A Mechanistic Link between Olfaction and Autism Spectrum Disorder

Liron Rozenkrantz, Ditza Zachor, Iris Heller, Anton Plotkin, Aharon Weissbrod, Kobi Snitz, Lavi Secundo, Noam Sobel

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


Internal action models (IAMs) are brain templates for sensory-motor coordination underlying diverse behaviors [1]. An emerging theory suggests that impaired IAMs are a common theme in autism spectrum disorder (ASD) [2-4]. However, whether impaired IAMs occur across sensory systems and how they relate to the major phenotype of ASD, namely impaired social communication [5], remains unclear. Olfaction relies on an IAM known as the sniff response, where sniff magnitude is automatically modulated to account for odor valence [6-12]. To test the failed IAM theory in olfaction, we precisely measured the non-verbal non-task-dependent sniff response concurrent with pleasant and unpleasant odors in 36 children - 18 with ASD and 18 matched typically developing (TD) controls. We found that whereas TD children generated a typical adult-like sniff response within 305 ms of odor onset, ASD children had a profoundly altered sniff response, sniffing equally regardless of odor valance. This difference persisted despite equal reported odor perception and allowed for 81% correct ASD classification based on the sniff response alone (binomial, p < 0.001). Moreover, increasingly aberrant sniffing was associated with increasingly severe ASD (r = -0.75, p < 0.001), specifically with social (r = -0.72, p < 0.001), but not motor (r < -0.38, p > 0.18), impairment. These results uncover a novel ASD marker implying a mechanistic link between the underpinnings of olfaction and ASD and directly linking an impaired IAM with impaired social abilities.

Original languageEnglish
Pages (from-to)1904-1910
Number of pages7
JournalCurrent Biology
Issue number14
StatePublished - 20 Jul 2015
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2015 The Authors.


This work was supported by pilot grants from the Benoziyo Center for Neurological Diseases and the Adelis Foundation, and major support came from ERC Adg # 670798. The results of this manuscript are under consideration of patent at the Weizmann Institute Office of Technology Transfer.

FundersFunder number
Adelis Foundation
Horizon 2020 Framework Programme670798
European Research Council
Nella and Leon Benoziyo Center for Neurological Diseases, Weizmann Institute of Science


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