27 RESULTS
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COMMENT This fly paper catches genetic evidence that Rac inhibition slows memory decay, constitutively increased Rac activation accelerates memory decay, and that cofilin hyperactivation gives rise to the same phenotype as seen with Rac inhibition. The authors co
COMMENT There are not that many transgenes that improve cognitive function over baseline, so it is always interesting when that happens, as with this report from the Kang lab on Fat-1 transgenics that synthesize DHA from Fat-1, resulting in elevated brain DHA, in
COMMENT This new data on curcumin stimulated neurogenesis look pretty good and the dosing at 500nM to get the effect in vitro and via stimulation of MAPK is credible and consistent with other literature. Their in vivo results are the most important demonstration
COMMENT I have been told that patients of colleagues received this treatment and it did not help them. I also have been told that the patients pay for it out of pocket, and that it is expensive. Last year the UCLA ADRC invited Dr. Tobinick to present his results
COMMENT The decision to market tramiprosate as a supplement is surprising news. It does not speak well of nutraceuticals as a refuge for drugs that fail in clinical trials. From my perspective, it would be okay to fail in a clinical trial if they had compelling b
COMMENT Sex and Drugs and Rac and Rho. How Can You Handle a Sick PAK? Sex-linked mental retardation genes are probably the best understood genetic causes of cognitive deficits. As proximate causes of cognitive dysfunction from birth, they may provide clues to any
COMMENT This new study from Freund-Levi et al. has solid data to show the negative result that at the dose used, DHA-enriched omega-3 fatty acid (fish oil base) supplementation does not produce cognitive benefits in the overall group of AD patients tested. Howeve
COMMENT We read this interesting paper, which offers a novel mechanism of action for PUFA-mediated neurite outgrowth. The mechanism involves fatty acid modulation of formation of syntaxin 3 complexes with SNARE proteins. The latter are required for regulating fus
COMMENT The identification of ACE as a possible AD gene and ACE inhibitors as potential risk factors for AD are both potentially very important observations. Similarly, the many reports on relatively nontoxic dietary factors modulating amyloidosis in animal model
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
COMMENT In response to the commentary by Robert Peers, I'd like to reply that part of his interpretation is plausible and part of it seems less likely to me. When Sally Frautschy and Marni Harris-White infused that particular preparation of Aβ oligomers into
COMMENT The epidemiology supporting an association of chronic and early NSAID use with reduced risk for AD is consistent enough to take seriously. Results from the recent Rotterdam and Cache County studies, as well as many others, suggest that risk for AD can be
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