Autism Studies and Related Medical Conditions, January 2009 - TACA

findings, which consisted of obstructive arteriopathy of small and medium size
vessels in delimited areas. A specific cause of the arteriopathy was not found in
any case. We discuss the treatment (corticosteroids and calcium antagonists)
and the course of the patients. In front of the possibility of being isolated cases,
we discuss the interest of performing cerebral angiographic studies in patients
with Landau-Kleffner syndrome in initial stage in order to confirm the consistence
of these findings and the adequate treatment.
Mazur-Kolecka, B., I. L. Cohen, et al. (2007). "Altered development of neuronal
progenitor cells after stimulation with autistic blood sera." Brain Res 1168: 11-20.
Changes of brain structure and functions in people with autism may result from
altered neuronal development, however, no adequate cellular or animal models
are available to study neurogenesis in autism. Neuronal development can be
modeled in culture of neuronal progenitor cells (NPCs) stimulated with serum to
differentiate into neurons. Because sera from people with autism and agematched
controls contain different levels of numerous biologically active factors,
we hypothesized that development of human NPCs induced to differentiate into
neurons with sera from children with autism reflects the altered early neuronal
development that leads to autism. The control and autistic sera were collected
from siblings aged below 6 years that lived in the same environment. The effect
of sera on differentiation of NPC neurospheres into neuronal colonies was tested
in 72-h-long cultures by morphometry, immunocytochemistry and
immunoblotting. We found that sera from children with autism significantly
reduced NPCs' proliferation, but stimulated cell migration, development of small
neurons with processes, length of processes and synaptogenesis. These results
suggest that development of network of processes and synaptogenesis--the
specific events in the brain during postnatal ontogenesis--are altered in autism.
Further studies in this cell culture model may explain some of the cellular
alterations described in autistic patients.
Ni, L., G. Acevedo, et al. (2007). "Toll-like receptor ligands and CD154 stimulate
microglia to produce a factor(s) that promotes excess cholinergic differentiation in the
developing rat basal forebrain: implications for neurodevelopmental disorders." Pediatr
Res 61(1): 15-20.
Maternal inflammation plays a role in the etiology of certain neurodevelopmental
disorders including autism and schizophrenia. Because maternal inflammation
can lead to activation of fetal microglia, we have examined effects of inflamed
microglia on cultured neural progenitors from rat embryonic septal region and
basal forebrain. These cells give rise to cholinergic neurons projecting to cortex
and hippocampus. Microglia stimulated with lipopolysaccharide (LPS),
peptidoglycan, Poly I:C and CD154 produce conditioned media (CM) that
promotes excessive numbers of cholinergic neurons and levels of choline
acetyltransferase (ChAT) activity 6-8 times that of untreated cultures. Expression
of the neural-specific transcription factor MATH1 increases substantially within 1
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