About

Allan Reiss is a professor in the Department of Psychology and Behavior Sciences at Stanford University, associated with the Center for Interdisciplinary Brain Sciences Research and Radiology. His research focuses on the brain sciences, particularly in the context of psychology and behavior sciences. Reiss's work involves interdisciplinary approaches to understanding brain functions and their relation to behavior, contributing to the broader field of human biology and neuroscience.

Research topics

• Neuroscience
• Biology
• Psychology
• Endocrinology
• Genetics
• Computer Science
• Medicine
• Developmental psychology
• Psychiatry
• Internal medicine
• Cognitive psychology
• Cognitive science
• Pediatrics

Selected publications

• Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion

  Molecular Psychiatry · 2026-02-20

  articleOpen access

  22q11.2 deletion (22qDel) and duplication (22qDup) carriers have an increased risk of neurodevelopmental disorders and exhibit altered brain structure, including white matter microstructure. However, the underlying cellular architecture and age-related changes contributing to these white matter alterations remain poorly understood. Neurite orientation dispersion and density imaging (NODDI) was used on mixed cross-sectional and longitudinal data to examine group differences and age-related trajectories in measures of axonal density (i.e., intracellular volume fraction; ICVF), axonal orientation (orientation dispersion index; ODI) and free water diffusion (isotropic volume fraction; ISO) in 50 22qDel (n scans = 69, mean age = 20.7, age range = 7.4-51.1, 64.0% female) and 24 22qDup (n scans = 34, mean age = 21.6, age range = 8.3-49.4, 54.2% female) carriers, and 890 controls (n scans = 901, mean age = 21.9, age range = 7.8-51.1, 54.5% female). The results showed widespread gene dosage effects, with higher ICVF in 22qDel and lower ICVF in 22qDup compared to controls, and region-specific effects of the 22qDel and 22qDup on ODI and ISO measures. However, 22qDel and 22qDup carriers did not exhibit altered age-related trajectories relative to controls. Observed differences in ICVF suggest higher white matter axonal density in 22qDel and lower axonal density in 22qDup compared to controls. Conversely, differences in ODI are highly localized, indicating region-specific effects on axonal dispersion in white matter. We do not find evidence for altered developmental trajectories of axonal density or dispersion among 22q11.2 CNV carriers, suggesting stable disruptions to neurodevelopmental events before childhood.

  PublisherOA PDFDOI

• P267: Neuropsychiatric manifestations in Myhre syndrome: Expanding the phenotype to guide early diagnosis and monitoring

  Genetics in Medicine Open · 2026-01-01

  articleOpen access

  Introduction: Undiagnosed adults presenting to genetics clinics often require exome and genome sequencing (ES/GS) to help identify the underlying cause of their condition.However, many insurance companies deny these tests based on the patient's age, despite the presence of symptoms that began in childhood.As a result, these individuals are frequently denied access to diagnostic methods that could reduce uncertainty, prevent misdiagnosis, and improve treatment outcomes.One of the primary goals of the Undiagnosed Diseases Network (UDN) is to provide access to comprehensive clinical evaluations, including ES/GS, for participants who have not had the opportunity to undergo these evaluations previously.Methods: This retrospective review focused on UDN participants who were at least 18 years old at the time of application and reported that their symptoms began at age 17 or younger.We included only those who had a completed medical records review conducted by the clinical site to which they were assigned.Participants who turned 18 after enrollment in the UDN were excluded.Data were obtained from the UDN Gateway.Demographic data, including age, were self-reported by participants.Phenotypic data and diagnostic outcomes were provided by the UDN clinical sites.Results: A total of 485 UDN participants were included in the analysis.Of these, 129 participants (26.7%) received at least one highly likely or certain diagnosis.Among the 51 adults who reported congenital symptoms, the diagnostic rate was 31.6%.The average age of symptom onset for the entire cohort was 6 years (median 3 years).In the diagnosed cohort, the average age of onset was 4 years (median 1 year).Of the diagnosed participants, 107 (82.9%) received their diagnosis through genome-scale sequencing, including exome and genome sequencing.Regarding the timing of diagnoses, 78 participants (60.4%) received their diagnosis after undergoing the UDN evaluation, 23 participants (17.8%) had a diagnosis made before the UDN evaluation, and 20 participants (15.5%) received their diagnosis during the UDN evaluation.Neurological conditions were the most common phenotype (45.2%) among adults with childhood-onset conditions.Conclusion: This study describes a cohort of undiagnosed adults with childhood-onset conditions who were evaluated by the UDN.Of these participants, 26.7% received a diagnosis, slightly lower than the 30% diagnostic rate reported for all UDN participants, but higher than the 19.9% diagnostic rate previously identified for all adult participants in earlier research.The majority of diagnoses were made using ES/GS.These findings highlight the importance of ES/GS for patients with symptoms that began in childhood, emphasizing that genetic testing can provide critical insights into their conditions.

  PublisherOA PDFDOI

• Atypical Inter-Brain Synchrony and Social Communication Deficits in Girls with Fragile X Syndrome: Evidence from Functional Near-infrared Spectroscopy Hyperscanning

  Research Square · 2025-10-17

  preprintOpen accessSenior author
  PublisherOA PDFDOI

• Relationship Between Intellectual Disability and Behavioral Comorbidity in Children With Fragile X Syndrome

  Journal of Autism and Developmental Disorders · 2025-10-23 · 1 citations

  article
  PublisherDOI

• Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-30

  preprintOpen access

  22q11.2 deletion (22qDel) and duplication (22qDup) carriers have an increased risk of neurodevelopmental disorders and exhibit altered brain structure, including white matter microstructure. However, the underlying cellular architecture and age-related changes contributing to these white matter alterations remain poorly understood. Neurite orientation dispersion and density imaging (NODDI) was used on mixed cross-sectional and longitudinal data to examine group differences and age-related trajectories in measures of axonal density (i.e., intracellular volume fraction; ICVF), axonal orientation (orientation dispersion index; ODI) and free water diffusion (isotropic volume fraction; ISO) in 50 22qDel (n scans = 69, mean age = 21.7, age range = 7.4-51.1, 65.2% female) and 24 22qDup (n scans = 34, mean age = 23.3, age range = 8.3-49.4, 55.0% female) carriers, and 890 controls (n scans = 901, mean age = 21.9, age range = 7.8-51.1, 54.5%). The results showed widespread gene dosage effects, with higher ICVF in 22qDel and lower ICVF in 22qDup compared to controls, and region-specific effects of the 22qDel and 22qDup on ODI and ISO measures. However, 22qDel and 22qDup carriers did not exhibit an altered age-related trajectory relative to controls. Observed differences in ICVF suggest higher white matter axonal density in 22qDel and lower axonal density in 22qDup compared to controls. Conversely, differences in ODI are highly localized, indicating region-specific effects on axonal dispersion in white matter. We do not find evidence for altered developmental trajectories of axonal density or dispersion among 22q11.2 CNV carriers, suggesting stable disruptions to neurodevelopmental events before childhood.

  PublisherOA PDFDOI

• Distinct and shared intrinsic resting-state functional networks in children with idiopathic autism spectrum disorder and fragile X syndrome

  Molecular Psychiatry · 2025-07-15 · 2 citations

  articleOpen access

  Autism spectrum disorder (ASD) and fragile X syndrome (FXS) are behaviorally overlapped. However, little is known about the functional patterns underlying the cognitive and behavioral characteristics of FXS and ASD. The present study aimed to identify the distinct or/and shared functional networks in young children with FXS and idiopathic ASD. We recruited 150 children consecutively in a group with FXS, a group with idiopathic ASD, and a group with typically developing (TD) children. Resting-state functional magnetic resonance imaging (fMRI) and behavioral data were collected and genetic information was obtained in the FXS group. We compared functional connectivity (FC) among the three groups and found that both FXS and ASD showed significantly decreased FC among the default mode network (DMN), sensorimotor network (SMN), cerebellum network (CN), and visual network (VN) relative to TD. FXS specifically demonstrated decreased FC within DMN, while both FXS and ASD exhibited significantly decreased FC within the CN and also between the CN and DMN, SMN, VN, respectively. Aberrant topological alterations of CN were identified in children with FXS and ASD, while ASD group showed significantly lower segregation in regions that integrate sensory and visual information, and motor coordination function. Moreover, correlations between the severity of social affect and mean FC of various cerebral-cerebellum networks in FXS exhibited significantly distinct trends from those observed in ASD. In the FXS group, the topological measure at crus I of the cerebellum is found to be negatively associated with DNA methylation levels. These results were statistically robust and demonstrated the shared and distinct profiles of intrinsic functional networks in FXS and ASD, two phenotypically overlapping developmental disorders.

  PublisherOA PDFDOI

• Aberrant neural activation during inhibitory control in girls with fragile X syndrome

  Cerebral Cortex · 2025-05-13

  articleSenior author

  Fragile X syndrome (FXS) is a genetic condition associated with risk for deficits in executive function, especially response inhibition. Under a clinical setting, this study employs a mobile neuroimaging technique, functional near-infrared spectroscopy (fNIRS), to examine differences in inhibition-elicited neural activation between girls with FXS and a control group matched for age, cognitive function, and clinical symptoms. fNIRS data were collected from 42 girls with FXS and 31 controls during a go/nogo task, with valid data available from 35 and 30 respectively. Relative to the control group, girls with FXS showed higher brain activation (NoGo>Go) in the right dorsolateral prefrontal cortex (DLPFC), angular gyrus, precentral gyrus, and left frontal pole, and lower activation in the right ventrolateral prefrontal cortex, frontal pole, precentral cortex, middle temporal cortex, parietal lobe, and left superior temporal cortex. A significant positive correlation was found between DLPFC activation and response inhibition deficits in girls with FXS. Girls with FXS show abnormal neural activation in response to inhibitory stimulus. Aberrant neural activation in DLPFC in girls with FXS is associated with executive function deficits. fNIRS is established to allow participants to engage in a task in relatively more "real world" conditions compared to the scanner environment.

  PublisherDOI

• Differences in White Matter Microstructure in Children With Type 1 Diabetes Persist During Longitudinal Follow-up: Relation to Dysglycemia

  Diabetes · 2025-06-02 · 6 citations

  articleOpen accessSenior author

  Type 1 diabetes has detrimental effects in white matter microstructure. In a longitudinal study, we investigated whether these reported findings change as children grow and enter puberty. At study entry, there were 143 children with type 1 diabetes and 71 control participants without diabetes, 4-9 years old. Brain MRI using diffusion tensor imaging, neurocognitive, and glycemic assessments were performed four times across 6-8 years of follow-up. Longitudinal mixed-effects modeling was used to examine changes in fractional anisotropy (FA), axial diffusivity (AD) (measures of myelination and fiber integrity), radial diffusivity (RD) (axonal leakage), and mean diffusivity (MD) (average diffusion). Associations with glycemic and cognitive measures were assessed. We observed in 182 children (121 type 1 diabetes vs. 61 control participants) who had testing at time 4 that FA increased, and RD, AD, and MD decreased significantly in both groups, with no differences between groups for FA, RD and MD over time. However, children with diabetes had lower AD than control participants at 6-10 years. Differences were not detected at 12 years (age imputed from data), when in puberty. Higher blood glucose levels are associated with lower FA and higher RD and MD. Higher glucose percentage time-in-range was associated with higher FA, reflecting better fiber integrity and myelination and higher cognitive metrics. Within the diabetes group, AD and MD showed no association with neurocognitive outcomes. In summary, white matter AD was decreased in children with diabetes, less so during puberty, and FA was reciprocally related to hyperglycemia. These data suggest continued negative impact of chronic hyperglycemia in the developing brain. ARTICLE HIGHLIGHTS: Type 1 diabetes has detrimental effects in white matter in young children. We performed a longitudinal study using brain MRI (diffusion tensor imaging) and cognitive assessments in 4- to 9-year-old children, control participants without diabetes (n = 71) and with type 1 diabetes (n = 143), plus continuous glucose monitoring, to assess changes at four time points as children grow over 6-8 years. White matter myelination and fiber integrity were assessed using axial diffusivity, which was decreased in the diabetes versus control group, less so during puberty, and fractional anisotropy was reciprocally related to hyperglycemia. Data suggest continued negative impact of chronic hyperglycemia in the developing brain.

  PublisherOA PDFDOI

• <b>Differences in White Matter Microstructure in Children With Type 1 Diabetes Persist During Longitudinal Follow up: Relation to Dysglycemia</b>

  2025-06-02

  preprintOpen accessSenior author

  <p dir="ltr">Type 1 diabetes has detrimental effects in white matter microstructure. In a longitudinal study, we investigated if these reported findings change as children grow and enter puberty.</p><p dir="ltr">143 children with type 1 diabetes and 71 non-diabetic controls, 4-9 years old at study entry had brain MRI using diffusion tensor imaging, neurocognitive and glycemic assessments at 4 time points across 6-8 years of follow-up. Longitudinal mixed-effects modeling was used to examine changes in fractional anisotropy (FA), axial diffusivity (AD) (measures of myelination and fiber integrity), radial diffusivity (RD) (axonal leakage) and mean diffusivity (MD) (average diffusion). Associations with glycemic and cognitive measures were assessed.</p><p dir="ltr">We observed in 182 children (121 type 1 diabetes, vs. 61 controls) who had testing at Time 4 that FA increased, and RD, AD, MD decreased significantly in both groups, with no differences between groups for FA, RD and MD over time. However, children with diabetes had lower AD than controls at 6-10 years, differences not detected at 12 years (age imputed from data), when in puberty. Higher blood sugars are associated with lower FA, higher RD and MD. Higher glucose %Time-in-Range was associated with higher FA, reflecting better fiber integrity and myelination, and higher cognitive metrics. Within the diabetes group AD and MD showed no association with neurocognitive outcomes.</p><p dir="ltr"><b>In summary, </b>white matter axial diffusivity was decreased in children with diabetes, less so during puberty, and fractional anisotropy was reciprocally related to hyperglycemia. These data suggest continued negative impact of chronic hyperglycemia in the developing brain.</p>

  PublisherDOI

• <b>Differences in White Matter Microstructure in Children With Type 1 Diabetes Persist During Longitudinal Follow up: Relation to Dysglycemia</b>

  2025-06-02

  preprintOpen accessSenior author

  <p dir="ltr">Type 1 diabetes has detrimental effects in white matter microstructure. In a longitudinal study, we investigated if these reported findings change as children grow and enter puberty.</p><p dir="ltr">143 children with type 1 diabetes and 71 non-diabetic controls, 4-9 years old at study entry had brain MRI using diffusion tensor imaging, neurocognitive and glycemic assessments at 4 time points across 6-8 years of follow-up. Longitudinal mixed-effects modeling was used to examine changes in fractional anisotropy (FA), axial diffusivity (AD) (measures of myelination and fiber integrity), radial diffusivity (RD) (axonal leakage) and mean diffusivity (MD) (average diffusion). Associations with glycemic and cognitive measures were assessed.</p><p dir="ltr">We observed in 182 children (121 type 1 diabetes, vs. 61 controls) who had testing at Time 4 that FA increased, and RD, AD, MD decreased significantly in both groups, with no differences between groups for FA, RD and MD over time. However, children with diabetes had lower AD than controls at 6-10 years, differences not detected at 12 years (age imputed from data), when in puberty. Higher blood sugars are associated with lower FA, higher RD and MD. Higher glucose %Time-in-Range was associated with higher FA, reflecting better fiber integrity and myelination, and higher cognitive metrics. Within the diabetes group AD and MD showed no association with neurocognitive outcomes.</p><p dir="ltr"><b>In summary, </b>white matter axial diffusivity was decreased in children with diabetes, less so during puberty, and fractional anisotropy was reciprocally related to hyperglycemia. These data suggest continued negative impact of chronic hyperglycemia in the developing brain.</p>

  PublisherDOI

Recent grants

• Research Training for Child Psychiatry and Neurodevelopment

  NIH · $6.9M · 1993–2026

• NIH Grant R01HD049653

  NIH · $6.0M · 2018

• NIH Grant K11MH000726

  NIH · $466k · 1992

• NIH Grant R01MH064708

  NIH · $8.1M · 2018

• NIH Grant K02MH001142

  NIH · $1.3M · 2004

Frequent coauthors

• Gary H. Glover

  Stanford University

  153 shared

• Amy Garrett

  The University of Texas Health Science Center at San Antonio

  149 shared

• Laurence L. Greenhill

  University of California, San Francisco

  110 shared

• Simon T. Tonev

  Clinical Research Institute

  110 shared

• Jeffery N. Epstein

  106 shared

• Julie Spicer

  106 shared

• Alan Vitolo

  Duke University

  106 shared

• Stephen P. Hinshaw

  University of California, San Francisco

  106 shared

Education

• Ph.D., Human Biology

  Stanford University

  1980

• M.D., Medicine

  Stanford University School of Medicine

  1976

• B.A., Human Biology

  Stanford University

  1972