32 Introduction to Autism Spectrum Disorders
compartments. As we have shown earlier, in the majority of cases, an ASD
child has a 30% larger frontal lobe, and an abnormally large amygdala, hip
pocampus, thalamus, and hypothalamus. Similarly, the ASD child has lost
olfactory capacity, the normal ability to smell, and also has damage to the part
of the brain that controls communication in the frontal lobe. Note the obvious
connection between the loss of olfactory capacity and the exposure to syn
thetic fragrances [9].
This idea of partial missing pieces of human brain or other parts of the body
due to selective damage is not a new concept. For example, Thalidomide was
used in Europe from 1958 to 1961. This resulted in limb abnormalities, where
the newborns’ limbs were partially developed (Figure 1.14).
As seen in Figure 1.17, the part of the brain that controls emotions, empathy,
and communication can show decreased capacity. In the case of Asperger’s, the
vastly increased number of synapses can dramatically increase brain size and
capacity in some ways, while presenting weaknesses in others.Pinpointing Critical Steps Where the Autistic Brain Emerges
To ascertain at what stage of fetal development autism emerges, what types of
approaches would reveal the potential extent of neuronal progenitor cell loss
that results in ASD? One has to develop a precise map of each compartment of
the human brain tree. The human brain represents an enormously intricate
puzzle, assembled from neurons derived from a series of committed progeni
tor cells, each cell representing a branch of a giant tree at the early stages of
fetal brain development. Lineage‐tracing analyses have demonstrated that
neuronal cohorts frequently derive from a common ancestor, and that com
mon progenitor cell types give rise to specific subtypes of neurons. In specific
regions of the brain, including the cortical columns, the assembling of func
tional circuits occurs, and this assembling draws on the same cell types that
grew out of specific progenitor cell types. Therefore, an all‐inclusive neuronal
circuit could display the same developmental alterations that had their genesis
in a common cell type progenitor. The skills and technology are becoming
available to analyze such structures at molecular, cellular and subcellular lev
els, and to characterize neurons with specific origins at various immunological
levels. Ultimately, it would be possible to dissect out entire population of origi
nal progenitor cells for the neurons from specific faculties of the brain; however,
this exceeds current capacity [107–110].
Nevertheless, preliminary investigations are being pursued to ascertain the
“leaves” and “branches” that stem from the so called human brain tree. One
approach involves tracking the miniscule genetic alternations that accompany