Animals, Newborn

Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Spinal muscular atrophy (SMA), a recessive neurodegenerative disease, is characterized by the selective loss of spinal motor neurons. No available therapy exists for SMA, which represents one of the leading genetic causes of death in childhood. SMA is caused by a mutation of the survival-of-motor-neuron 1 (SMN1) gene, leading to a quantitative defect in the survival-motor-neuron (SMN) protein expression. All patients retain one or more copies of the SMN2 gene, which modulates the disease severity by producing a small amount of stable SMN protein.

Branchu, Julien
Biondi, Olivier
Chali, Farah
Collin, Thibault
Leroy, Felix
Mamchaoui, Kamel
Makoukji, Joelle
Pariset, Claude
Lopes, Philippe
Massaad, Charbel
Chanoine, Christophe
Charbonnier, FrÈdÈric
Publication Title: 
Methods in Molecular Biology (Clifton, N.J.)

Intrauterine gene therapy (IUGT) potentially enables the treatment and possible cure of monogenic -diseases that cause severe fetal damage. The main benefits of this approach will be the ability to correct the disorder before the onset of irreversible pathology and inducing central immune tolerance to the vector and transgene if treatment is instituted in early gestation.

Mattar, Citra N.
Biswas, Arijit
Choolani, Mahesh
Chan, Jerry K. Y.
Publication Title: 
Brain Research

Diet restriction of rodents during adult life is known to cause an increased life span. It has been hypothesised that this increase may be related to effects on the anti-oxidant defence systems. However, it has been suggested that undernutrition during the gestation and pre-weaning may reduce their life span as it is known to have other deleterious effects on a rodent's growth and development.

Partadiredja, G.
Worrall, S.
Bedi, K. S.
Publication Title: 
Obesity (Silver Spring, Md.)

OBJECTIVE: Increasing prevalence of childhood obesity and associated risks of adult type disease have led to worldwide concern. It remains unclear how genetic predisposition, environmental exposure to obesogenic food, and developmental programming interact to lead to overweight and obese children. The development of a nonhuman primate model of obesity, and particularly juvenile obesity, is an important step to elucidating the factors associated with obesity and evaluating intervention strategies. DESIGN AND METHODS: Infant marmosets were followed from birth to 12 months of age.

Ross, Corinna N.
Power, Michael L.
Artavia, Joselyn M.
Tardif, Suzette D.
Publication Title: 
Aging Cell

Cockayne syndrome (CS) is a rare autosomal recessive segmental progeria characterized by growth failure, lipodystrophy, neurological abnormalities, and photosensitivity, but without skin cancer predisposition. Cockayne syndrome life expectancy ranges from 5 to 16 years for the two most severe forms (types II and I, respectively). Mouse models of CS have thus far been of limited value due to either very mild phenotypes, or premature death during postnatal development prior to weaning. The cause of death in severe CS models is unknown, but has been attributed to extremely rapid aging.

Brace, Lear E.
Vose, Sarah C.
Vargas, Dorathy F.
Zhao, Shuangyun
Wang, Xiu-Ping
Mitchell, James R.
Publication Title: 
Neuroscience and Biobehavioral Reviews

In mammals the neonatal period is a time of significant social interaction. This is true even in solitary species as females spend a significant amount of time nursing and caring for their offspring. In social species interactions may also include the father, older siblings and extended family members. This period is a time of significant development, including organization of the central nervous system, and therefore a time when the degree and type of social interaction influences the development and expression of social behavior in adulthood.

Cushing, Bruce S.
Kramer, Kristin M.
Publication Title: 
Journal of Pharmacological Sciences

Early brain development has a tremendous impact on the success of humans throughout their lives. During early development, neural circuit formation proceeds in a strictly regulated manner. In addition to genetic and epigenetic programs, recent studies using animal models have demonstrated that certain maternal bio-active agents are essential for normal neural development, with deficiencies adversely affecting offspring brain function and behavior.

Tozuka, Yusuke
Wada, Etsuko
Wada, Keiji
Publication Title: 
Genes, Brain, and Behavior

Epigenetic mechanisms may moderate genetic and environmental risk (GxE) for mood disorders. We used an experimental rhesus macaque model of early life stress to test whether epigenetic regulation of serotonin transporter (5-HTT) may contribute to GxE interactions that influence behavior and emotion.

Kinnally, E. L.
Capitanio, J. P.
Leibel, R.
Deng, L.
LeDuc, C.
Haghighi, F.
Mann, J. J.
Publication Title: 
Biological Psychiatry

BACKGROUND: Prenatal cannabis exposure has been linked to addiction vulnerability, but the neurobiology underlying this risk is unknown. METHODS: Striatal dopamine and opioid-related genes were studied in human fetal subjects exposed to cannabis (as well as cigarettes and alcohol). Cannabis-related gene disturbances observed in the human fetus were subsequently characterized with an animal model of prenatal ?-9-tetrahydrocannabinol (THC) (.15 mg/kg) exposure.

DiNieri, Jennifer A.
Wang, Xinyu
Szutorisz, Henrietta
Spano, Sabrina M.
Kaur, Jasbir
Casaccia, Patrizia
Dow-Edwards, Diana
Hurd, Yasmin L.
Publication Title: 
Schizophrenia Research

INTRODUCTION: To improve the understanding of psychotic abnormalities and their non-Mendelian inheritance patterns, the epigenetic regulation of the psychotic disorder-associated GABRB2, gene for the type A ?-aminobutyric acid receptor ?(2)-subunit, was investigated. METHODS: Expression of GABRB2, and the epigenetic regulatory enzymes histone deacetylases (HDACs) and DNA methyltransferases (DNMTs) in mouse and postmortem human brains was analyzed using real-time PCR.

Zhao, Cunyou
Wang, Feng
Pun, Frank W.
Mei, Lingling
Ren, Lihuan
Yu, Zhiliang
Ng, Siu-Kin
Chen, Jianhuan
Tsang, Shui-Ying
Xue, Hong


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