I promise I’ll stop now.

My comment above would make more sense if I added the following:

Just to add my two cents into the neuroinflammation discussion (or more correctly, to wordsmith someone else’s thoughts):

According to Dr Casanova’s minicolumns and autism hypothesis (see a-shade-of-grey.blogspot.com/2006/09/autism-and-minicolumns.html for an overview (http omitted to get past the spam filter)), the autistic brain has a higher number of minicolumns of narrower than average width, with smaller than average neurons. (Note that this is part of the normal distribution of minicolumnar widths – albeit at the tail end – and does not automatically result in autism.) Estimates suggest that each minicolumn is connected to 10^3 similar modules, so therefore a higher number of columns means a higher number of overall connections.

Just to add my two cents into the neuroinflammation discussion (or more correctly, to wordsmith someone else’s thoughts):

According to Dr Casanova’s minicolumns and autism hypothesis (see http://a-shade-of-grey.blogspot.com/2006/09/autism-and-minicolumns.html for an overview), the autistic brain has a higher number of minicolumns of narrower than average width, with smaller than average neurons. (Note that this is within the normal distribution of minicolumnar widths – albeit at the tail end – and does not automatically result in autism.) Estimates suggest that each minicolumn is connected to 10^3 similar modules, so therefore a higher number of columns means a higher number of overall connections.

Just to add my two cents into the neuroinflammation discussion (or more correctly, to wordsmith someone else’s thoughts):

According to Dr Casanova’s minicolumns and autism hypothesis (see here for an overview), the autistic brain has a higher number of minicolumns of narrower than average width, with smaller than average neurons. (Note that this is within the normal distribution of minicolumnar widths – albeit at the tail end – and does not automatically result in autism.) Estimates suggest that each minicolumn is connected to 10^3 similar modules, so therefore a higher number of columns means a higher number of overall connections.

From Casanova (2006):

“During development, the number of oligodendrocytes is adjusted to ensure even spacing along the length of the axons. This results in the death of oligodendrocytes along regions of cellular crowding (Barres and others 1992). Dying cells provide chemotactic signals for monocytes and their differentiation to form macrophages and microglia (Perry and others 1985; Perry and Gordon 1988). Not surprisingly, microglia activation is prominent in the gray-white matter junction of autistic patients (Vargas and others 2005). It may be the case that the innate immune response observed in the neocortex and adjacent white matter of autistic patients is the result of tissue modeling, a fetal pattern of development that persists to the postnatal years.”

Other oligodendrocyte alternatives are also discussed in the paper, but from the above it should be clear that microglial activation in a brain with a higher number of narrower width minicolumns (again, whether autistic or not) could result in microglial activation that in this case would be beneficial.

According to Dr Casanova’s minicolumns and autism hypothesis (see http://a-shade-of-grey.blogspot.com/2006/09/autism-and-minicolumns.html for an overview), the autistic brain has a higher number of minicolumns of narrower than average width, with smaller than average neurons. (Note that this is within of the normal distribution of minicolumnar widths – albeit at the tail end – and does not automatically result in autism.) Estimates suggest that each minicolumn is connected to 10^3 similar modules, so therefore a higher number of columns means a higher number of overall connections. Connections consist of axons and oligodendrocytes necessary to myelinate them.

From Casanova’s “Neuropathological and Genetic Findings in Autism: The Significance of a Putative Minicolumnopathy” Neuroscientist (2006) paper:

“During development, the number of oligodendrocytes is adjusted to ensure even spacing along the length of the axons. This results in the death of oligodendrocytes along regions of cellular crowding (Barres and others 1992). Dying cells provide chemotactic signals for monocytes and their differentiation to form macrophages and microglia (Perry and others 1985; Perry and Gordon 1988). Not surprisingly, microglia activation is prominent in the gray-white matter junction of autistic patients (Vargas and others 2005). It may be the case that the innate immune response observed in the neocortex and adjacent white matter of autistic patients is the result of tissue modeling, a fetal pattern of development that persists to the postnatal years.”

Other oligodendrocyte alternatives are also discussed, but from the above it should be clear that microglial activation in a brain with a higher number of narrower width minicolumns (again, whether autistic or not) could result in microglial activation that in this case would be beneficial.