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Minicolumnar pathology in autism
Abstract
OBJECTIVE: To determine whether differences exist in the configuration of minicolumns between the brains of autistic and control patients. BACKGROUND: Autism is a severe and pervasive developmental disturbance of childhood characterized by disturbances in both social interactions and communication, as well as stereotyped patterns of interests, activities, and behaviors. Postmortem neuropathologic studies remain inconclusive. METHODS: The authors used a computerized imaging program to measure details of cell column morphologic features in area 9 of the prefrontal cortex and areas 21 and posterior 22 (Tpt) within the temporal lobe of nine brains of autistic patients and controls. RESULTS: The authors found significant differences between brains of autistic patients and controls in the number of minicolumns, in the horizontal spacing that separates cell columns, and in their internal structure, that is, relative dispersion of cells. Specifically, cell columns in brains of autistic patients were more numerous, smaller, and less compact in their cellular configuration with reduced neuropil space in the periphery. CONCLUSIONS: In autism, there are minicolumnar abnormalities in the frontal and temporal lobes of the brain.
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“Changes in the structure and function of excitatory synapses, and alterations in the local versus long-range dendritic connectivity of neurons, have both been associated with the development of neuropsychiatric conditions involving imbalances of excitation and inhibition, such as ASD and SCZ.73,74”
From The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines (2014) · cites this paper as [73]
In the citing paper
“Patients with ASD have smaller and more numerous minicolumns with more dispersed neurons in Brodmann’s areas 9, 21, and 22 [57, 58], and patients with Asperger’s syndrome have smaller, less compact minicolumns in the temporal neocortex [56].”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [57]
In the citing paper
“A number of the neural models cited above suggest that there is a proliferation of neural connections in the sensory cortex of individuals with ASD (Belmonte et al., 2004;Casanova et al., 2002;see Baron-Cohen & Belmonte, 2005;Minshew et al., 2007, for reviews)”
From Vision in autism spectrum disorders (2009) · cites this paper as Casanova et al., 2002
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Metadata
- Authors
- Casanova, M. F., Buxhoeveden, D. P., Switala, A. E., & Roy, E.
- Affiliations
- University of South Carolina (US)
- Venue
- Neurology
- Published
- 2002-02-12
- Volume
- 58
- Issue
- 3
- Pages
- 428-432
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2042999794
- Cited by
- 846
- References
- 32
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 18 · 2023: 22 · 2022: 25 · 2021: 18 · 2020: 60 · 2019: 23 · 2018: 24 · 2017: 26 · 2016: 34 · 2015: 49 · 2014: 44 · 2013: 48 · 2012: 47
- FWCI
- 19.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Autism Research Foundation
- School of Medicine, Boston University
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Child Nutrition and Feeding Issues
- Keywords
- autism spectrum disorder, minicolumns, prefrontal cortex, temporal lobe, column spacing, postmortem neuropathology, frontal lobe
- MeSH terms
- Adult, Autistic Disorder, Child, Child, Preschool, Humans, Image Processing, Computer-Assisted, Neurons, Temporal Lobe, Multivariate Analysis, Prefrontal Cortex, Neuropil
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