ABSTRACT
Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) regulates several cellular processes including survival, proliferation, and metabolism. In the brain, PTEN is a key modulator of synaptic function, and is involved in regulating synaptogenesis, connectivity, and synaptic plasticity. Herein we discuss how alterations in PTEN can disturb these mechanisms, thus compromising normal synaptic function and consequently contributing to behavioral and cognitive phenotypes observed in autism spectrum disorder (ASD). As the role of PTEN in synaptic function is linked to ASD, a deeper understanding of this interaction will shed light on the pathological mechanisms involved in ASD, contributing to the development of new therapies.
Subject(s)
Autism Spectrum Disorder/metabolism , Autism Spectrum Disorder/physiopathology , Neuronal Plasticity/physiology , PTEN Phosphohydrolase/metabolism , Female , Humans , Male , Signal Transduction/physiologyABSTRACT
The present study represents an ex post facto non-experimental study of undergraduate nursing students (Nâ¯=â¯1,176) residing in Mexico whereby we examined the association between substance use and depressive symptomatology. The sample was composed primarily of women (70.1%), between the ages of 18 and 23 years (89.5%). Outcomes suggest a significant association between current clinically relevant depressive symptomatology 3-month marijuana, alcohol, and sedative use. Additionally, current depressive symptomatology was significantly associated with lifetime alcohol and sedative use. Lastly, current depressive symptomatology was significantly associated with both moderate/high risk level due to alcohol and sedative use. The present study is innovative as it examines possible associations between depressive symptomatology and 10 classes of substances concurrently for a group that is largely understudied, further contributing to the international literature in this area. Findings are discussed with regards to study limitations.