Primary olfactory cortex in autism and epilepsy: increased glial cells in autism

Abstract

Autism Spectrum Disorder is characterized by sensory anomalies including impaired olfactory identification. Between 5 and 46 percent of individuals with autism have a clinical diagnosis of epilepsy. Primary olfactory cortex (piriform cortex) is central to olfactory identification and is an epileptogenic structure. Cytoarchitectural changes in olfactory cortex may underlie olfactory differences seen in autism. Primary olfactory cortex was sampled from 17 post-mortem autism cases with and without epilepsy, 11 epilepsy cases without autism and 11 typically developed cases. Stereological and neuropathological methods were used to quantify glial, pyramidal and non-pyramidal cell densities in layers of the piriform as well as identify pathological differences in this area and its neighbouring region, the olfactory tubercle. We found increased layer II glial cell densities in autism with and without epilepsy, which were negatively correlated with age and positively correlated with levels of corpora amylacea in layer I. These changes were also associated with greater symptom severity and did not extend to the olfactory tubercle. Glial cell organization may follow an altered trajectory of development with age in autism. The findings are consistent with other studies implicating increased glial cells in the autism brain. Altered cytoarchitecture may contribute to sensory deficits observed in affected individuals. This study provides evidence that autism is linked to alterations in the cytoarchitectural structure that underlies primary sensory processes and is not restricted to heteromodal ("higher") cognitive centers.

Behavioural and brain ultrastructural changes following the systemic administration of propionic acid in adolescent male rats. Further development of a rodent model of autism

“…Activation of astrocytes and microglia is common in the ASD autopsy material (Menassa, Sloan, & Chance, ; Pardo, Vargas, & Zimmerman, ; Vargas, Nascimbene, Krishnan, Zimmerman, & Pardo, ) and represents the important feature of PPA action (Choi et al, ; De Almeida, Funchal, Gottfrield, Wajner, & Pessoa‐Pureur, ; MacFabe, ). It is proposed, that in normal and pathological conditions PPA and butyrate increase neuronal histone acetylation, but are metabolized mainly in glia (Nguyen et al, ).…”

Cell-Type-Specific Whole-Brain Direct Inputs to the Anterior and Posterior Piriform Cortex

“…As one of the primary olfactory cortex, the PC is involved in encoding odor identification (Gottfried et al, 2006;Howard et al, 2009;Wilson and Sullivan, 2011;Bekkers and Suzuki, 2013;Courtiol and Wilson, 2017), odor associated values or contexts (Gottfried and Dolan, 2003;Calu et al, 2007;Roesch et al, 2007), and odor memory (Zelano et al, 2011;Strauch and Manahan-Vaughan, 2018). Besides, the PC is also implicated in various neurological disorders, such as epilepsy (Loscher and Ebert, 1996;Vismer et al, 2015;Young et al, 2019), Alzheimer's disease (Samudralwar et al, 1995;Saiz-Sanchez et al, 2015), autism spectrum disorder (Menassa et al, 2017;Koehler et al, 2018) and Parkinson's disease (Wu et al, 2011).…”

An fMRI Feature Selection Method Based on a Minimum Spanning Tree for Identifying Patients with Autism

“…Many studies have pointed out that the olfactory cortex has a great influence on basic cognitive processes and is associated with a variety of mental disorders [50][51][52]. The symptoms of patients with autism include abnormal smell recognition, and 5% to 46% of patients with autism have been diagnosed with epilepsy; notably, the olfactory cortex is the key to smell recognition and a structure that leads to epilepsy [53]. In addition, based on a study of structural and functional magnetic resonance imaging of the olfactory changes in patients with ASD, alterations in olfaction in patients with ASD are rooted in the primary olfactory cortex [54].…”