26 RESULTS
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COMMENT In this interesting paper, Kukar and colleagues report that many NSAIDs and their derivatives selectively raise Aβ42 and lower Aβ38 secretion. These results are surprising, given the group’s original finding that another subset of NSAIDs do just the oppos
COMMENT Recent epidemiological studies (Jick et al., 2000; Wolozin et al., 2000; Heart Protection Study Group, 2002; Shepherd et al., 2002; Zandi et al., 2005) have led to contradictory conclusions regarding the efficacy of statin treatment for AD. As Dr. Wolozin
COMMENT Recently there has been much debate as to whether statin therapy offers a benefit for Alzheimer disease (AD), and whether statins reduce AD incidence and/or progression remains an open question (Jick et al., 2000; Wolozin et al., 2000; Shepherd et al., 20
COMMENT As reported in our J. Neurosci. paper, the 5XFAD mice display obvious neuron loss of large pyramidal neurons in layer 5 of the cortex and in the subiculum at 9 months of age. It appears that the neuron loss may be related to an increase in p25, the activa
COMMENT Gary Landreth’s group (Ostrowski et al.) has published a very interesting and thorough study demonstrating that the isoprenylation status of specific Ras-related GTPases can have a significant impact on APP metabolism and Aβ genesis. Through a set of eleg
COMMENT Reply to comment by Greg Hook I don't see solid evidence for the argument that BACE1 is not β- secretase. Dr. Hook claims that cathepsin B, not BACE1, is the β-secretase for wild-type APP. If so, then BACE1 knockouts mated to wild-type APP transgenic
COMMENT The paper by Kovacs and colleagues reports the discovery that a significant proportion of APP in the cell is palmitoylated and enriched in lipid rafts. APP palmitoylation increased the colocalization of APP with BACE1, the β-secretase. Consequently, BACE1
COMMENT Research spanning the last two decades has increasingly implicated the Aβ peptide as a critical early player in the pathogenesis of AD. However, the mechanisms of Aβ-mediated toxicity and neurodegeneration in AD have been intensely debated and remain poor
COMMENT Researchers have long speculated that the Aβ peptide might have a physiological function. Unfortunately, evidence of a normal role for Aβ in cellular processes has been notoriously difficult to obtain and has led to the prevailing notion that Aβ is merely
COMMENT Kotti et al., present an elegant study in which they use behavioral and electrophysical and biochemical analysis of wild type and 24-hydroxylase knockout (KO) mice to delineate a novel role for geranylgeraniol, an immediate precursor of the isoprenoid ger
COMMENT This is a fascinating paper. It presents a strong case that normal translation of proteins under hypoxic conditions can lead to cell death, and that reducing protein synthesis can therefore be protective when oxygen (and probably glucose, too) is limiting
COMMENT This paper fits with our hypothesis that glucose deprivation increases BACE1 mRNA translation and hence increases the risk of AD, as type 2 diabetes has been shown to do epidemiologically. However, the study has not investigated mechanism, so the jury is
COMMENT This paper by Gang Yu and colleagues describes a very interesting study to identify the set of RNAs that bind to TDP-43, a protein that has been implicated in a wide range of neurodegenerative diseases. The authors performed an unbiased screen of TDP-43 R
COMMENT Research spanning the last two decades has increasingly implicated the Aβ peptide as a critical early player in the pathogenesis of AD. However, the mechanisms of Aβ-mediated toxicity and neurodegeneration in AD have been intensely debated and remain poor
COMMENT The discovery of η-secretase processing of APP is an intriguing finding that may have important implications for BACE inhibition as a therapeutic approach for AD. Willem and colleagues convincingly show that BACE inhibition increases the Aη-α fragment in
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