11622 RESULTS
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
COMMENT Recent research offers new clues into the pathogenesis of prion diseases Glycation Involved in the Formation of Aberrant Prion Protein Isoform PrPSc Mark E. Obrenovich and Vincent M. Monnier Prion diseases comprise a group of neurodegenerative diseases, t
COMMENT The finding of no effect on synaptic integration prior to plaque accumulation seems at variance with other data (e.g. Redwine et al., 2003; Oddo et al., 2003) showing significant effects on parameters such as LTP prior to plaque accumulation in transgenic
COMMENT I recommend this paper. 0 emueller3586
COMMENT Nice try; but is it in package form and availible over the counter? Bugs are close relatives but without applicable results it's just another nice direction without building blocks. herbywalker 0
COMMENT When all that shines is not golden: Metals in Alzheimer disease This review provides a good summary of the old and new mechanisms by which aluminium, zinc and lead might mediate neurotoxicity, and suggests that multiple downstream mechanism are involved.
COMMENT Would there be room for the suggestion that AML stem cells may also migrate to the brain to form astrocytes? It seems of interest that Baldus et al(1) find overexpression of APP, ETS2 and ERG genes in AML. Wolvetang and colleagues (2)show that ETS2 transa
COMMENT ABAD—The New/Old Good/Bad Guy in Alzheimer's Disease Lustbader and colleagues [1] present a complex potential mechanism for the role of amyloid β in Alzheimer's disease (AD) pathology. The authors created a crystal form of amyloid β-binding alco
COMMENT The effects of unfractionated (Neurobiol Aging 2002;23:531) and now fractionated heparins on Aß bioactivity (in vitro) and deposition (in vivo) are clearly intriguing, though it remains unclear how to tie these in-vitro and in- vivo findings together. The
COMMENT We published a paper recently which might be interesting given the topic: Serum testosterone levels in males with Alzheimer's disease. mikko.laakso 0 Serum testosterone levels in males with Alzheimer's disease.
COMMENT Embalming Amyloid-β: The Role for Aldehyde Stress in Alzheimer's Disease Zhang and colleagues present novel findings demonstrating that cholesterol derivative-aldehydes resulting from ozonolysis can accelerate the aggregation of Aβ into fibers. This
COMMENT This is a very thoughtful minireview of presenilin gene action and its significance for AD pathogenesis and therapy, as would be expected from Bart De Strooper and his colleagues. I certainly agree that we need research initiatives that reflect thinking &
COMMENT Parkin and Mitochondria: Are They Allies in the War Against Parkinson’s Disease? This exciting study by Palacino and colleagues shows an alliance between two of the best-studied features of Parkinson's disease, namely, mitochondrial dysfunction and p
COMMENT Curcumin and Protein Misfolding The most common cause of cystic fibrosis is the δF508 mutation that causes ER misfolding and retention/degradation of the cystic fibrosis transmembrane conductance regulator (CFTR). This leads to a temperature-dependent fai
