11549 RESULTS
COMMENT Interesting link between glucocorticoids (stress) and toxicity due to beta amyloid and glutamate. [However,] The clonal cell line has not proven its value as a model for hippocampal pyramidal cell. 0 gf224
COMMENT cystatin C is implicated in dementia and this paper provides a mechanism. 0 bwolozin
COMMENT It is obscure whether apoptosis is involved in AD apthogenesis. Study of bcl-2 and p53 and other related molecules are interesting for understanding neuronal viability in AD brain. 0 mori
COMMENT Dr. Kay is the world leader in band 3 work, and in this review paper presents preliminary evidence for differences between AD and controls in posttranslational processing of this protein. 0 Paul_Coleman
COMMENT Bleomycin is a chemical of interest in AD and its metabolic enzyme must be something [of significance]. 0 mori
COMMENT This paper contains important implication and experimental explanation for gammma-secretase which is believed to play a crucial role in Abeta production 0 mori
COMMENT NGF was considered once a promising drug for AD treatment. Unfortunately it seems to have serious side effects (very common with growth factors). Maybe a better administration route will be found with less side effects. 0 nikos.robakis
COMMENT Estrogen is a potent drug to block AD pathogenesis and any information on this issue should be an attractive study. This paper is interesting because the authors studied the possibility of interact estrogen with amyloid and neurite bioactivity. 0 mori
COMMENT A turning point in the molecular history of neurodegenerative disorders. 0 andre.delacourte
COMMENT Soluble APP and ApoE4 are not my bag, but a major weakness in this line of research is that it is conducted in cultured neurons which are immature isolated cells that may march to a different tune than neurons in the intact adult aging brain. 0 OlneyJ
COMMENT In the abstract the authors comment that " No differences between Bcl-2 and Bax
COMMENT The abstract states "Our data show that the decreased activity of nucleus basalis neurons in AD is ApoE epsilon 4 dependent and suggest that ApoE epsilon 4 participates in the pathogenesis of AD by decreasing neuronal metabolism." Neuronal metab
COMMENT Oxidative stress is a potent mechanism of cell death in AD brain. This review may be interesting for a route to address such studies. 0 mori
COMMENT We believe that the dramatic reduction of the calmodulin binding protein, PEP-19, in basal ganglia in Huntington's disease, but not in Parkinson's disease or Downs, may relate to the regional neuronal vulnerability of this disease as well as to
COMMENT Interesting. 0 emufson
