# Beyond Baby Siblings: Early Developmental Trajectories and Biomarkers of Risk for ASD

> **NIH NIH P50** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2020 · $301,396

## Abstract

PROJECT SUMMARY
Identification of the earliest markers of risk for ASD holds tremendous clinical relevance, as it informs the
implementation of early interventions that may attenuate symptoms and even prevent the development of ASD.
Historically, infant siblings of children with ASD have constituted the primary focus of research in early
markers. However, other high risk groups based on genetic diagnosis have been identified over the past
several years. Studying infants at heightened genetic risk for ASD affords us a valuable opportunity to examine
both distinct and shared neurobiological pathways to the core features that define autism symptoms. Such
investigations not only shed light on mechanisms underlying atypical development in high-risk infants, but they
can also clarify the ideal timing and target of early interventions that may modulate developmental trajectories.
Here, we take a genetics-first approach and investigate biomarkers of risk for ASD and predictors of outcome
in early infancy in three genetically defined groups with elevated risk: infants with an older sibling with ASD
(familial risk), infants with Tuberous Sclerosis Complex (TSC), and infants with 22q11.2 deletion syndrome
(22q11). We select these groups both because of our unique ability to study these populations at UCLA and
because they allow us to examine ASD as it emerges in the context of three genetic pathways: polygenic risk
(familial risk), single gene mutations (TSC), and copy number variation (22q11.2 deletion). We combine
electrophysiology (EEG) with magnetic resonance imaging (MRI) to examine neurodevelopmental processes in
the first year of life that may underlie the impairments that define ASD: (1) resting state/baseline neural
synchrony and connectivity, (2) low level sensory processing and (3) brain activity and connectivity in language
and salience networks. We study infants at 1.5, 3, 6, 9, 12 months with MRI (1.5 and 9 months), EEG (3-12
months), and behavioral (3-12 months) assays and then perform standardized assessments of cognition and
autism symptoms at 12, 24 and 36 months. The project has synergy with the other ACE projects. Infants
demonstrating early signs of ASD in this project will be referred to the infant intervention study in Project II (PI:
Kasari). With Project III (PI: Dapretto), we share leadership and employ common measures of brain activity
and connectivity. This project also will rely on the Diagnostic and Phenotyping Core (PI: McCracken, Co-PI
Gulsrud) for developmental and diagnostic testing. We also will integrate with the Biomarkers Core (PI:
Geschwind, Co-PI Jeste), with data collection performed in the Jeste and Dapretto labs and imaging/EEG data
combined with data from the other projects for larger scale analyses of heterogeneity from infancy to
adolescence. Saliva samples for genetics will be gathered at baseline from all participants for analysis of
CNV's and polygenic risk. Each aim of this project is grounded in the overarc...

## Key facts

- **NIH application ID:** 9984495
- **Project number:** 5P50HD055784-14
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Shafali Spurling Jeste
- **Activity code:** P50 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $301,396
- **Award type:** 5
- **Project period:** 2007-08-06 → 2022-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9984495

## Citation

> US National Institutes of Health, RePORTER application 9984495, Beyond Baby Siblings: Early Developmental Trajectories and Biomarkers of Risk for ASD (5P50HD055784-14). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9984495. Licensed CC0.

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