Data from this study validated the previously proposed PS3 system, which was found to more accurately predict shunt-dependent chronic hydrocephalus in patients with aSAH compared with other such systems in the neurosurgical literature, such as the chronic hydrocephalus ensuing from SAH score, Barrow Neurological Institute, and shunt dependency in aSAH systems.
We provide strong genetic and biochemical evidence that hydrocephaly and white spotting in B3glct mutants resulted from loss of ADAMTS20, eye abnormalities from partial reduction of ADAMTS9, and cleft palate from loss of ADAMTS20 and partially reduced ADAMTS9 function.
These data demonstrate that altered neuronal proliferation/apoptosis and disrupted ependymal cilia are the main factors contributing to hydrocephalus in PAC1-overexpressing mice.
The increased frequency of hydrocephalus among sibs of probands with a NTD and vice versa suggests that, following the birth of a child with either malformations, subsequent pregnancies should be monitored at mid-gestation by amniotic fluid AFP and serial ultrasound examination.
Mutations in the AP1S2 gene encoding the sigma 2 subunit of the adaptor protein 1 complex are associated with syndromic X-linked mental retardation with hydrocephalus and calcifications in basal ganglia.
Concentrations of amyloid precursor protein (APP), soluble APPα (sAPPα), soluble APPβ, neural cell adhesion molecule-1 (NCAM-1), L1 cell adhesion molecule (L1CAM), tau, phosphorylated tau, and total protein (TP) were measured in lumbar CSF from neonates in 6 groups: (1) no known neurological disease (n = 33); (2) IVH grades I to II (n = 13); (3) IVH grades III to IV (n = 12); (4) PHH (n = 12); (5) ventricular enlargement without hydrocephalus (n = 10); and (6) hypoxic ischemic encephalopathy (n = 13).
With advancing hydrocephalus, expression of AQPs 1 and 4 increased at the brain-CSF interfaces; AQP1 was localized to the endothelium of cortical capillaries with increased AQP4 expression in surrounding astrocytes end feet.
The reduced ventricular size in AQP1-deficient mice following kaolin-induced hydrocephalus suggests AQP1 inhibition or down-regulation as a potential adjunctive treatment for hydrocephalus.
Here we have explored, in young and aged mice exposed to hypoxia, whether aquaporin-4 and aquaporin-1 participate in the development of age-related hydrocephalus.
AQP-4 expression was higher in the sixth than in the first month after inoculation (P = 0.016) and also occurred in animals that received antigen inoculation but did not develop hydrocephalus, suggesting that AQP-4 may constitute an alternative route of cerebrospinal fluid absorption under inflammatory conditions.
With advancing hydrocephalus, expression of AQPs 1 and 4 increased at the brain-CSF interfaces; AQP1 was localized to the endothelium of cortical capillaries with increased AQP4 expression in surrounding astrocytes end feet.