Dr. Geschwind is the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics, Neurology and Psychiatry at UCLA.
In his capacity as Senior Associate Dean and Associate Vice Chancellor of Precision Health, he leads the Institute for Precision Health (IPH) at UCLA, where he oversees campus precision health initiatives. In his laboratory, his group has pioneered the application of systems biology methods in neurologic and psychiatric disease, with a focus on autism spectrum disorders (ASD) and neurodegenerative conditions.
Dr. Geschwind is a pioneer in the transcriptomic and functional genomic analyses of the nervous system. His laboratory showed that gene co-expression has a reproducible network structure that can be used to understand neurobiological mechanisms in health and disease. He led the first studies to define the molecular pathology of autism and several other major psychiatric disorders and has made major contributions to defining the genetic basis of autism. He demonstrated the utility of using gene network approaches to discover new pathways involved in neurodegeneration and new approaches to facilitate neural regeneration. More recently, his laboratory demonstrated how knowledge of 3-dimensional chromatin structure can be used to understand the functional impact of human genetic variation.
Dr. Geschwind has trained over 70 graduate students and post-doctoral research fellows and is among the highest cited scientists in neurology, neuroscience and genetics (H index > 140).
In addition to serving on several scientific advisory boards, including the Faculty of 1000 Medicine, the Scientific Advisory Board for the Allen Institute for Brain Science, the NIMH Advisory Council and the NIH Council of Councils, he currently serves on the editorial boards of the journals Cell, Neuron and Science. He has received several awards for his laboratory’s work is an elected Member of the American Association of Physicians and the National Academy of Medicine.
Medical Board Certifications
Neurology, American Board of Psychiatry and Neurology, 1996
UCLA School of Medicine, 1997
UCLA School of Medicine, 1995
UCLA School of Medicine, 1992
Yale University School of Medicine, MD, 1991
Super doctors, Southern California, 2021
Ronald Reagan UCLA Medical Center
- Scientific Service Award from Autism Speaks, 2008
- Derek Denny-Brown Neurological Scholar Award from the American Neurological Association, 2004
Circa May 25, 2011
The brains of people with autism are chemically different from those without autism, according to researchers.
A study, published in the journal Nature, showed the unique characters of the frontal and temporal lobes had disappeared.
Different genes should be active in each region, but autistic brains had the same pattern of gene expression.
The National Autistic Society said the results could be important for future treatments.
Autism spectrum disorders, including Asperger’s syndrome, are common and affect more than 500,000 people in the UK.
They are thought to be caused by a combination of genetics and the environment.
Professor Daniel Geschwind, from the University of California, Los Angeles, said: “If you randomly pick 20 people with autism, the cause of each person’s disease will be unique.
“Yet when we examined how genes and proteins interact in autistic people’s brains, we saw well-defined shared patterns. This common thread could hold the key to pinpointing the disorder’s origins.”
The scientists in the UK, US and Canada compared samples from 19 autistic brains and 17 without.
They noticed that 209 genes linked to the way brain cells work and talk to each other were working at a lower level in autistic brains while 235 genes linked to immune and inflammatory responses were expressed more strongly.
The researchers said many of these genes had already been linked to the condition.
They also noted that there was no longer a difference in the genes expressed in the frontal and temporal lobes in the brain.
Professor Daniel Geschwind said: “Instead, the frontal lobe closely resembles the temporal lobe.”
It is likely due to defective brain development, they argue.
Richard Mills, director of research at the National Autistic Society said: “We are beginning to better understand the differences between the brains of people with autism and those without.
“If replicated these findings are important for the development of interventions which may reduce the more disabling effects of autism.
“They also confirm the importance of research that can shed light on underlying mechanisms. It is critical that we continue our investment in high quality research consortia.”
April 6, 2012
LOS ANGELES, April 6 (UPI) — U.S. researchers estimate there are likely about 1,000 or more genes that contribute to autism spectrum disorder risk, but mutations might be the key.
Dr. Daniel Geschwind, a professor of neurology and psychiatry at the University of California, Los Angeles, and colleagues from Yale University, Carnegie Mellon University and the University of Pittsburgh, completed “whole-exome sequencing” of 238 parent-child quartets.
A quartet is defined as two parents and one child without autism spectrum disorder and one child with autism spectrum disorder. Whole-exome sequencing is an efficient strategy to sequence the coding regions of the genome selectively, as a cheaper but still effective alternative to whole genome sequencing.
The researchers compared mutation rates between unaffected individuals and those with autism spectrum disorder within a family, and then compared autism spectrum disorder mutations to the entire study.
They found multiple variations between unaffected and affected groups. Specifically, among a total of 279 coding mutations, they identified a single instance in individual children with autism spectrum disorder — and not in siblings — in which two independent mutations disrupt the gene SCN2A.
That same mutation was found in all the unrelated children with autism spectrum disorder, confirming its importance.
The study was published in the journal Nature.
SFARI > Spectrum
February 7, 2017
People from minority groups have traditionally been underrepresented in autism research, and genetic studies are no exception.
For example, African-Americans constituted just over 2 percent of individuals in the Autism Genetic Resource Exchange, a large repository of genetic information, in 2008. African-Americans make up 13 percent of the total U.S. population, according to the 2015 census.
This lack of diversity is a serious shortcoming for the studies. For example, researchers can miss variants that crop up only in certain populations.
Daniel Geschwind’s team at the University of California, Los Angeles (UCLA), along with researchers at three other universities set out in 2013 to increase the number of African-Americans in autism studies. One aim of the project is to see whether patterns of variants tied to autism in people of European descent also augur risk in African-Americans. So far, the answer seems to be no.
We asked Geschwind what strategies his team is using to recruit families, and why the work is important. … Full story on Spectrum.
Note: Spectrum is part of the SFARI and Simons Foundation family.
February 9, 2018
Shared molecular neuropathology across major psychiatric disorders parallels polygenic overlap
Published February 9, 2018 in Science, Gandal, Haney, et al
Research led by Daniel Geschwind of the University of California, Los Angeles used postmortem brain tissue, including resources from Autism BrainNet, found similar gene expression patterns in the brains of those with autism, schizophrenia, and bipolar disorder. All three conditions show an activation of genes in star-shaped brain cells called astrocytes, and suppression of genes that function at synapses, the junctions between neurons. The autism brains also show a unique increase in the expression of genes specific to immune cells called microglia. Below is the abstract from the report, followed by a link to the full text.
The predisposition to neuropsychiatric disease involves a complex, polygenic, and pleiotropic genetic architecture. However, little is known about how genetic variants impart brain dysfunction or pathology. We used transcriptomic profiling as a quantitative readout of molecular brain-based phenotypes across five major psychiatric disorders—autism, schizophrenia, bipolar disorder, depression, and alcoholism—compared with matched controls. We identified patterns of shared and distinct gene-expression perturbations across these conditions. The degree of sharing of transcriptional dysregulation is related to polygenic (single-nucleotide polymorphism–based) overlap across disorders, suggesting a substantial causal genetic component. This comprehensive systems-level view of the neurobiological architecture of major neuropsychiatric illness demonstrates pathways of molecular convergence and specificity.