Hiroshi Mori on The Glu318Gly substitution in presenilin 1 is not causally related to Alzheimer disease.
COMMENT This site is the hot spot we have to conclude immediately. 0 mori
264 RESULTS
COMMENT This site is the hot spot we have to conclude immediately. 0 mori
COMMENT This clearly denies the association of a gene near BCHE with AD. 0 mori
COMMENT Post-translational modification is a characteristic event in AD and related disorders because of abnormal accumulation of cellular inclusions and extracellular deposition. There is still not much known about related enzymes and molecules other than ubiqui
COMMENT It is interesting to know the effect of tau mutations on their fibril formation. Several lines of evidence must accumulate for different aspects of the tau mutations because of a wide variety of tauopathy. 0 mori
COMMENT His hypothesis that G protein is tightly associated with AD degeneration is very unique and interesting on the viewpoint of signal transduction disorder. 0 mori
COMMENT Since alpha-2-macroglobulin is claimed to be associated with sproadic AD, factors such as immune reacion and lipid metabolism should be of greater interest. 0 mori
COMMENT Ab1-42/43 is likely to be associated with presenilin-1 but this paper indicates the possible interaction between Ab1-40 and presenilin-1. 0 mori
COMMENT This suggests superoxide production by PS-1 mutations. What remains to be seen is the relationship between radical species and amyloidgenesis, both of which were caused by PS-1. 0 mori
COMMENT Caspase is a family of apoptosis-related protease and now known to be comprised of more than 13 species. Some of them could be related to AD pathogenesis. 0 mori
COMMENT The high radical scavenger activity in ApoE null mice may be related with the lack of amyloid deposition. 0 mori
COMMENT His aminopeptidase hypothesis is a new one which explains in vivo amyloid deposition. 0 mori
COMMENT The detailed analysis on tau is very informative for elucidating in vivo condition of tau in Alzheimer's PHF. 0 mori
COMMENT It is very interesting and desiralbe to enhance the present study because cerebral LRP blockade may be a new anti-AD therapy. 0 mori
COMMENT This is important because it shows the presence of gene expression of ApoE in neuron as well as glial cells which were supposed to be the sole cell type to produce ApoE. 0 mori
COMMENT Any trials to improve cognitive dysfunction of AD must be welcomed even if they are completely denied theoretically or clinically. We certainly need the mass examination of such trials. Estrogen is one of such trials we need to study clinically. 0 mori