11527 RESULTS
COMMENT Contrary to assumptions that mutant superoxide dismutase (mSOD) causes ALS via peroxynitrite-mediated oxidative injury, Subramaniam et al. provide compelling evidence that mSOD toxicity is not due to the copper-dependent catalytic activity of peroxynitrit
COMMENT This paper presents data suggesting that chronic use of a NO-releasing NSAID attenuates Aβ plaque load in an animal model of Aβ neuropathology. Additionally, the data indicate that the efficacy of this NO-releasing NSAID was mediated by microglia activati
COMMENT The paper by Subramaniam et al. demonstrates for the first time that chaperone-mediated copper loading is not required for mutant SOD protein to produce ALS-like disease. Mutant SOD protein-mediated motor neuron disease was not affected in the absence of
COMMENT The new genome screen on Alzheimer's and Parkinson's diseases reported by Pericak-Vance et al. is a very interesting and provocative paper using age-at-onset (AAO) as a quantitative trait to search for novel AD and PD genes. The most interesting
COMMENT Authors' Reply We appreciate Dr. Beach's comment on our publication, and his comments
COMMENT It appears that expression of Cox-1 and 2 varies with species, dose, route and type of insult. Neurons, microglia, astrocytes and also the peripheral macrophages that migrate into the brain following injury can all express Cox-2. The expression of Cox-1 h
COMMENT Our published work indicates that (1) COX-2 expression in the AD brain tissues involves blood-derived macrophages, not neurons; (2) macrophages are infiltrating the neuritic plaques and phagocytizing amyloid-beta. COX-2 activation in the brain appears to
COMMENT The study by DeKosky does not allow for conclusions about whether or not the cholinergic deficit is present at early stages of AD. The data show that there are differences in ChAT activity between a "no cognitive impairment" (NCI) group and a &q
COMMENT In this prospective study, Seshadri et al. measured plasma homocysteine levels in normal elderly individuals and then followed the same individuals for eight years and reassessed their clinical status as well as homocysteine levels. They found that plasma
COMMENT This study shows very similar results to what we reported at the last Neuroscience meeting in San Diego. We found that secreted-type AβPP dose-dependently increased glial differentiation of normal human neural stem cells, and that transfection of the wild
COMMENT Data obtained in the recent prospective epidemiological studies of Wolf et al. and in our studies of a mouse model of Alzheimer's disease (AD) provide a strong case for folic acid supplementation as a preventative approach for AD. The study of the Fr
COMMENT One problem in the Bahn et al. paper is that it lacks confirmation that these changes occur with real Down's syndrome cells, like primary neurons or astrocytes in culture, or in the Down's brain. When they looked at the expression of the AβPP ge
COMMENT The Alzheimer's Society in the UK welcomes all new advances in the treatment of Alzheimer's disease. Memantine is a drug that has been used for many years in Germany, and will now shortly have a Europe-wide license. Memantine works by blocking t
COMMENT I think this is a good paper, and it adds to our transgenic toolbelt. It may, for example, allow us to turn pathology and off, to see if lesions such as plaques can be resolved once the source (e.g., elevated Aβ from an AβPP or PS1 transgene) is removed.
COMMENT This is indeed the first report that newborn neurons in adult brain have morphological and electrophysiological characteristics of adult granule cells, and thereby demonstrates that these new neurons are functional. This represents a major advance by prov
