User:Rlstatton/sandbox

Article Evaluation
The types of Gene Therapy section has a lot of information. However, there should be more detail in the "Current Treatments" and "Gene Therapy Backround" sections; there are good ideas mentioned but not enough information about them for the reader to connect it with the main idea. Everything written is relevant to the topic. The article is written in a neutral tone. Links to sources work, are reliable, and support claims made. The "Talk" section discusses external links that were updated and changed. The article is rated a C-Class low importance and is part of WikiProject Genetics.

Article Selection

 * Bipolar disorder in children - needs updated, lead section not adequate
 * Controversies in autism - needs more medical references (relies on primary sources too much), it's written like a personal essay
 * Heritability of autism - too many primary sources, possibly contains original research, needs reorganized

Draft Edits
I chose to rewrite the "Genetics" section of Controversies in Autism due to lack of neutrality and recent sources.

Genetics
The role of genetic influence on the Autism Spectrum Disorder has been heavily researched over the past years.

ASD is considered to have polygenic traits since there is not a single risk factor, but multiple ones.

Multiple twin and family studies have been conducted in order to observe any genetic influence in diagnosing ASD. The chance of both twins having ASD was significantly higher in identical twins than fraternal twins, concluding that ASD is heritable. A reoccurring finding is that de novo (new mutation) copy number variants are a primary cause of ASD - they alter synaptic functions; germ line mutations can produce de novo CNVs. These mutations can only be passed on to offspring; this explains the phenomenon that occurs when the child has symptoms of ASD, but the parents have no symptoms or history of ASD. De novo variants differ from person to person i.e one variant can cause ASD in one person, whereas another person would need multiple variants to cause the same disorder. Loss of function variants occur in 16-18% of ASD diagnoses, which is nearly double the normal population. These loss of function variants reduce function in the protein neurexin, which connects neurons at the synapse and is important for neurological development; deletion mutations of neurexin are also very common in people with autism, as well as other neurological disorders like schizophrenia, bipolar disorder, and ADHD.

Gut microbiome has a relation to ASD. Excessive Clostridia spp. was found in children with ASD and gastrointestinal difficulties; Clostridia spp produces propionic acid which is impaired or in excess in people with ASD. Specifically, C.tetani and C.histolyticum are two species of this bacteria that affect people with ASD. C.tetani is a tetanus neurotoxin that is formed in the intestinal tract; C.histolyticum is a toxin producer that is abundant in people diagnosed with ASD. Both of these could contribute to neurological symptoms.

There is always conversation over the Nature vs. Nurture debate. According to family studies, genetic and environmental factors have an equal influence on risk of ASD.