Benjamin Wolozin on alpha-Synuclein membrane interactions and lipid specificity.

COMMENT Important contribution to understanding synuclein biology. 0 bwolozin

Nikolaos K. Robakis on New susceptibility gene for Alzheimer's disease on chromosome 12?

COMMENT If replicated, the importance of this finding is obvious 0 nikos.robakis

Paul Coleman on Striation is the characteristic neuritic abnormality in Alzheimer disease.

COMMENT The authors suggest that the neuritic striations they describe may disrupt the microtubule system and, thus, block fast axonal transport. This could be an important component of both the disrupted synapses as well as altered retrograde transmission of mat

Hiroshi Mori on Effects of frontotemporal dementia FTDP-17 mutations on heparin-induced assembly of tau filaments.

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

John Olney on Effect of beta-amyloid block of the fast-inactivating K+ channel on intracellular Ca2+ and excitability in a modeled neuron.

COMMENT This would appear to be a theoretical effort to solve the AD mystery by a mathematical model that speculates upon potential links between beta amyloid, potassium currents, intracellular calcium, etc. We need more empirical science and less arm chair specu

Hiroshi Mori on A new paradigm for neurotoxicity by FAD mutants of betaAPP: a signaling abnormality.

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

Carl Cotman on Requirement of the familial Alzheimer's disease gene PS2 for apoptosis. Opposing effect of ALG-3.

COMMENT A key new lead. Specificity may be dependent on the PC12 line 0 cwcotman

Hiroshi Mori on Complement C1-inhibitor expression in Alzheimer's disease.

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

Nikolaos K. Robakis on Cell activation by glycated proteins. AGE receptors, receptor recognition factors and functional classification of AGEs.

COMMENT This is a good review for the production and clearance of cellular proteins modified by advanced glycation endproducts (AGE). It has been proposed that Glycation products may be important for AD (see also next Abstract) 0 nikos.robakis

Hiroshi Mori on Evidence for presenilin-1 involvement in amyloid angiopathy in the Alzheimer's disease-affected brain.

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

Hiroshi Mori on Superoxide mediates the cell-death-enhancing action of presenilin-1 mutations.

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

Hiroshi Mori on Antibody to caspase-cleaved actin detects apoptosis in differentiated neuroblastoma and plaque-associated neurons and microglia in Alzheimer's disease.

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

Elliott Mufson on Comparison of site specific injections into the basal forebrain on water maze and radial arm maze performance in the male rat after immunolesioning with 192 IgG saporin.

COMMENT Interesting. 0 emufson

Hiroshi Mori on Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury.

COMMENT The high radical scavenger activity in ApoE null mice may be related with the lack of amyloid deposition. 0 mori

Richard Mayeux on Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease.

COMMENT Timing is everything. This study suggests that COX2 may be upregulated in AD (assuming that animal models are an accurate reflection of the disease) at later stages in the pathogenesis of the disease. Thus, inhibitors of COX2 might be more useful in prima