Talk:Animal model of autism

Wiki Education Foundation-supported course assignment

This article was the subject of a Wiki Education Foundation-supported course assignment, between 19 January 2021 and 16 April 2021. Further details are available on the course page. Student editor(s): WikiWizard3286.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 17:19, 17 January 2022 (UTC)

DYK hook

I have added a scientific consensus statement to the statement about thimerosal and autism (my edit summary: required statement per NPOV; "avoid stating seriously contested assertions as facts". Content from Thimerosal controversy. Also move out of first paragraph of section due to WP:WEIGHT concern). However, I think it may be useful to discuss here whether the content has the WP:WEIGHT to be in the article at all; it is furthermore a violation of WP:MEDRS, our requirements on medical sourcing (it is sourced to a primary study and a news article). I would remove it myself, but the statement is currently a DYK hook so this seems like the best temporary solution. Sunrise (talk) 07:32, 18 December 2013 (UTC)

I agree. I reviewed it and I can't believe I missed that. I wasn't familiar with the controversy and just checked out the Thimerosal article, which didn't raise any red flags. I am One of Many (talk) 07:49, 18 December 2013 (UTC)

Added: I have reported the issue to FTN here and to DYK here. Sunrise (talk) 07:51, 18 December 2013 (UTC)

Maternal Immune Activation

I will be creating a new paragraph under the "Environmental Factors of ASD" subheading that addresses maternal immune activation. This is an environmental risk factor that is known to be correlated with the development of neurodevelopmental disorders such as autism and schizophrenia.WikiWizard3286 (talk) 15:51, 15 April 2021 (UTC)

I just added the paragraph about maternal immune activation as a risk factor for autism. I think this is important to mention as it is currently being extensively studied and is well-known as a risk factor. Here is my sandbox: https://en.wikipedia.org/wiki/User:WikiWizard3286/Animal_model_of_autism WikiWizard3286 (talk) 17:24, 16 April 2021 (UTC)

Wiki Education assignment: Psychology Capstone

This article was the subject of a Wiki Education Foundation-supported course assignment, between 8 May 2023 and 11 August 2023. Further details are available on the course page. Student editor(s): Corri123 (article contribs). Peer reviewers: Zafomby, LaDonna205, AddieGrace, Ddmiller12, Jkp0103, April Sala.

— Assignment last updated by Rahneli (talk) 19:54, 13 June 2023 (UTC)

Merger proposal

User:Mruanova added a merger template on Autism spectrum in animals for it to be merged here.

• Oppose. The topics are distinct. Autism spectrum in animals also has no useful information to be merged into this article; it has serious sourcing issues. SomeoneDreaming (talk) 23:01, 14 June 2023 (UTC)

• Update: I think a redirect is probably what makes most sense, because there doesn't seem to be anything notable and reliable on (natural/pre-existing, not induced) autism in animals to be in the other article.

SomeoneDreaming (talk) 23:23, 14 June 2023 (UTC)

• Oppose merging as well as redirecting. See this comment on why animal models of a condition and a condition occurring in animals are not the same thing and should not be confused with each other.--TempusTacet (talk) 07:50, 15 June 2023 (UTC)

Closing, given that the other page no longer exists. Klbrain (talk) 10:01, 20 July 2023 (UTC)

Wiki Education assignment: Psychology Capstone

This article was the subject of a Wiki Education Foundation-supported course assignment, between 9 January 2024 and 26 April 2024. Further details are available on the course page. Student editor(s): Grahamal (article contribs). Peer reviewers: Lizmtay, Lkshephe, Sara8887, Zclayt, Peytonmk.

— Assignment last updated by Rahneli (talk) 17:06, 11 February 2024 (UTC)

Asl1021's edit in May 2020

Hi, I've been reading this page and have some concerns. Specifically this contribution here by Asl1021 has meant a large portion of the article has no source. They have no prior contributions and it's coming up on 6 years of it being in the article without any citations to the information they provided. I think it should be removed until changes are made to back-up the paragraphs they wrote. How2function (talk) 03:52, 6 May 2026 (UTC)

That makes sense to me. Feel free to do it yourself! And I'd encourage you to be bold about things like this. Cadddr (talk) 03:58, 6 May 2026 (UTC)

Just going to dump the removed section here for when I get around to finding the citations for each section.

=== Genetic and phenotypic factors ===

There are six autism-related genes that are linked to the X chromosome. The first gene that has been linked to autism is the Fragile X gene (FMR1). For example, rodents with this gene exhibit elevated cortical spine densities that are similar to those found in autism, as well as decreased social behaviors. Another gene that has been linked to autism is the methyl-CpG-binding protein type 2 gene (MECP2). In the rodent models that have MECP2 disruption, the rodents are usually normal up until the sixteenth week of age, at which point they start to develop extreme anxiety in the field, reduced nest building, and poor social interactions, which are all symptoms of autism.

The third and fourth genes that have been linked to autism are neuroligin (NLGN) 3 and 4 genes. One study found that mutations in the NLGN 3 and 4 genes lead to loss of neuroligin processing to stimulate the formation of synapses, which is a feature of autistic spectrum disorders. The fifth and sixth genes that are linked to autism are the tuberous sclerosis genes (TSC1 and TSC2). Mutations in either of these two genes cause multiple benign tumors to grow in multiple tissues like the brain. Lastly, many of the abnormalities found in autistic spectrum disorders involve the mTOR signaling pathway, the GABA-containing neurons, and the immune system.

=== Human autism spectrum disorder ===

All disorders have different implications when it comes to genetic makeup, both in expression and genotype, which generally impacts specific brain regions. In ASD, it is generally seen in reduced developmental growth within the brain, specifically reduced gray matter within the medial temporal lobe, which is where the amygdala and hippocampus are located. This region of the brain controls emotions and learning, which are symptomatically linked to ASD. This supports the need for animal models that establish a greater understanding of what effects these particular brain regions and genetics have on development, as well as potential measures that could be taken in order to prevent the development of the disorder in utero.

=== Neuropathology of the underdeveloped synapse ===

Autism is caused by developmental delays that cause the brain to have lower connectivity within important regions. Alterations in the timing of critical periods in brain development have been observed in autism models, potentially impacting synaptic formation, cognitive outcomes, and the ability to create stronger synapses for basic communication and stimulus recognition. Furthermore, the brain's lessened development and cognitive delays are usually observable within the genetics and grey matter within the brain.

Researchers often use rodent models to study ASD because rodent's brains are similar to humans in makeup and because they have similar social interactions and structures, allowing for social development symptoms often used to diagnose ASD to emerge. To replicate ASD, the rodents are lesioned prior to birth using prenatal valproate and compared to rodents of a control group. These rodents experience symptoms and developmental changes similar to humans with ASD. Humans with ASD are identified to have a single-gene mutation at Neuroligin-3, or NL-3 R451C.

=== Neuropathology of GABA receptors ===

When exposed to prenatal valproate during pregnancy, the mice are born with basic deformities and the developmental delays seen symptomatically in humans. This is particularly advantageous and easier to study, as mice and most rodents have relatively short lifespans. This allows researchers to observe genetic factors, subtle effects, and potential interventions over a compressed time frame. As a result, they can more efficiently develop and test methods to delay the onset of the disorder, ultimately accelerating the development of new treatments for individuals with ASD. Additionally, these rodents may help trace how developmental delays occur in relation to GABA5. GABA is a neurotransmitter that is generally seen as inhibitory, but prior to birth and in early development of the brain it is often excitatory while neurons establish proper brain chemistry.

During development, there are specific times—called critical periods—where the brain is more capable of acquiring neural connections which usually leads to new behavioral and psychological skills. GABA's change from excitatory to inhibitory, as well as other neurotransmitter changes during these critical developmental stages, can impact brain development. If the critical period is early, growth can be limited, slowed, or stunted. If it is later, the brain's development is measured as complete incorrectly which may limit its ability to improve connectivity. Overall, the brain's circuitry and communication is often limited or poor within ASD, so using rodent models to study these limitations and where they come about increases researchers' understanding of the disorder and potential ways to prevent it. How2function (talk) 04:37, 6 May 2026 (UTC)