Carl Cotman on Does Alzheimer's disease start early in life?
COMMENT Interesting 0 cwcotman
11518 RESULTS
COMMENT Interesting 0 cwcotman
COMMENT Glycation which is another post-translational modification beside hyperphosphorylation is described in soluble PHF-tau as well as insoluble PHF from AD brains. The question remains which isoforms suffer such modification? 0 mori
COMMENT The paper indicates the difference of radical action on neurotoxicity between SOD enzyme and ascorbate chemical. This suggests the mode of action of radical species, if any, is not unique. 0 mori
COMMENT `Decoy peptides' are interesting because of their activity as a potent agent to prevent amyloid accumulation or toxicity. 0 mori
COMMENT The abstract suggests that the combined blockade produced may be a pharmacologic model of the memory deficits of AD. Whether this models a major mechanism of memory defect in AD depends on the relation of transmitter status to synaptic loss, hippocampal d
COMMENT Estrogen could be a potent drug to treat dementia. It is important to know its mode of action in brain. This paper examined the changes of expression of trkA, BDNF, NGF genes. The authors study these interesting molecules as the second regulator to respon
COMMENT There are at least three mutation sites in the APP sequence. They influence processing of APP to produce beta-amyloid protein in a different fashion. This is undoubtedly one of the papers that will contribute to our understanding of the biological effects
COMMENT The substantial overlap pointed out by the authors limits the diagnostic potential of this measure as conducted in this study. 0 Paul_Coleman
COMMENT Important new gene for AD risk. 0 bwolozin
COMMENT Intracellular distribution of presenilins must be examined by several approaches to understand the physiological functions. This presents clear evidence for Golgi compartmentation segregated with fragmentation of presenilins. 0 mori
COMMENT Interesting. 0 emufson
COMMENT At neutral pH, PI influences amyloidosis of in vitro Ab1-42 but not Ab1-40. This may be relevant with the presence of diffuse plaque formation. 0 mori
COMMENT The abstract states 'these transgenic mice surprisingly reproduce many aspects of the pathological alterations observed in Alzheimer's disease patients.' There is no inofrmation in the abstract as to which aspects are reproduced. 0 Paul_Col
COMMENT Molina et al review the role of nitric oxide in neurodegeneration and correctly conclude that at present the clinical effects of nitric oxide enzyme inhibitors is unknown. 0 OlneyJ
COMMENT Cytochrome C is a key mediator of apoptosis. Understanding the factors that cause its release is therefore very important. The observation that the mechanism of release differs between neurons and peripheral cells is quite provocative and could explain th