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The amygdala, cerebellum, and many other brain regions have been implicated in autism. [15]Unlike some brain disorders which have clear molecular hallmarks that can be observed in every affected individual, such as Alzheimer's disease or Parkinson's disease, autism does not have a unifying mechanism at the molecular, cellular, or systems level.
Rett syndrome brain samples and autism brain samples show immaturity of dendrite spines and reduction of cell-body size due to errors in coupled regulation between MECP2 and EGR2. [62] However, because of the multigene involvement in autism, the MECP2 gene has only been identified as a vulnerability factor in autism. [63]
The severity of symptoms and functional impairment vary between individuals. [3] There are many known environmental, genetic, and biological causes of autism. Research indicates that genetic factors predominantly contribute to its appearance. The heritability of autism is complex and many of the genetic interactions involved are unknown. [1]
An individual exhibiting intellectual disability and other symptoms similar to LFS was found to have a terminal deletion of the subtelomeric region in the short arm of chromosome 5. [25] Deletion of this area of chromosome 5 is associated with intellectual disability, psychotic behavior, autism, macrocephaly and hypernasal-like speech, as well ...
Autism has multiple causes. This article focuses on heritable causes. The heritability of autism is the proportion of differences in expression of autism that can be explained by genetic variation; if the heritability of a condition is high, then the condition is considered to be primarily genetic. Autism has a strong genetic basis.
Of the PDDs, Asperger syndrome was closest to classic autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with it, but were understood to potentially have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical autism) was diagnosed when the criteria were not met for ...
The connections between the terminal nerve and the olfactory system have been extensively studied in human embryos. olfactory nerve fibers enter the brain at stage 17, fibers from the vomeronasal organ and fibers of the terminal nerve enter the brain at stages 17 and 18. [9] During prenatal development some of the ganglion cells are lost. [7]
Brain MRI, T1 weighted on a transversal plane, of an 8-month old boy with lissencephaly. Note the scarce and wide gyri, mostly on the parietal, temporal and occipital lobes, the absence of a true Sylvian fissure, and the augmented thickness of the gray matter. The boy had a severe developmental delay and seizures. Specialty: Neurology