Evidence map›Paper›PMID 28929566›Full record

ArticleThe Journal of comparative neurology2018

Protracted dendritic growth in the typically developing human amygdala and increased spine density in young ASD brains.

R K Weir, M D Bauman, B Jacobs, C M Schumann

Abstract read
In one paragraph

Article in The Journal of comparative neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed.

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  12. Molecular psychiatry · 2025
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  20. Microglia and Microbiome-Gut-Brain Axis.Advances in neurobiology · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

R K WeirDepartment of Psychiatry and Behavioral Sciences, University of California at Davis MIND Institute, Sacramento, California.ORCID http://orcid.org/0000-0002-7268-7038
M D BaumanDepartment of Psychiatry and Behavioral Sciences, University of California at Davis MIND Institute, Sacramento, California.
B JacobsLaboratory of Quantitative Neuromorphology, Department of Psychology, Colorado College, Colorado Springs, Colorado.ORCID http://orcid.org/0000-0002-4662-3401
C M SchumannDepartment of Psychiatry and Behavioral Sciences, University of California at Davis MIND Institute, Sacramento, California.

Funding

National Institute on Aging (NIA) ColonyP51OD011107 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Simon J. Atkinson · 2012 to 2026
$191.5M
Rodent Behavior CoreU54HD079125 · NICHD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SIMON, TONY J · 2013 to 2019
$8.5M
Typical and Pathological Cellular Development of the Human AmygdalaR01MH097236 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SCHUMANN, CYNTHIA · 2011 to 2022
$3.9M
NICHD NIH HHS U54 HD079125NIH HHS P51 OD011107NIMH NIH HHS R01 MH097236
6 · The paper itself

Abstract

The amygdala is a medial temporal lobe structure implicated in social and emotional regulation. In typical development (TD), the amygdala continues to increase volumetrically throughout childhood and into adulthood, while other brain structures are stable or decreasing in volume. In autism spectrum disorder (ASD), the amygdala undergoes rapid early growth, making it volumetrically larger in children with ASD compared to TD children. Here we explore: (a) if dendritic arborization in the amygdala follows the pattern of protracted growth in TD and early overgrowth in ASD and (b), if spine density in the amygdala in ASD cases differs from TD from youth to adulthood. The amygdala from 32 postmortem human brains (7-46 years of age) were stained using a Golgi-Kopsch impregnation. Ten principal neurons per case were selected in the lateral nucleus and traced using Neurolucida software in their entirety. We found that both ASD and TD individuals show a similar pattern of increasing dendritic length with age well into adulthood. However, spine density is (a) greater in young ASD cases compared to age-matched TD controls (<18 years old) and (b) decreases in the amygdala as people with ASD age into adulthood, a phenomenon not found in TD. Therefore, by adulthood, there is no observable difference in spine density in the amygdala between ASD and TD age-matched adults (≥18 years old). Our findings highlight the unique growth trajectory of the amygdala and suggest that spine density may contribute to aberrant development and function of the amygdala in children with ASD.

Indexed as

AdolescentAdultAge FactorsAmygdalaAutism Spectrum DisorderChildDendritic SpinesFemaleHumansMaleMiddle AgedNeuronsSilver StainingYoung Adultamygdalaautism spectrum disordergolgi-kopschneuromorphologyRRID:SCR_003131spines

Identifiers

PMID28929566
PMCPMC5728110

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.