Learn More
Mutations of amyloid precursor protein (APP) and presenilin-1 (PS1) lead to an increase in beta-amyloid (Abeta) production. Despite the fact that a number of transgenic mice develop cerebral Abeta plaques, few have been subjected to ultrastructural investigation and the sequence of events leading to Abeta plaque formation is unclear. We therefore(More)
Ts65Dn mice are partially trisomic for the distal region of MMU16, which is homologous with the obligate segment of HSA21 triplicated in Down syndrome (DS). Ts65Dn mice are impaired in learning tasks that require an intact hippocampus. In order to investigate the neural basis of these deficits in this mouse model of Down syndrome, quantitative light and(More)
Septic encephalopathy is a complication of sepsis, and it is closely associated with the increased mortality of the sufferers. Pathophysiology of septic encephalopathy is not still completely understood. In an attempt to provide insight into the pathogenesis of septic encephalopathy, a light and electron microscopic investigation has been carried out in a(More)
Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a(More)
PURPOSE The objective of this study was to compare the effects of two neuroprotective agents; melatonin, a free radical scavenger and topiramate, AMPA/kainate receptor antagonist, administered alone or in combination in neonatal hypoxic-ischemic model. METHODS After being anesthetized, 7-day-old pups underwent ischemia followed by exposure to hypoxia. The(More)
Down syndrome results from triplication of human chromosome 21. The distal end of mouse chromosome 16 shares a large region of genetic homology with the Down syndrome 'critical region' of human chromosome 21. Therefore, a partially trisomic mouse (Ts65Dn) that possesses a triplication of the distal region of chromosome 16 has been developed as a putative(More)
Senile plaques composed mainly of beta-amyloid (Abeta) and neurofibrillary tangles principally composed of hyperphosphorylated tau are the major pathological features of Alzheimer's disease (AD). Despite the fact that increased expression of amyloid precursor protein (APP) and presenilin-1 (PS1) transgenes in mice lead to increased Abeta deposition in(More)
The deposition of amyloid beta (A beta) protein plays a central role in the neuropathology of Alzheimer's disease (AD) and it constitutes the core of classical senile plaques. However, little is known about its intracellular distribution. An immunogold electron microscope study was therefore carried out on biopsies of brain tissue from patients with AD(More)
Sepsis and septic shock are the commonest causes of death in the intensive care units. Although recent research have improved our understanding of the progress and pathophysiology of sepsis and septic shock, underlying mechanisms in sepsis-associated encephalopathy is still poorly understood. The incidence of sepsis-associated encephalopathy has been(More)
Paired helical filaments (PHFs) are one of the hallmark pathologies of Alzheimer's disease (AD). PHFs occur in three intracellular locations, although hitherto, it was not known whether all PHFs are structurally homogeneous. Parietal cortex biopsies were taken from five patients with a clinical and histopathological diagnosis of AD and processed for(More)