Pediatric Intracranial Abscess From Sinusitis Leading to Status Epilepticus: A Clinical Case Report.

This case study presents the rare incidence of an eight-year-old female with a pediatric intracranial abscess, a life-threatening complication of sinusitis. The patient manifested focal neurological deficits and experienced status epilepticus before presenting to the Emergency Department. She had been diagnosed with sinusitis and prescribed amoxicillin one day prior. The case underscores the importance of early recognition and intervention in managing this rare but potentially fatal complication of a common pediatric illness.

Reduction of synaptojanin 1 ameliorates synaptic and behavioral impairments in a mouse model of Alzheimer's disease.

Decades of research have correlated increased levels of amyloid-ß peptide (Aß) with neuropathological progression in Alzheimer's disease (AD) patients and transgenic models. Aß precipitates synaptic and neuronal anomalies by perturbing intracellular signaling, which, in turn, may underlie cognitive impairment. Aß also alters lipid metabolism, notably causing a deficiency of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)], a phospholipid that regulates critical neuronal functions. Haploinsufficiency of the gene encoding synaptojanin 1 (Synj1), a major PI(4,5)P(2) phosphatase in the brain, provided protection against PI(4,5)P(2) breakdown and electrophysiological deficits attributable to Aß. Based on these data, we tested whether reduction of Synj1 could rescue cognitive deficits and Aß-induced morphological alterations of synapses. We found that hemizygous deletion of Synj1 in the context of a mouse model expressing the Swedish mutant of amyloid precursor protein rescues deficits in learning and memory without affecting amyloid load. Synj1 heterozygosity also rescued PI(4,5)P(2) deficiency in a synaptosome-enriched fraction from the brain of Tg2576 mice. Genetic disruption of Synj1 attenuated Aß oligomer-induced changes in dendritic spines of cultured hippocampal neurons, sparing mature spine classes, which corroborates the protective role for Synj1 reduction against Aß insult at the synapse. These results indicate that Synj1 reduction ameliorates AD-associated behavioral and synaptic deficits, providing evidence that Synj1 and, more generally, phosphoinositide metabolism may be promising therapeutic targets. Our work expands on recent studies identifying lipid metabolism and lipid-modifying enzymes as targets of AD-associated synaptic and behavioral impairment.