Treatments

Autism Science Foundation President Alison Singer Speaks

Source: 
BlogHer
Date Published: 
October 7, 2009
Abstract: 

Autism Science Foundation president Alison Singer is well known in the autism community for her formative role at Autism Speaks, for her controversial participation in their Autism Every Day video, and for leaving Autism Speaks to found the Autism Science Foundation.

She a role model for autism parents struggling to balance advocacy with positivity and work with family, especially those who tirelessly investigate ways to help our children lead fulfilling lives, actively respect neurodiversity, and continue to educate ourselves and others about autism perspectives and attitudes.

Read on to learn about the founding and goals of the Autism Science Foundation.

Op-Ed: Fight to Overcome Autism Gets Major Boost, Higher Priority

Source: 
HHS Secretary Kathleen Sebelius
Date Published: 
October 5, 2009
Abstract: 

The federal government will provide nearly twice as much funding for autism research in the upcoming fiscal year as we had just three years ago. President Obama has made autism a focus from the first days of his presidency in hopes to counterbalance some of the new challenges Autism has created for for families, schools, and health care providers.

Seaside Therapeutics Secures $30 Million Financing

Source: 
Reuters
Date Published: 
September 17, 2009
Abstract: 

Seaside Therapeutics LLC today announced that it has secured $30 million in financing from a private, family investment firm which is committed to advancing research in the field of autism and Fragile X Syndrome.

Lack of Efficacy of Citalopram in Children With Autism Spectrum Disorders and High Levels of Repetitive Behavior

Source: 
Archives of General Psychiatry, King, Hollander, Sikich, McCracken, Scahill, Bregman, Donnelly, Anagnostou, Dukes, Sullivan, Hirtz, Wagner, Louise Ritz; for the STAART Psychopharmacology Network
Date Published: 
June 2009
Year Published: 
2009

Citalopram (Celexa), a medication commonly prescribed to children with autism spectrum disorders (ASD), was no more effective than a placebo at reducing repetitive behaviors, according to a multi-site clinical trial guided by lead author Bryan King, MD, director of child and adolescent psychiatry at Seattle Children's Hospital and professor and vice chair of psychiatry at the University of Washington School of Medicine.

Because citalopram is also prescribed for patients with obsessive compulsive disorders (OCD), these study results may challenge the widely held premise that repetitive behaviors in children with ASD are similar to repetitive behaviors often found in cases of OCD.

Researchers identify how PCBs may alter in utero, neonatal brain development

Source: 
PLoS-Biology, Pessah, et al
Date Published: 
April 2009
Year Published: 
2009

In three new studies — including one appearing in the Public Library of Science - Biology (PLoS - Biology) — UC Davis researchers provide compelling evidence of how low levels of polychlorinated biphenyls (PCBs) alter the way brain cells develop.

The findings could explain at last — some 30 years after the toxic chemicals were banned in the United States — the associations between exposure of the developing nervous system to PCBs and behavioral deficits in children.

 

Partial reversal of Rett Syndrome-like symptoms in MeCP2 mutant mice

Source: 
PNAS, Sur, Tropea, Giacometti, et al.
Date Published: 
February 2009
Year Published: 
2009

Rett Syndrome (RTT) is a severe form of X-linked mental retardation caused by mutations in the gene coding for methyl CpG-binding protein 2 (MECP2). Mice deficient in MeCP2 have a range of physiological and neurological abnormalities that mimic the human syndrome. Here we show that systemic treatment of MeCP2 mutant mice with an active peptide fragment of Insulin-like Growth Factor 1 (IGF-1) extends the life span of the mice, improves locomotor function, ameliorates breathing patterns, and reduces irregularity in heart rate. In addition, treatment with IGF-1 peptide increases brain weight of the mutant mice. Multiple measurements support the hypothesis that RTT results from a deficit in synaptic maturation in the brain: MeCP2 mutant mice have sparse dendritic spines and reduced PSD-95 in motor cortex pyramidal neurons, reduced synaptic amplitude in the same neurons, and protracted cortical plasticity in vivo. Treatment with IGF-1 peptide partially restores spine density and synaptic amplitude, increases PSD-95, and stabilizes cortical plasticity to wild-type levels. Our results thus strongly suggest IGF-1 as a candidate for pharmacological treatment of RTT and potentially of other CNS disorders caused by delayed synapse maturation.

Fragile X: Translation in Action

Source: 
Neuropshcyopharmacology, Bear, Dolen et al
Date Published: 
2008

Fragile X is a synapsopathy--a disorder of synaptic function and plasticity. Recent studies using mouse models of the disease suggest that the critical defect is altered regulation of synaptic protein synthesis. Various strategies to restore balanced synaptic protein synthesis have been remarkably successful in correcting widely varied mutant phenotypes in mice. Insights gained by the study of synaptic plasticity in animal models of fragile X have suggested novel therapeutic approaches, not only for human fragile X but also for autism and mental retardation of unknown etiology.

Reversal of Learning Deficits in a Ts2+/- Mouse Model of Tuberous Sclerosis

Source: 
Nature Medicine, Ehninger, Han, et al
Date Published: 
2008
Year Published: 
2008

Tuberous sclerosis is a single-gene disorder caused by heterozygous mutations in the TSC1 (9q34) or TSC2 (16p13.3) gene and is frequently associated with mental retardation, autism and epilepsy. Even individuals with tuberous sclerosis and a normal intelligence quotient (approximately 50%) are commonly affected with specific neuropsychological problems, including long-term and working memory deficits. Here we report that mice with a heterozygous, inactivating mutation in the Tsc2 gene (Tsc2(+/-) mice) show deficits in learning and memory. Cognitive deficits in Tsc2(+/-) mice emerged in the absence of neuropathology and seizures, demonstrating that other disease mechanisms are involved. We show that hyperactive hippocampal mammalian target of rapamycin (mTOR) signaling led to abnormal long-term potentiation in the CA1 region of the hippocampus and consequently to deficits in hippocampal-dependent learning. These deficits included impairments in two spatial learning tasks and in contextual discrimination. Notably, we show that a brief treatment with the mTOR inhibitor rapamycin in adult mice rescues not only the synaptic plasticity, but also the behavioral deficits in this animal model of tuberous sclerosis. The results presented here reveal a biological basis for some of the cognitive deficits associated with tuberous sclerosis, and they show that treatment with mTOR antagonists ameliorates cognitive dysfunction in a mouse model of this disorder.

Thimerosal Disappears but Autism Remains

Source: 
Archives of General Psychiatry, Fombonne
Date Published: 
2008
Year Published: 
2008

 

Parents of autistic children should be reassured that autism in their child did not occur through immunizations. Their autistic children, and their siblings, should be normally vaccinated, and as there is no evidence of mercury poisoning in autism, they should avoid ineffective and dangerous
"treatments" such as chelation therapy for their children.

Can Children with Autism Recover? If so, How?

Source: 
Neuropsychology Review, Helt, Kelley, et al
Date Published: 
2008
Year Published: 
2008

Although Autism Spectrum Disorders (ASD) are generally assumed to be lifelong, we review evidence that between 3% and 25% of children reportedly lose their ASD diagnosis and enter the normal range of cognitive, adaptive and social skills. Predictors of recovery include relatively high intelligence, receptive language, verbal and motor imitation, and motor development, but not overall symptom severity. Earlier age of diagnosis and treatment, and a diagnosis of Pervasive Developmental Disorder-Not Otherwise Specified are also favorable signs. The presence of seizures, mental retardation and genetic syndromes are unfavorable signs, whereas head growth does not predict outcome. Controlled studies that report the most recovery came about after the use of behavioral techniques. Residual vulnerabilities affect higher-order communication and attention. Tics, depression and phobias are frequent residual co-morbidities after recovery. Possible mechanisms of recovery include: normalizing input by forcing attention outward or enriching the environment; promoting the reinforcement value of social stimuli; preventing interfering behaviors; mass practice of weak skills; reducing stress and stabilizing arousal. Improving nutrition and sleep quality is non-specifically beneficial.