.

Now you can search all such registers to identify clinical trial research around the world!




Pregnancy Timeline

Prescription Drug Effects on Pregnancy

Pregnancy Calculator

Female Reproductive System


Disclaimer: The Visible Embryo web site is provided for your general information only. The information contained on this site should not be treated as a substitute for medical, legal or other professional advice. Neither is The Visible Embryo responsible or liable for the contents of any websites of third parties which are listed on this site.

Content protected under a Creative Commons License.
No dirivative works may be made or used for commercial purposes.


Pregnancy Timeline by SemestersDevelopmental TimelineFertilizationFirst TrimesterSecond TrimesterThird TrimesterFirst Thin Layer of Skin AppearsEnd of Embryonic PeriodEnd of Embryonic PeriodFemale Reproductive SystemBeginning Cerebral HemispheresA Four Chambered HeartFirst Detectable Brain WavesThe Appearance of SomitesBasic Brain Structure in PlaceHeartbeat can be detectedHeartbeat can be detectedFinger and toe prints appearFinger and toe prints appearFetal sexual organs visibleBrown fat surrounds lymphatic systemBone marrow starts making blood cellsBone marrow starts making blood cellsInner Ear Bones HardenSensory brain waves begin to activateSensory brain waves begin to activateFetal liver is producing blood cellsBrain convolutions beginBrain convolutions beginImmune system beginningWhite fat begins to be madeHead may position into pelvisWhite fat begins to be madePeriod of rapid brain growthFull TermHead may position into pelvisImmune system beginningLungs begin to produce surfactant
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development

Developmental Biology - Down Syndrome

A Down Syndrome Treatment?

Rutgers-led team uses stem cell-based disease models to pinpoint Down syndrome gene link to impaired memory...

Targeting a key gene before birth could someday help lead to a treatment for Down syndrome by reversing abnormal embryonic brain development and improving cognitive function after birth, according to a Rutgers-led study.

Using stem cells that can turn into other cells, researchers developed two experimental models (1) a living 3D "organoid" model of the brain and (2) a mouse brain model with implanted human cells to investigate early brain development linked to Down's. The study appears in Cell Stem Cell, and focused on human chromosome 21 gene OLIG2.
"Our results suggest the OLIG2 gene is potentially an excellent prenatal therapeutic target to reverse abnormal embryonic brain development, rebalance the two types of neurons in the brain excitatory and inhibitory, as a healthy balance is critical as well as improve postnatal cognitive function."

Peng Jiang PhD, Assistant Professor, Department of Cell Biology and Neuroscience, Rutgers University-New Brunswick, New Jersey, USA.

Usually, a baby is born with 46 chromosomes, but babies with Down syndrome have an extra copy of chromosome 21. That changes how a baby's body and brain develops, which can lead to mental and physical challenges, according to the U.S. Centers for Disease Control and Prevention. Down syndrome patients often develop early-onset Alzheimer's disease as well.
Down syndrome is the most common chromosomal condition diagnosed in the United States. It affects about one in 700 babies, about 6,000 infants are born with the condition each year.

Researchers collected skin cells from Down patients and genetically reprogrammed those cells into human-induced pluripotent stem cells (hiPSCs). Resembling embryonic stem cells, these special cells can develop into many different types of cells, including brain cells, during early life and growth and are useful tools for drug development and disease modeling, according to the National Institutes of Health.

Using brain cells derived from stem cells with an extra copy of chromosome 21, the scientists developed the 3D brain organoid model resembling the early developing human brain. They also developed the mouse brain model, using stem cell-derived human brain cells implanted into the mouse brains within 24 hours of the mice being born. They found that inhibitory neurons - which make our brain function smoothly - were overproduced in both models. The adult mice had impaired memory. They also found the OLIG2 gene is critical to those effects inhibiting it led to improvements.
Reducing OLIG2 function normalizes interneuron production and behavioral deficits.

These results support that working with both brain organoids and a mouse brain model can be useful in studying neurodevelopmental disorders such as autism spectrum disorder. Both tools may also help better explain mechanisms behind Alzheimer's disease.
Down syndrome (DS) brain organoids overproduce OLIG2+ progenitors
DS brain organoids and chimeric mouse brains exhibit excessive interneuron production
OLIG2 directly upregulates expression of transcriptional regulators of interneuron fate
Reducing OLIG2 expression normalizes interneuron production and behavioral deficits

Down syndrome (DS) is a common neurodevelopmental disorder, and cognitive defects in DS patients may arise from imbalances in excitatory and inhibitory neurotransmission. Understanding the mechanisms underlying such imbalances may provide opportunities for therapeutic intervention. Here, we show that human induced pluripotent stem cells (hiPSCs) derived from DS patients overproduce OLIG2+ ventral forebrain neural progenitors. As a result, DS hiPSC-derived cerebral organoids excessively produce specific subclasses of GABAergic interneurons and cause impaired recognition memory in neuronal chimeric mice. Increased OLIG2 expression in DS cells directly upregulates interneuron lineage-determining transcription factors. shRNA-mediated knockdown of OLIG2 largely reverses abnormal gene expression in early-stage DS neural progenitors, reduces interneuron production in DS organoids and chimeric mouse brains, and improves behavioral deficits in DS chimeric mice. Thus, c in DS patients.

RanjieXu, Andrew T. Brawner, Shenglan Li, Jing-Jing Liu, Hyosung Kim, Haipeng Xue, Zhiping P.Pang, Woo-Yang Kim, Ronald P.Hart, Ying Liu and Peng Jiang.

The study's lead author is Ranjie Xu, a postdoctoral researcher in Jiang's lab. Other Rutgers co-authors include Hyosung Kim, a former post-doc in Jiang's lab; Ronald P. Hart, a professor in the Department of Cell Biology and Neuroscience at Rutgers-New Brunswick; Zhiping P. Pang, an associate professor in the Department of Neuroscience and Cell Biology at Rutgers Robert Wood Johnson Medical School, and Jing-Jing Liu, a former post-doc in Pang's lab. Scientists at the University of Texas Health Science Center, Kent State University, and University of Nebraska Medical Center contributed to the study.

Return to top of page

May 29 2019   Fetal Timeline   Maternal Timeline   News  

A living 3D "organoid" model of the brain generated from Down syndrome human stem cells.
CREDIT Ranjie Xu/Rutgers University-New Brunswick, New Jersey, USA.

Phospholid by Wikipedia