11633 RESULTS
COMMENT In a human brain one can see three main types of plaques: first Abeta 42 diffuse plaques, then amyloid plaques and at the end senile plaques also named neuritic plaques. Senile plaques, with dystropic neurites filled with a tau pathology, represent the tw
COMMENT This interesting paper shows that our perception of AD physiopathology is getting more complex, but more realistic. We are far away from the simple explanation of the amyloid cascade hypothesis (ACH). To summarize, neurodegeneration is associated with a d
COMMENT The role of statins in modifying both cholesterol- and isoprenoid-related Abeta production is of consierable interest, as reported here. Alternatively, however, the effects of statins on endothelial integrity and function (via increase of eNOS and decreas
COMMENT Very useful reference. 0 laurenmbell2003
COMMENT More support for what might be called the axonal "traffic jam" hypothesis for the pathogenesis of AD- from Larry Goldstein's lab. This paper should be read in conjunction with Orly Lazarov et al., J Neurosci March 2, 2005, which integrates
COMMENT New methodology provides evidence that tau binds to single stranded DNA as well as to dsDNA. With a limited range of oligonucleotides, there was evidence of sequence specificity in the binding of ssDNA. The authors speculate that tau may have a role in ch
COMMENT This excellent paper very elegantly untangled the differential and independent mechanisms by which Ab production is affected by isoprenoids and cholesterol. Unfortunately, the above discussion whether statin treatment in humans could increase intracellula
COMMENT This is a very well-designed study that adds up to the accumulating evidence on cannabinoid-mediated neuroprotection. It shows many aspects of their beneficial effects, in experimental models (both in-vitro and in-vivo), and highlights the effect of canna
COMMENT One could add that it is safer to vaccinate against the pathological Abeta species (N-truncated Ab 42) involved in the first steps of amyloidosis rather than against the physiological one, to avoid an auto-immune effect and to be closer to the physiopatho
COMMENT Pat McGeer makes an interesting point, but further review of the research shows that agonists of CB1 receptors can in fact be neuroprotective. It is quite possible to manipulate CB1 receptors to induce apoptosis in affected neurons (i.e. those with amyloi
COMMENT I find this paper encouraging to research in the area of statins and effects on various esters, their constituents and other biochmeical markers in Alzheimers. I am curious, though, how we may be able to maximize isoprenoid activity, lower cholesterol, (p
COMMENT Kinesin molecular motor protein is involved axonal transport along microtubules. Tau protein is a major constituent of mircrotubules and thus disruption of tau (hyperphophorylation as an example) or any other part of microtubules have been shown to interf
COMMENT Downregulation of clathrin-mediated intracellular transport; desensitization of receptor-mediated ester endocytosis, and RNAi antisense against cell synthesis of cholesterol could prove a powerful synergy of therapeutic treatment in this area. Decreased h
COMMENT LXR¹s are nuclear hormone receptors that bind to hydroxylated forms of cholesterol and promote transcription of genes involved in lipid homeostasis (e.g., ApoE, ABCA1). Cholesterol homeostasis is poorly understood in the brain, but of obvious importance b
COMMENT Fragile X mental retardation syndrome (FXS), the most common form of inheritable retardation, results from a trinucleotide repeat expansion in the FMR1 gene, which ultimately results in transcriptional silencing of the Fragile X mental retardation protein
