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.

COMMENT Interesting 0 emufson

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

Carl Cotman on The effects of additional pathology on the cognitive deficit in Alzheimer disease.

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

Paul Coleman on Diabetes and dementia in long-term care.

COMMENT Interesting from the point of view of issues regarding potential relationship between metabolic status and AD. 0 Paul_Coleman

Benjamin Wolozin on Presenilin-1 P264L knock-in mutation: differential effects on abeta production, amyloid deposition, and neuronal vulnerability.

COMMENT Important clarification in an ongoing debate. 0 bwolozin

Paul Coleman on Elevated expression of p21ras is an early event in Alzheimer's disease and precedes neurofibrillary degeneration.

COMMENT Another study with implications for cell cycle-relayed genes in AD. 0 Paul_Coleman

John Olney on Evidence that 4-hydroxynonenal mediates oxidative stress-induced neuronal apoptosis.

COMMENT See my remarks on the Barger & Mattson review. 0 OlneyJ

Hiroshi Mori on Age-related alteration of PKC, a key enzyme in memory processes: physiological and pathological examples.

COMMENT Racial comparison of ApoE alleles will provide some information of molecular mechanism of the disease etiology. 0 mori

Hiroshi Mori on Cholesterol depletion inhibits the generation of beta-amyloid in hippocampal neurons.

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

Hiroshi Mori on ApoE polymorphism in Polish patients with Alzheimer's disease.

COMMENT It is important to see the ApoE allelic frequency of AD patients in various ethnic groups. 0 mori

Hiroshi Mori on The apolipoprotein E epsilon4 allele is not a significant risk factor for frontotemporal dementia.

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