Early Brain Developmental Process Linked to Autism, Schizophrenia and Epilepsy

Anju Vasudevan, Ph.D., Brain Research Expert and Schizophrenia Expert
Anju Vasudevan, Ph.D.

In the continuing search for glitches in brain development that may give rise later on to serious illnesses such as schizophrenia, autism spectrum disorder (ASD) and epilepsy, research done by a team at Harvard University offers a new perspective. They found that blood vessel-related defects that originate during the brain’s earliest developmental stages may play a role in the development of these disorders. This research was led by 2009 NARSAD Young Investigator Grantee Anju Vasudevan, Ph.D., Director of the Angiogenesis & Brain Development Laboratory at McLean Hospital and Assistant Professor of Psychiatry at Harvard Medical School. The research team includes 2009 NARSAD Young Investigator Grantee Zhicheng Lin, Ph.D., from McLean Hospital and Harvard Medical School.

In this study published on July 16th in Nature Communications, Dr. Vasudevan and colleagues report that networks of blood vessels in the developing brain play an important role in regulating a type of brain cell (or neuron) essential to healthy brain function. The neurons in question are called GABA neurons, after the main chemical neurotransmitter that conveys “inhibitory” signals in the brain. Without a properly working network of GABA neurons deployed at strategic points throughout the brain, “excitatory” signals can propagate unchecked, causing overload and severe epilepsy-like seizures.

Well before birth, in the earliest days of brain development in people, rodents and other mammals, GABA neurons are “born” in a portion of the emerging brain that is like an incubator for various types of brain cells. The immature GABA cells have to migrate from this region of their birth to assume places in the emerging cerebral cortex, the place in the mature brain where essential functions like memory, attention, thought, perception and language are performed.

In this current work, the researchers made the surprising discovery that migrating GABA cells follow a route into the cortex for which blood vessels lay down a kind of guide, but also interact with the neurons in a manner that “molds their development” in important ways. Additionally, many of the genes linked to ASD, schizophrenia and epilepsy are expressed not only in neurons, as traditionally believed, but also in endothelial cells signifying the new possibility of common molecular signals defective specifically in blood vessels.

Since blood vessels interact with neurons and help regulate them in the earliest stages of the brain’s emergence, it is now possible to think that angiogenesis―the process by which blood vessels develop―may play a role never before anticipated. The emergence of blood vessels may be involved, in other words, in the pathology of disorders like ASD and schizophrenia, which many scientists suspect begin to develop in the period when the brain is “wiring up.”

Article comments

often wondered if our grandson was affected by some Autism Disorder, screamed and shrieked a lot, highly emotional and touchy, sensory issues, ADHD-like symptoms, separation anxiety..learning problems,,didn't formally communicate quickly, many pronounced tendancies. Was premature, low birth weight, now teenager, diagnosed schizoaffective, bipolar sybtype or schizophrenic

Schizophrenia is a very trumatic disorder. It is the worst of mental disorders. I am happy to see that the team is on to something by studying GABA, neurons, and the blood vessel connection. The team is definately on to something. Genetics is the main indicator of mental disorders, together with environmental factors. I believe the environment is also a collaborator of early onset schizophrenia.

Schizophrenia is a very trumatic disorder. It is the worst of mental disorders. I am happy to see that the team is on to something by studying GABA, neurons, and the blood vessel connection. The team is definately on to something. Genetics is the main indicator of mental disorders, together with environmental factors. I believe the environment is also a collaborator of early onset schizophrenia.

Very interesting as we suspect research: We still suspect with proof that our son's schizophrenia was a result of a delayed cesarean that might have damaged parts of his brain sufficient to impede a proper early child-brain development. Our son is remarkably highly intelligent (memory,creativity, and sensitivity-perceptive) in certain other cognitive aspects ( sequencing-organisation, writing-dexterity) he struggled throughout his youth-teens. At age 12 years he declared that his brain was racing with thoughts which he could not stop, he was worried that something was not right......and he developed a noticeable tremor in his hand in his teens which began impeding his writing ability (he always had difficulty in writing, but it until then legible), an increase in auditory processing disorder, and loss of smell became very obvious in his teens. We thought these symptoms were a neurological disorder which it might have been, and in time these interfered with his ability to cope with stressful demands (academic/social) resulting in schizophrenia....???? Damage at birth (during birth) might also be another factor.

Great Going..... Go Ahead !!!

There are increasing evidences that favor the prenatal beginning of schizophrenia. These evidences point toward intra-uterine environmental factors that act specifically during the second pregnancy trimester producing a direct damage of the brain of the fetus. The current available technology doesn't allow observing what is happening at cellular level since the human brain it is not exposed to a direct analysis in that stage of the life. In 1977 we began a direct research of the brain of fetuses of schizophrenic mothers in order to finding differences at cellular level in relation to controls. In these studies we have observed within the nuclei of neurons the presence of complete and incomplete viral particles that reacted in positive form with antibodies to herpes simplex hominis type I [HSV1] virus, and mitochondria alterations. The importance of these findings can have practical applications in the prevention of the illness keeping in mind its direct relation to the aetiology and physiopathology of schizophrenia

Defective blood vessels in the fetal brain is an exciting pathway to follow. A viral connection in the fetal brain of schizophrenic mothers is also of high interest in terms of proof of a genetic cellular model. But schizophrenia does not develop until late adolescence or early adulthood in many persons, often after relatively successful or- at least uneventful- childhood and adolescence. IOn light of all we have learned about neuroplasticity, one would think that through those developmental periods, the brain should have had time to heal itself of birth defecits

Have you seen the "Ambien Effect"? Apparently, Ambien has been helpful to some folks with traumatic brain injury, stroke, and other brain traumas and disease, somehow by acting on GABA receptors. It seems to "awaken" neurons thought to be dead. I wonder if this mechanism could be found and be helpful to people with schizophrenia? We must leave no stoned unturned. I thank these people for their hard work. Because of continued research, I believe someday people won't suffer so much.

in reference to neuroplasticity,I would like to suggest that Carla Schatz (former head of neuroscience at Harvard,now at Stanford) has discovered immune molecules known as MHCI"s that can and do cross the brain- blood barrier and can be involved in the development of schizophrenia ,autism,parkinsons etc.!

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