Evidence map›Paper›PMID 23801940›Full record

ArticleFrontiers in cellular neuroscience2013

Autism as early neurodevelopmental disorder: evidence for an sAPPα-mediated anabolic pathway.

Debomoy K Lahiri, Deborah K Sokol, Craig Erickson, Balmiki Ray, Chang Y Ho, Bryan Maloney

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 8% of its field
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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  19. Cerebrospinal fluid and the early brain development of autism.Journal of neurodevelopmental disorders · 2018
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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

6 authors at 3 institutions in 1 country.

Debomoy K LahiriDepartment of Psychiatry, Indiana University School of Medicine Indianapolis, IN USA ; Laboratory of Medical and Molecular Genetics, Indiana University School of Medicine Indianapolis, IN, USA ; Institute of Psychiatric Research, Indiana University School of Medicine Indianapolis, IN, USA.
Deborah K Sokol
Craig Erickson
Balmiki Ray
Chang Y Ho
Bryan Maloney
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USCincinnati Children's Hospital Medical Center · US

Funding

Regulation of APP Pathway Gene Promoters in Alzheimer'sR01AG018379 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2000 to 2011
$3.1M
Mechanisms of Cholinesterase Inhibitors on Beta-amyloidR01AG018884 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2002 to 2012
$2.9M
NIA NIH HHS R01 AG018379NIA NIH HHS R01 AG018884
6 · The paper itself

Abstract

Autism is a neurodevelopmental disorder marked by social skills and communication deficits and interfering repetitive behavior. Intellectual disability often accompanies autism. In addition to behavioral deficits, autism is characterized by neuropathology and brain overgrowth. Increased intracranial volume often accompanies this brain growth. We have found that the Alzheimer's disease (AD) associated amyloid-β precursor protein (APP), especially its neuroprotective processing product, secreted APP α, is elevated in persons with autism. This has led to the "anabolic hypothesis" of autism etiology, in which neuronal overgrowth in the brain results in interneuronal misconnections that may underlie multiple autism symptoms. We review the contribution of research in brain volume and of APP to the anabolic hypothesis, and relate APP to other proteins and pathways that have already been directly associated with autism, such as fragile X mental retardation protein, Ras small GTPase/extracellular signal-regulated kinase, and phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin. We also present additional evidence of magnetic resonance imaging intracranial measurements in favor of the anabolic hypothesis. Finally, since it appears that APP's involvement in autism is part of a multi-partner network, we extend this concept into the inherently interactive realm of epigenetics. We speculate that the underlying molecular abnormalities that influence APP's contribution to autism are epigenetic markers overlaid onto potentially vulnerable gene sequences due to environmental influence.

Indexed as

Alzheimer’s-autism continuumanabolic hypothesiscranial volumeneurite overgrowth

Identifiers

PMID23801940
PMCPMC3689023
OpenAlexW2066724281

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.