Morphometric changes at the craniocervical junction during childhood.

Objective: Current understanding of how the pediatric craniocervical junction develops remains incomplete. Measurements of anatomical relationships at the craniocervical junction can influence clinical and surgical decision-making. The purpose of this analysis was to quantitatively define clinically relevant craniocervical junction measurements in a population of children with CT scans that show normal anatomy.

Outcomes and factors associated with infant abusive head trauma in the US.

OBJECT Head trauma is the leading cause of death in abused children, particularly prior to the age of 2 years. An awareness of factors associated with this condition as well as with a higher risk of mortality is important to improve outcomes and prevent the occurrence of these events. The objective of this study was to evaluate outcomes and factors associated with poor outcomes in infants with diagnosed abusive head trauma (AHT).

Therapeutic effects of glatiramer acetate and grafted CD115⁺ monocytes in a mouse model of Alzheimer's disease.

Weekly glatiramer acetate immunization of transgenic mice modelling Alzheimer's disease resulted in retained cognition (Morris water maze test), decreased amyloid-β plaque burden, and regulation of local inflammation through a mechanism involving enhanced recruitment of monocytes. Ablation of bone marrow-derived myeloid cells exacerbated plaque pathology, whereas weekly administration of glatiramer acetate enhanced cerebral recruitment of innate immune cells, which dampened the pathology. Here, we assessed the therapeutic potential of grafted CD115(+) monocytes, injected once monthly into the peripheral blood of transgenic APPSWE/PS1ΔE9 Alzheimer's disease mouse models, with and without weekly immunization of glatiramer acetate, as compared to glatiramer acetate alone.

Angiotensin-converting enzyme overexpression in myelomonocytes prevents Alzheimer's-like cognitive decline.

Cognitive decline in patients with Alzheimer's disease (AD) is associated with elevated brain levels of amyloid β protein (Aβ), particularly neurotoxic Aβ(1-42). Angiotensin-converting enzyme (ACE) can degrade Aβ(1-42), and ACE overexpression in myelomonocytic cells enhances their immune function. To examine the effect of targeted ACE overexpression on AD, we crossed ACE(10/10) mice, which overexpress ACE in myelomonocytes using the c-fms promoter, with the transgenic APP(SWE)/PS1(ΔE9) mouse model of AD (AD⁺).