Research: Everyone has Unique Brain Anatomy

Apparently this wasn’t thought much 30 years ago. It is also a bit surprising that some of the differences are driven primarily by repeated experiences.

Like with fingerprints, no two people have the same brain anatomy, a study by researchers of the University of Zurich has shown. This uniqueness is the result of a combination of genetic factors and individual life experiences.

The fingerprint is unique in every individual: As no two fingerprints are the same, they have become the go-to method of identity verification for police, immigration authorities and smartphone producers alike. But what about the central switchboard inside our heads? Is it possible to find out who a brain belongs to from certain anatomical features? This is the question posed by the group working with Lutz Jäncke, UZH professor of neuropsychology. In earlier studies, Jäncke had already been able to demonstrate that individual experiences and life circumstances influence the anatomy of the brain.

Experiences make their mark on the brain

Professional musicians, golfers or chess players, for example, have particular characteristics in the regions of the brain which they use the most for their skilled activity. However, events of shorter duration can also leave behind traces in the brain: If, for example, the right arm is kept still for two weeks, the thickness of the brain’s cortex in the areas responsible for controlling the immobilized arm is reduced. “We suspected that those experiences having an effect on the brain interact with the genetic make-up so that over the course of years every person develops a completely individual brain anatomy,” explains Jäncke.

Magnetic resonance imaging provides basis for calculations

To investigate their hypothesis, Jäncke and his research team examined the brains of nearly 200 healthy older people using magnetic resonance imaging three times over a period of two years. Over 450 brain anatomical features were assessed, including very general ones such as total volume of the brain, thickness of the cortex, and volumes of grey and white matter. For each of the 191 people, the researchers were able to identify an individual combination of specific brain anatomical characteristics, whereby the identification accuracy, even for the very general brain anatomical characteristics, was over 90 percent.

Combination of circumstances and genetics

“With our study we were able to confirm that the structure of people’s brains is very individual,” says Lutz Jäncke on the findings. “The combination of genetic and non-genetic influences clearly affects not only the functioning of the brain, but also its anatomy.” The replacement of fingerprint sensors with MRI scans in the future is unlikely, however. MRIs are too expensive and time-consuming in comparison to the proven and simple method of taking fingerprints.

Progress in neuroscience

An important aspect of the study’s findings for Jäncke is that they reflect the great developments made in the field in recent years: “Just 30 years ago we thought that the human brain had few or no individual characteristics. Personal identification through brain anatomical characteristics was unimaginable.”

Prolonged Exposure to Air Pollution Linked to Negative Genetic Changes in Mice

Air pollution — consistently being shown to be a pretty significant issue to public health.

Prolonged exposure to particulate matter in air pollution in the Los Angeles Basin triggered inflammation and the appearance of cancer-related genes in the brains of rats, a Cedars-Sinai study has found.

While previous research has documented the association between air pollution and a variety of diseases, including cancer, the study found markers indicating certain materials in coarse air pollution — nickel, in particular — may play a role in genetic changes related to disease development, said Julia Ljubimova, MD, PhD.

Ljubimova, director of the Nanomedicine Research Center at Cedars-Sinai, is the lead author of the paper, published April 9 in Scientific Reports.

“This study, which looked at novel data gathered in the Los Angeles area, has significant implications for the assessment of air quality in the region, particularly as people are exposed to air pollution here for decades,” Ljubimova said.

44 Genomic Variations Linked to Major Depression in New Research

Genetic variations (variants) are the roughly 0.5% share of DNA that makes individuals unique, as about 99% of human DNA is shared across humans. The word genome represents the entire set of genetic material someone’s made of. With that being said, this research is important because major depressive disorder can be a really crippling affliction, and the more that’s known about it, the more effectively it can be treated or prevented.

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A new meta-analysis of more than 135,000 people with major depression and more than 344,000 controls has identified 44 genomic variants, or loci, that have a statistically significant association with depression.

Of these 44 loci, 30 are newly discovered while 14 had been identified in previous studies. In addition, the study identified 153 significant genes, and found that major depression shared six loci that are also associated with schizophrenia.

Results from the multinational, genome-wide association study were published April 26 in Nature Genetics.

The study was an unprecedented global effort by over 200 scientists who work with the Psychiatric Genomics Consortium. Co-leaders of the study are Patrick F. Sullivan, MD, FRANZCP, Yeargen Distinguished Professor of Psychiatry and Genetics and Director of the Center for Psychiatric Genomics at the University of North Carolina School of Medicine; and Naomi Wray, PhD, Professorial Research Fellow at the University of Queensland in Australia.

“This study is a game-changer,” Sullivan said. “Figuring out the genetic basis of major depression has been really hard. A huge number of researchers across the world collaborated to make this paper, and we now have a deeper look than ever before into the basis of this awful and impairing human malady. With more work, we should be able to develop tools important for treatment and even prevention of major depression.”

“We show that we all carry genetic variants for depression, but those with a higher burden are more susceptible,” Wray said. “We know that many life experiences also contribute to risk of depression, but identifying the genetic factors opens new doors for research into the biological drivers.”

“This pioneering study is incredibly important, for two reasons,” said Josh Gordon, MD, PHD, Director of the U.S. National Institute of Mental Health. Dr. Gordon was not an author on this paper.

“First, it reaffirms the value of large-scale collaborations, particularly in identifying the complex genetics underlying psychiatric illness. Second, it confirms the genetic roots for depression, offering important biological clues that we hope will lead to new and better treatments.”

“Major depression represents one of the world’s most serious public health problems,” said Steven E. Hyman, MD, former director of the U.S. National Institute of Mental Health who is now Director of the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard. Dr. Hyman was not an author on this paper. “Despite decades of effort there have been, until now, only scant insights into its biological mechanisms. This unfortunate state of affairs has severely impeded treatment development, leaving the many people who suffer from depression with limited options. This landmark study represents a major step toward elucidating the biological underpinnings of depression,” Hyman said.

Other findings of the study include:

  • The results can be used for improved therapies — targets of known antidepressant medications were enriched in the genetic findings
  • The genetic basis of depression overlaps importantly with other psychiatric disorders like bipolar disorder and schizophrenia
  • Intriguingly, the genetic basis of depressive disorder also overlaps with that for obesity and multiple measures of sleep quality, including daytime sleepiness, insomnia and tiredness

Studying Mental Illness by Using Artificial 3D Human “Mini-Brains”

A better understanding of mental illness allows for more effective treatments of it, and this highly complex research looks to be a positive contribution to that.

Article: 3-D human ‘mini-brains’ shed new light on genetic underpinnings of major mental illness

Major mental illnesses such as schizophrenia, severe depression and bipolar disorder share a common genetic link. Studies of specific families with a history of these types of illnesses have revealed that affected family members share a mutation in the gene DISC1. While researchers have been able to study how DISC1 mutations alter the brain during development in animal models, it has been difficult to find the right tools to study changes in humans. However, advancements in engineering human stem cells are now allowing researchers to grow mini-organs in labs, and gene-editing tools can be used to insert specific mutations into these cells.

Researchers from Brigham and Women’s Hospital are leveraging these new technologies to study the effects of DISC1 mutations in cerebral organoids — “mini brains” — cultured from human stem cells. Their results are published in Translational Psychiatry.

“Mini-brains can help us model brain development,” said senior author Tracy Young-Pearse, PhD, head of the Young-Pearse Lab in the Ann Romney Center for Neurologic Diseases at BWH. “Compared to traditional methods that have allowed us to investigate human cells in culture in two-dimensions, these cultures let us investigate the three-dimensional structure and function of the cells as they are developing, giving us more information than we would get with a traditional cell culture.”

The researchers cultured human induced pluripotent stem cells (iPSCs) to create three-dimensional mini-brains for study. Using the gene editing tool CRISPR-Cas9, they disrupted DISC1, modeling the mutation seen in studies of families suffering from these diseases. The team compared mini-brains grown from stem cells with and without this specific mutation.

DISC1-mutant mini-brains showed significant structural disruptions compared to organoids in which DISC1 was intact. Specifically, the fluid-filled spaces, known as ventricles, in the DISC1-mutant mini-brains were more numerous and smaller than in controls, meaning that while the expected cells are present in the DISC1-mutant, they are not in their expected locations. The DISC1-mutant mini-brains also show increased signaling in the WNT pathway, a pathway known to be important for patterning organs and one that is disrupted in bipolar disorder. By adding an inhibitor of the WNT pathway to the growing DISC1-mutant mini-brains, the researchers were able to “rescue” them — instead of having structural differences, they looked similar to the mini-brains developed from normal stem cells. This suggests that the WNT pathway may be responsible for the observed structural disruption in the DISC1-mutants, and could be a potential target pathway for future therapies.