Hiroshi Mori on Quantification of sub-femtomole amounts of Alzheimer amyloid beta peptides.

COMMENT This is a third method to measure Abeta. 0 mori

Benjamin Wolozin on The effects of nicotine on Parkinson's disease.

COMMENT This is important because it complements a recent report suggesting that caffeine is beneficial in PD. Both caffeine and nicotine elevate cAMP, so this report strengthens a putative link between cAMP and neuroprotection in PD. 0 bwolozin

Elliott Mufson on A cellular mechanism for the neuronal changes underlying Alzheimer's disease.

COMMENT Interesting. 0 emufson

Hiroshi Mori on Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology.

COMMENT There are some transgenic mice to show amyloid plaques but this is the first study to show the presence of tau alteration to suggest the occurrence of PHF. 0 mori

Benjamin Wolozin on Testosterone stimulates rapid secretory amyloid precursor protein release from rat hypothalamic cells via the activation of the mitogen-activated protein kinase pathway.

COMMENT Novel mechanism for regulating APP processing. 0 bwolozin

Hiroshi Mori on No association of apolipoprotein epsilon 4 allele with schizophrenia even in cognitively impaired patients.

COMMENT This is important to show the pathological specificity of ApoE to AD. 0 mori

Hiroshi Mori on The effects of aging and neurodegeneration on apoptosis-associated DNA fragmentation and the benefits of nicotinamide.

COMMENT Smoking is easy and may be certainly useful to prevent dementia. Such study is worth further examination. Several lines of evidence should be gathered pertaining to approaches that do NOT enhance another diseases such as lung cancer. 0 mori

Paul Coleman on Mechanisms of neurofibrillary degeneration and the formation of neurofibrillary tangles.

COMMENT This whole supplement is obviously a must read for those wishing to learn more about AD from some of the major players in the field. A beta and tau continue to be emphasized as the constituents of the lesions described by Alzheimer. However, mounting evid

John Olney on Infracortical interstitial cells concurrently expressing m2-muscarinic receptors, acetylcholinesterase and nicotinamide adenine dinucleotide phosphate-diaphorase in the human and monkey cerebral cortex.

COMMENT Smiley et al. use histological methods to describe a unique population of infracortical interstitial cells that have m2 muscarinic receptors and contain cholinesterase in the human and monkey cortex. This information is a useful addition to other neuroana

Hiroshi Mori on Multiple pathways of apoptosis in PC12 cells. CrmA inhibits apoptosis induced by beta-amyloid.

COMMENT Apoptotic pathways occur independently on bcl-2 and crmA. Abeta42-dependent pathway may be related with oxidative and non-oxidative ways. 0 mori

Elliott Mufson on Automated identification and quantitative morphometry of the senile plaques of Alzheimer's disease.

COMMENT Noteworthy. 0 emufson

Paul Coleman on The level of cerebrospinal fluid tau correlates with neurofibrillary tangles in Alzheimer's disease.

COMMENT A correlation of 0.44 produces an R squared of 0.19, meaning that the correlation of CSF tau with NFT scores accounts for only 19% of the variability in the NFT data. The magnitide of the correlation also suggests that there may be significant overlap bet

Hiroshi Mori on Perlecan binds to the beta-amyloid proteins (A beta) of Alzheimer's disease, accelerates A beta fibril formation, and maintains A beta fibril stability.

COMMENT A different Kd of perlecan with two Abeta species in the binding should provide a mechanism for cofactors to enhance amyloid fibriol formation. 0 mori

Paul Coleman on Dementia with Lewy bodies.

COMMENT The clinical diagnosis of Lewy body disease is an important issue, but the precise definition of definitive clinical criteria remains unsettled. 0 Paul_Coleman

John Olney on [Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection].

COMMENT Holsboer reviews the evidence for a unified hypothesis to explaiin the neuropathology of AD in terms of an oxidative stress mechanism. This is a well written review, but it does not present any new data or novel ideas that have not been presented before.