Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Dec 8:8:64.
doi: 10.1186/s13229-017-0181-5. eCollection 2017.

No preliminary evidence of differences in astrocyte density within the white matter of the dorsolateral prefrontal cortex in autism

Ting Ting Lee  1   2 , Efstratios Skafidas  1   2   3 , Mirella Dottori  2   4   5 , Daniela Zantomio  6 , Christos Pantelis  1   2   7   3 , Ian Everall #  1   2   3   8 , Gursharan Chana #  1   2   9   3
Affiliations

No preliminary evidence of differences in astrocyte density within the white matter of the dorsolateral prefrontal cortex in autism

Ting Ting Lee et al. Mol Autism. .

Abstract

Background: While evidence for white matter and astrocytic abnormalities exist in autism, a detailed investigation of astrocytes has not been conducted. Such an investigation is further warranted by an increasing role for neuroinflammation in autism pathogenesis, with astrocytes being key players in this process. We present the first study of astrocyte density and morphology within the white matter of the dorsolateral prefrontal cortex (DLPFC) in individuals with autism.

Methods: DLPFC formalin-fixed sections containing white matter from individuals with autism (n = 8, age = 4-51 years) and age-matched controls (n = 7, age = 4-46 years) were immunostained for glial fibrillary acidic protein (GFAP). Density of astrocytes and other glia were estimated via the optical fractionator, astrocyte somal size estimated via the nucleator, and astrocyte process length via the spaceballs probe.

Results: We found no evidence for alteration in astrocyte density within DLPFC white matter of individuals with autism versus controls, together with no differences in astrocyte somal size and process length.

Conclusion: Our results suggest that astrocyte abnormalities within the white matter in the DLPFC in autism may be less pronounced than previously thought. However, astrocytic dysregulation may still exist in autism, even in the absence of gross morphological changes. Our lack of evidence for astrocyte abnormalities could have been confounded to an extent by having a small sample size and wide age range, with pathological features potentially restricted to early stages of autism. Nonetheless, future investigations would benefit from assessing functional markers of astrocytes in light of the underlying pathophysiology of autism.

Keywords: Astrocytes; Autism; Cell density; Dorsolateral prefrontal cortex (DLPFC); Glia; White matter.

PubMed Disclaimer

Conflict of interest statement

Ethics approval and consent to participate

Brain tissue for this study was provided by the NICHD Brain and Tissue Bank for Developmental Disorders (NBTBD), Baltimore, Maryland (supported by NICHD contract #HHSN275200900011C, Ref. No. N01-HD-9-0011; University of Melbourne ethics approval ID: 1339835.1), with informed consent from donors and/or families.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Optical fractionator results of ASD and controls. Estimated density of a astrocytes (GFAP positive), b negative glia (GFAP-negative glia), and c total glia, in the DLPFC of ASD and control subjects
Fig. 2
Fig. 2
Astrocyte morphology estimates. Astrocytes reactivity measures of a cell somal area via nucleator probe, and b cell processes length using spaceballs probe
See this image and copyright information in PMC

References

    1. Weintraub K. The prevalence puzzle: autism counts. Nature. 2011;479(7371):22–24. doi: 10.1038/479022a. - DOI - PubMed
    1. Baxter AJ, et al. The epidemiology and global burden of autism spectrum disorders. Psychol Med. 2015;45(3):601–613. doi: 10.1017/S003329171400172X. - DOI - PubMed
    1. Petrelli F, Pucci L, Bezzi P. Astrocytes and microglia and their potential link with autism spectrum disorders. Front Cell Neurosci. 2016;10:21. doi: 10.3389/fncel.2016.00021. - DOI - PMC - PubMed
    1. Voineagu I, et al. Transcriptomic analysis of autistic brain reveals convergent molecular pathology. Nature. 2011;474(7351):380–384. doi: 10.1038/nature10110. - DOI - PMC - PubMed
    1. Fan LW, Pang Y. Dysregulation of neurogenesis by neuroinflammation: key differences in neurodevelopmental and neurological disorders. Neural Regen Res. 2017;12(3):366–371. doi: 10.4103/1673-5374.202926. - DOI - PMC - PubMed

Publication types

Substances