11633 RESULTS
COMMENT The recent epidemiological study by Rea and colleagues adds yet more complexity (and confusion) to the issue of statin use and AD risk. It’s difficult to draw any firm conclusions from the study, since the reported outcomes vary so distinctly as a functio
COMMENT Given the termination of ADAPT, it may be many years before we know whether nonsteroidal drugs can truly inhibit or delay the onset of AD. Still, the strong observational evidence in favor of this idea warrants further investigation. Here is a paper showi
COMMENT The findings reported by Dr. Love, while having some overlap with the tissue transplant studies, show significant differences, particularly with regard to neuronal resprouting and also to the involvement of the substantia nigra. It seems likely that GDNF
COMMENT SantaCruz and colleagues manipulated transgenic tau levels using the tet-off system. Their results indicate that NFT accumulation is not sufficient to cause neuronal death and cognitive decline. This result was a bit of a surprise, because NFT formation i
COMMENT In this study, SantaCruz and colleagues have created an inducible mutant tau transgenic model, and observed the neuropathological consequences of strategically turning on and off tau expression for set periods. Profound forebrain neurodegeneration and mem
COMMENT FAD mutations inhibit cleavage at the ε site of many PS/γ-secretase substrates. Inhibition at the ε site is predicted to increase cleavage at the γ site, thus increasing Aβ production. This paper offers experimental evidence for this concept. 0 nikos.roba
COMMENT Bae et al. present compelling evidence for a crucial role of p53, a protein well-known for its role in programmed cell death, in the cellular dysfunction and associated motor abnormalities in Huntington disease (HD) (1). They establish an association betw
COMMENT The cholesterol and statin story in AD has been a never-ending battle since its inception in the late 1980s, and the current paper sends a mixed message. It seems that if the authors exclude the final year of medications from consideration, there is no re
COMMENT The new paper raises legitimate questions regarding the potential for artifactual associations emerging from epidemiological studies. My position remains cautiously optimistic because of the faint but positive signal emerging from the Sparks et al. trial
COMMENT The report by Love and colleagues in Nature Medicine provides intriguing preliminary evidence for a biological effect of GDNF in humans with Parkinson disease. The greater area of staining for tyrosine hydroxylase in the striatum on the side previously mo
COMMENT I understand that further animal toxicity studies are in progress. However, over 100 patients have received intracerebral GDNF infusion by one route or another with no clinical toxicity and I can't believe that GDNF treatment won't be available
COMMENT Prion disorders include Creutzfeldt Jakob disease in humans, bovine spongiform encephalopathy in cattle, and chronic wasting disease in the deer and elk population of North America. The underlying pathogenic and infectious particle in all prion disorders
COMMENT DNA Fragmentation Mechanism Involving Oxidative Stress: Relevance to Alzheimer Disease While DNA strand breaks are stereotypical of an apoptotic program, their presence in Alzheimer disease (AD) is of such a widespread nature and numerically high scale (S
COMMENT Rubinsztein and colleagues present strong evidence that macroautophagic turnover of proteins requires dynein, possibly to transport autophagosomes and lysosomes into juxtaposition for fusion and initiation of digestion. This role of dynein may be especial
COMMENT The recent finding from Junn and the Mouradian group on DJ-1 interacting with Daxx is very interesting. First, by using the two hybridization system, Junn et al. found that DJ-1 can bind Daxx, which is a component of the Fas death receptor signal transduc
