11170 RESULTS
COMMENT The validity of this article has been called into serious question by three journals. In January 2004, the British Medical Journal reported that its statistical reviewer concluded that the data in this trial had "all the hallmarks of being entirely i
COMMENT This report by Deisseroth and colleagues, that excitatory transmission stimulates neurogenesis in the hippocampus of rats, could have important implications for the pathogenesis and treatment of Alzheimer’s disease (AD). In AD, as in several other neurolo
COMMENT Presenilin (PS) 1 and 2 rose to prominence in the mid 90’s, when mutations in these genes were shown to be associated with sub-forms of Alzheimer’s disease characterized by the early onset of symptoms and their dominant inheritance. Many years of intense
COMMENT In this study, the authors investigate the role of notch signaling during mammalian neural development. The authors use a number of intricate, crafty conditional knockout mouse models to address whether notch signaling regulates apoptotic cell death durin
COMMENT Dr. Yang and colleagues report finding VEGF coaccumulates markedly with amyloid plaques in the brain of patients with AD. Their study shows VEGF directly binds to Aβ peptides with high affinity and specificity and is slowly released from the coaggregated
COMMENT This group of German and Belgian investigators has produced what is apparently the first evidence that a member of the ADAM family of proteases functions as an alpha secretase for the beta amyloid precursor protein substrate in vivo. An attractive feature
COMMENT The recent news on structural studies on Nerve Growth Factor (NGF), in relation to its interaction with the p75 receptor provide important new data. It will help in gaining insight into the emerging role of NGF, its precursor form(s), and of its complex r
COMMENT My Mother entered a nursing home walking, talking, eating and going to the bathroom by herself. She had Alzheimer's but ate breakfast out daily. She entered the home when Dad was hospitalized with a heart attack. She was prescribed zyprexa upon admis
COMMENT In this study, the authors provide the first in- vivo demonstration of an effect on plaque formation and neuronal function by stimulating the α-secretase pathway involved in APP processing. Presently, there are two known pathways by which APP is processed
COMMENT This is an excellant paper showing the effects of knocking out PS-1 and PS-2. The major differenct it seems between the Feng el al. paper and Saura et al., is the question of how the neurodegeneration is taking place? Feng el al., suggest an apoptotic pat
COMMENT Following quickly on the heels of the excellent Neuron paper by Carlos Saura and colleagues is this complementary work by Ruiben Feng et al. Both groups of investigators crossed a knock-out PS2 KO line, made by traditional transgenic methods (and revealin
COMMENT By Akihiko Takashima In this paper, Feng and colleagues showed that neurodegeneration occurred in mice deficient in both presenilins. Overlapping results have been reported in Neuron by Jie Shen’s lab. Their results also showed that aged PS1/2 double knoc
COMMENT Feng et al. describe cortical degeneration in the forebrain of mice lacking the Alzheimer’s disease genes presenilin (PS) 1 and 2. The mice help to define essential roles of presenilins in the maintenance of brain function. These results confirm previous
COMMENT This work largely confirms the earlier conditional KO study by Saura et al., 2004. There is a dramatic reduction in cortical tissue and a massive hydrocephalic-like appearance in animals that lack both presenilins. I wonder how significant and relevant th
COMMENT This study confirms some of our results. It reproduces the neurodegeneration phenotype we saw in an independently generated presenilin double conditional KO. Feng et al. report an increase in apoptosis; we tested for this but did not see it in our mice. F
