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Neuroimmunol Neuroinflammation 2019;6:15 I http://dx.doi.org/10.20517/2347-8659.2019.019 Page 17 of 24

enzyme that degrades another monoamine (dopamine), but only significantly around two years after birth.
The consequent long-term imbalance of synaptic monoamines is assumed here to impact the architecture
[1]
of sleep and learning , inducing a range of developmental problems.
This theory is drawn on Guided Propagation Networks (GPNs), the computer simulations of which show
the growth of aberrant structures when modulation parameters akin to monoamines do not satisfy inner
learning constraints. Comparisons are made between a reference well-tuned network and others grown
with shifted parameters, all using the same learning data. Unlike the reference network, impaired GPNs
display features that have been observed in the autistic brain: (1) more local connections (here underlying
either repetitive behavior or over-activity); (2) missing or impaired long-distance connections (which
convey emotional conditioning towards decision-making modules); and (3) overgrowth: the overall
[2]
connectivity can involve 1.5 more cells and links. Apart from these computer experiments , the 4:1 sex
ratio observed in autism can be calculated in a family tree which combines genetic variants and epigenetic
regulations. According to this calculation, which involves two types of genetic masking of the relevant
epigenetic traits (i.e., X-silencing and low-COMT), in addition to 1.5% of the population having developed
an overt form of autism, about 6% of men and 24% of women would be “healthy carriers” of the enzymatic
(dys) regulation at issue.

On the medical side, an epileptic 11-year-old boy with severe autism received sodium valproate daily
for its ability to both stimulate MAOA and treat epilepsy. In this case study, behavioral changes have
been recorded for one year by parents and caregivers unaware of the autism target. This one-year
monitoring showed improvement of sleep and then gaze, followed by a gradual decrease of stereotypy
among other behavioral changes arising nine months after the treatment initiation. Hyperactivity, which
hindered learning across this treatment, could afterwards be reduced by low-dose of the methylphenidate
psychostimulant. The proposed dual therapy thus involves a MAOA inducer and a psychostimulant,
together with re-education, all monitored by relevant biomarkers. If validated by future investigations, this
approach is first intended to prevent early gestation from environmental factors that are likely to stimulate
the production of MAOA, including small-sized fatty acids.

REFERENCES
1. Béroule DG. Offline encoding impaired by epigenetic regulations of monoamines in the guided propagation model of autism. BMC
Neuroscience 2018;19:80.
2. Available from: https://perso.limsi.fr/domi/Movie-S1_DGB_nov16.mov [Last accessed on 18 Dec 2019]

24. Neuropsychology intervention in Williams syndrome: a clinic case

Carlos Alberto Serrano-Juárez, Prieto-Corona Dulce María Belén, Ma. Guillermina Yáñez-Téllez

Laboratorio de neurometría, FES Iztacala, UNAM

Williams syndrome (WS) is a neurodevelopmental disorder caused by the removal of 7q11.23. Patients
with WS present neuroanatomical alterations that are reflected in neuropsychological alterations mainly
in visuospatial abilities, attention, and executive functions. The objective of the study was to apply a
neuropsychological intervention program to improve attention and visuospatial skills. The program was
applied for 10 months in sessions of 1.5 h to an 8-year-old girl with WS from Mexico City. The tasks
were designed based on neuropsychological clinical models. The pre- and post-intervention results were
compared with a clinical sample of five patients with WS, which allowed identifying if there were an