Hiroshi Mori on Solution structure of amyloid beta-peptide(1-40) in a water-micelle environment. Is the membrane-spanning domain where we think it is?

COMMENT Physicochemical information on amyloid peptide could be applied to disease indication as well as to basic results. 0 mori

Paul Coleman on Differential regional dysfunction of the hippocampal formation among elderly with memory decline and Alzheimer's disease.

COMMENT It appears that the results of this fMRI study may be roughly consistent with the stereological hippocampal regional cell counting study of M.J. West et al. in Lancet. 0 Paul_Coleman

Paul Coleman on Examination of the validity of the hierarchical model of neuropathological staging in normal aging and Alzheimer's disease.

COMMENT A useful exploration of the validity of a widely used approach to neuropathological staging of AD. 0 Paul_Coleman

Benjamin Wolozin on The role of prion peptide structure and aggregation in toxicity and membrane binding.

COMMENT Looks important for understanding the biology of protein aggregates. 0 bwolozin

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

COMMENT Very interesting knock-in transgenic mice models where neither APP nor PS were overexpressed. 0 edkoo

John Olney on Presenilins upregulate functional K+ channel currents in mammalian cells.

COMMENT The article by Malin et al presents interesting new evidence pertaining to the potential role of presenilins in the brain. The authors data are consistent with the hypothesis that presenilins regulate neuronal K+ channel expression which suggests the poss

Hiroshi Mori on Association of alpha1-antichymotrypsin polymorphism with cerebral amyloid angiopathy.

COMMENT This report is negative but it is important to know the conclude derived from more than 100 cases that no significant association of the ACT genotypes (AA, AT, and TT) with the severity of CAA. 0 mori

Hiroshi Mori on Microglia, scavenger receptors, and the pathogenesis of Alzheimer's disease.

COMMENT Well documented, microglial scavenger receptors may be novel targets for therapeutic interventions in Alzheimer's disease. They show further explanation here. 0 mori

Hiroshi Mori on Presenilin-1 mutations associated with familial Alzheimer's disease do not disrupt protein transport from the endoplasmic reticulum to the Golgi apparatus.

COMMENT This claims the effect of PS1 mutation on protein trafficking with two different co-transfections. It is an interesting suggestion that mutant forms of PSI cause elevated production of A beta(42) by a mechanism that is independent of a major disruption of

Benjamin Wolozin on Distinct properties of wild-type and the amyloidogenic human cystatin C variant of hereditary cerebral hemorrhage with amyloidosis, Icelandic type.

COMMENT Provide clear and important information on the biochemical mechanisms underlying the accumulation of cystatin C in disease. 0 bwolozin

Paul Coleman on Cortical load of PHF-tau in Alzheimer's disease is correlated to cholinergic dysfunction.

COMMENT It appears the data of this paper may be interpreted in several classes of ways. One class might involve directly causative mechanisms. The other might simply be that as disease progresses the load of PHF-tau increases and the cholinergic deficit also inc

Paul Coleman on Elevated neuronal Cdc2-like kinase activity in the Alzheimer disease brain.

COMMENT This paper appears to be based on the premise that 'tau hyperphosphorylation in AD may result in part from deregulation of Ndlk' (neuronal cdc2-like kinase). Ratio of this kinase activity in prefrontal vs. cerebellare cortex was found to be high

Elliott Mufson on Choline acetyltransferase mRNA expression in the striatal neurons of patients with Alzheimer's disease.

COMMENT Noteworthy. 0 emufson

Hiroshi Mori on Oxidative metabolism in cultured fibroblasts derived from sporadic Alzheimer's disease (AD) patients.

COMMENT Changes of redob enzyme associated with AD brain is interesting from the viewpoint that the possilbe radical contribution on AD pathogenesis. 0 mori

Benjamin Wolozin on Essential role for cholesterol in synaptic plasticity and neuronal degeneration.

COMMENT Cholesterol appears to be increasingly important in neurodegeneration, but is understudied. This paper provides novel insight into the manner in which abnormalities in cholesterol metabolism can modulate the biology of proteins involved in neurodegenerati