# Neurophysiologic investigation of somatosensory dysfunction in Autism Spectrum Disorders

> **NIH NIH R21** · BOSTON CHILDREN'S HOSPITAL · 2020 · $502,535

## Abstract

Project Summary
Autism spectrum disorders (ASD) are the cause of large health-related and economical costs in the U.S. Thus,
interventions that relieve symptoms for ASD patients are urgently needed. There are currently no treatments
approved by the Food and Drug Administration for ASD. The development of novel therapeutic interventions
will require early and reliable biomarkers and improved understanding of the underlying ASD pathophysiology.
Most of the research on ASD so far has focused on mechanisms and circuits specific to the central nervous
system with little attention to the contributions of abnormal signaling in the peripheral nervous system and
spinal cord to the pathophysiology and core symptoms of ASD. Critically, most ASD patients exhibit enhanced
responses to sensory stimuli, including tactile stimuli. Moreover, the degree of tactile hypersensitivity is
strongly correlated with increased anxiety behaviors and social-behavior deficits observed in ASD. However,
there are currently no neurophysiologic indices of tactile hypersensitivity and its contribution to dysfunction of
brain networks.
In cohorts of 40 ASD young adults, and 40 neurotypical young adults, we will compare the responses to paired
associative stimulation (PAS) of the median nerve and the primary motor cortex between individuals with ASD
and the control group – this will serve as a primary measure of the lasting effects on cortical cuntion that
aberrant (pathologically heightened) peripheral signaling may have in ASD. Second, we will examine the
correlation between the extent of abnormal PAS response in the ASD group and the degree of tactile
hypersensitivity as objectively quantified by tactile prepulse inhibition (PPI) and mechanical detection threshold
with von Frey fibers. Third, we will test the contribution of the common Val66Met single-nucleotide
polymorphism (SNP) in the brain-derived neurotrophic factor (BDNF) gene to PAS measures.
Each participant will undergo 4 visits, including two visits for quantitative tactile assessments and two visits for
assessment of PAS-induced plasticity. All participants will undergo baseline assessment, including detailed
screening, physical/neurological exam, neuropsychological assessment, and assessment of saliva samples for
the BDNF SNP to explore predictors of PAS response.
The proposed studies will be the first to validate well-formulated hypotheses from animal ASD research with
PAS measures of tactile hypersensitivity. Favorable results from proposed experiments will validate
standardized tools as biomarkers of tactile hypersensitivity in ASD and will provide measures of target
engagement in future therapeutic trials aimed at improving tactile hypersensitivity and associated anxiety and
social behavior deficits among ASD patients.

## Key facts

- **NIH application ID:** 10057023
- **Project number:** 1R21MH120438-01A1
- **Recipient organization:** BOSTON CHILDREN'S HOSPITAL
- **Principal Investigator:** Alexander Rotenberg
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $502,535
- **Award type:** 1
- **Project period:** 2020-05-11 → 2023-05-10

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10057023

## Citation

> US National Institutes of Health, RePORTER application 10057023, Neurophysiologic investigation of somatosensory dysfunction in Autism Spectrum Disorders (1R21MH120438-01A1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10057023. Licensed CC0.

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