Benjamin Wolozin on Biochemical identification of the neutral endopeptidase family member responsible for the catabolism of amyloid beta peptide in the brain.
COMMENT Important information on how Abeta is eliminated. 0 bwolozin
11642 RESULTS
COMMENT Important information on how Abeta is eliminated. 0 bwolozin
COMMENT Interesting hypothesis [that in AD combined with cerebrovascular disease, the total plaque density makes a significant contribution to cognitive deficit, while NFTs do not.] 0 cwcotman
COMMENT Interesting from the point of view of issues regarding potential relationship between metabolic status and AD. 0 Paul_Coleman
COMMENT Important clarification in an ongoing debate. 0 bwolozin
COMMENT Another study with implications for cell cycle-relayed genes in AD. 0 Paul_Coleman
COMMENT See my remarks on the Barger & Mattson review. 0 OlneyJ
COMMENT Racial comparison of ApoE alleles will provide some information of molecular mechanism of the disease etiology. 0 mori
COMMENT This paper shows that cholesterol is a key for APP metabolism to produce A-beta. This may be relevant to the function of ApoE. 0 mori
COMMENT It is important to see the ApoE allelic frequency of AD patients in various ethnic groups. 0 mori
COMMENT Apo e4 was not found to be a risk factor for frontotemporal dementia (FTD) in this paper but still remains to be studied further to reach the final conclusion. 0 mori
COMMENT Interesting 0 cwcotman
COMMENT These data appear to be at some variance with other data in the literature. 0 Paul_Coleman
COMMENT This report deserves further attention as it suggests for the first time that soluble Ab 1-40 may correlate closer to AD than either Ab1-42 or NFTs. 0 nikos.robakis
COMMENT The effect of PS1 mutation on amyloid is significant. Little concern was paid to amyloid speceis in the insoluble fraction including intracellular beside the soluble fraction. This paper gives us further knowledge to understand the PS1 function in cells.
COMMENT It is interesting to see the relationship between immuno response and amyloid plaque fomation. Evidence is not enough to discuss the etiology but this paper is one of studies on this route. 0 mori