Hiroshi Mori on mtDNA polymorphisms in Japanese sporadic Alzheimer's disease.

COMMENT Since their study is on the linking between Apo E receptor and AD, they examine more risk factors to explain other sporadic cases. 0 mori

Nikolaos K. Robakis on Somatic mutation analysis of the APP and Presenilin 1 and 2 genes in Alzheimer's disease brains.

COMMENT This paper helps to resolve the very important issue of the involvement of PS mutations in sporadic AD. 0 nikos.robakis

Hiroshi Mori on Laminin inhibits Abeta42 fibril formation in vitro.

COMMENT Laminin's effect on Abeta 42 may be a clue for the possible treatment in future. 0 mori

Paul Coleman on Multivariate analysis of laminar patterns of neurodegeneration in posterior cingulate cortex in Alzheimer's disease.

COMMENT 'In conclusion, multivariate pattern recognition shows that AD is composed of independent neuropathological subtypes and NFT in area 23 do not account for most neuron losses.' Another study showing that NFT are not obligatory for the excess neur

Hiroshi Mori on Alteration of proteins regulating apoptosis, Bcl-2, Bcl-x, Bax, Bak, Bad, ICH-1 and CPP32, in Alzheimer's disease.

COMMENT Upregulation of Bak, Bad, Bcl-2 and Bcl-x are observed in AD brains but it is still not known what the primary event is that is responsible for these changes. 0 mori

Hiroshi Mori on Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis of proteins in human cerebrospinal fluid.

COMMENT The recent advance of Mass spectrometry is great. It is useful to analyze protein chemistry of normal and abnormal peptide and its derivative in human material even in the presence of sait. 0 mori

Elliott Mufson on Induction of a specific tau Alzheimer epitope in SY-5Y neuroblastoma cells.

COMMENT Interesting 0 emufson

Hiroshi Mori on Glucocorticoids in Alzheimer's disease. The story so far.

COMMENT The inflammatory hypothesis is an attractive one for the treatment of Alzheimer's disease. Specific inflammatory to AD pathogenesis must be clinically and experimentally studied from multiple viewpoints. 0 mori

Hiroshi Mori on Heparin-binding properties of the amyloidogenic peptides Abeta and amylin. Dependence on aggregation state and inhibition by Congo red.

COMMENT Cofactors to promote amyloid fibrils are expected to have some important role in pathogenesis of Alzheimer's disease. HEPARIN is one of these factors and attractive from the view point of PHF formation. 0 mori

Nikolaos K. Robakis on Laminin inhibits Abeta42 fibril formation in vitro.

COMMENT If replicated, this is an interesting finding as it may indicate a way to inhibit Ab production. 0 nikos.robakis

Hiroshi Mori on Cytochrome oxidase in Alzheimer's disease: biochemical, histochemical, and immunohistochemical analyses of the visual and other systems.

COMMENT Staining for cytochrome oxidase activity is well used to see cortex layer architechture and barell analysis. It may be helpful to understand cellular disorders of AD pathology. 0 mori

Hiroshi Mori on Apolipoprotein E and antioxidants have different mechanisms of inhibiting Alzheimer's beta-amyloid fibril formation in vitro.

COMMENT It is important to look at amyloid fibril formation on different viewpoint as seen in this article. ApoE is worth to be examined because of its risky function for AD. The paper may be extended to two amyloid species or allelic difference in future. 0 mori

Hiroshi Mori on Appearance of sodium dodecyl sulfate-stable amyloid beta-protein (Abeta) dimer in the cortex during aging.

COMMENT The dimer is a species of amyloid protein which may be important for pathogenesis. 0 mori

Hiroshi Mori on Evidence that levels of presenilins (PS1 and PS2) are coordinately regulated by competition for limiting cellular factors.

COMMENT PS1 and PS2 are currently hot tips in AD field and the relationship between the causal genes such as PS1, PS2 and APP must be interesting because they introduce the same neuropathology. 0 mori

Elliott Mufson on Insulin-like growth factor I protects and rescues hippocampal neurons against beta-amyloid- and human amylin-induced toxicity.