Amyloid beta (Abeta) protein immunotherapy lowers cerebral Abeta and improves cognition in mouse models of Alzheimer's disease (AD). Here we show that Caribbean vervet monkeys (Chlorocebus aethiops, SK) develop cerebral Abeta plaques with aging and that these deposits are associated with gliosis and neuritic dystrophy. Five aged vervets were immunized with Abeta peptide over 10 months. Plasma and cerebral spinal fluid (CSF) samples were collected periodically from the immunized vervets and five aged controls; one monkey per group expired during the study. By Day 42, immunized animals generated plasma Abeta antibodies that labeled Abeta plaques in human, AD transgenic mouse and vervet brains; bound Abeta1-7; and recognized monomeric and oligomeric Abeta but not full-length amyloid precursor protein nor its C-terminal fragments. Low anti-Abeta titers were detected in CSF. Abetax-40 levels were elevated approximately 2- to 5-fold in plasma and decreased up to 64% in CSF in immunized vervets. Insoluble Abetax-42 was decreased by 66% in brain homogenates of the four immunized animals compared to archival tissues from 13 age-matched control vervets. Abeta42-immunoreactive plaques were detected in frontal cortex in 11 of the 13 control animals, but not in six brain regions examined in each of the four immunized vervets. No T cell response or inflammation was observed. Our study is the first to demonstrate age-related Abeta deposition in the vervet monkey as well as the lowering of cerebral Abeta by Abeta vaccination in a non-human primate. The findings further support Abeta immunotherapy as a potential prevention and treatment of AD.

Objective. This study aims to investigate whether posttraumatic stress disorder (PTSD) symptoms exist >1 year after neonatal intensive care unit (NICU) experience and whether PTSD symptomatology differs across parents of infants of different gestational age categories. Methods. A survey was given to parents at routine NICU follow-up visits. Parents completed the PTSD CheckList–Civilian (PCL-C), a standardized scale comprising 17 key symptoms of PTSD. Parents also rated how traumatic their birth experience, first day in the NICU, and first week in the NICU were from “Not Traumatic at All” to “Most Traumatic.” Fisher’s exact test was used to compare PCL-C responses across gestational age categories (Extremely Preterm, Very Preterm, Moderate to Late preterm, and Full Term). Results. Eighty parents participated. In total, 15% of parents had “Moderate to High Severity” PTSD symptoms. There were no statistical differences in PTSD prevalence between parents of children <1 year old and parents of children >1 year old ( P = .51). There was also no statistical difference in prevalence of “Moderate to High Severity” level of PTSD symptoms across gestational age ( P = .16). Overall, 38% of parents rated at least one experience as “Most traumatic.” Conclusion. A high percentage of parents who had a recent NICU experience and parents who had a NICU experience more than a year ago demonstrated PTSD symptoms. In light of these results, many parents of NICU graduates—both mothers and fathers—would benefit from access to long-term counseling services.

The intestine plays a crucial role in regulating wholebody lipid homeostasis through dietary fat absorption and secretion, and through its endocrine secretions of incretin hormones and immune mediators. The intestine synthesizes a specialized lipoprotein, the chylomicron, which contains both dietary triglyceride (TAG) and cholesterol, in addition to both structural and functional apolipoprotein cargo. apoB-48 provides structure to the nascent chylomicron, while apoA-IV, apoA-I, and apoC-III function in the periphery to modify plasma lipid metabolism and clearance, interact with inflammatory apparatus for efficient clearance of dietary lipopolysaccharide and oxidized lipids, and modulate insulin signaling and glucose metabolism (1-3). Therefore, the intestine and its secreted chylomicron are critical regulators of metabolic disease.Despite the importance of the intestine in raising plasma TAG levels in the postprandial state and in apolipoprotein secretion, mechanistic studies are difficult to carry out. This is due to a lack of suitable ex vivo cell culture models that are nontransformed yet stable enough in culture for extended studies and genetic manipulations. The intestine is difficult to model ex vivo because enterocytes are in constant turnover, and are only replenished by intestinal stem cells