George Siegel on Does Aβ Normally Rein in Excited Synapses?

COMMENT The physiologic effect of Abeta in depressing excitatory transmission in hippocampal slices as reported by Kamenetz et al may be due to the effect of Abeta in causing depletion of presynaptic SNAP-25 from hippocampus in transgenic mice, since SNAP-25 is r

John Hardy on Substantial linkage disequilibrium across the insulin-degrading enzyme locus but no association with late-onset Alzheimer's disease.

COMMENT Reply to comment by Rudy Tanzi. Phillipp Kahle's and Bart De Strooper's comments on the

Xiongwei Zhu on Involvement of DNA damage and repair systems in neurodegenerative process.

COMMENT Oncogenic Processes in Alzheimer’s Disease: A Common Link? While the Alzheimer’s disease (AD) research community has historically focused almost exclusively on how the two hallmark lesions of the disease, namely senile plaques and neurofibrillary tangles,

Kiminobu Sugaya on Stem Cell Fusion Is for Real

COMMENT There is much evidence that bone marrow stem cells acquire environmental cell characteristics by cell fusion (see ARF related news story; Spees et al., 2003). The fusion may be enough to reprogram gene expression patterns and result in changing cell fate

Robert Peers on Memantine in moderate-to-severe Alzheimer's disease.

COMMENT Any glutamate excess in Alzheimer's may be of glial origin. Aldehydic products of lipid peroxidation apparently inactivate glial glutamate uptake transporters. The correct approach to the problem is at a primary level, by correcting the lipid peroxid

Rudy Tanzi on Substantial linkage disequilibrium across the insulin-degrading enzyme locus but no association with late-onset Alzheimer's disease.

COMMENT be most responsible to hold off from making definitive comments of "fact' one way or the

Craig Atwood on Ironing out the Role of Metals in Neurodegenerative Diseases

COMMENT Chelation as a Therapeutic for Neurodegenerative Diseases In this study by Kaur and colleagues, transgenic mice generated by the embryonic injection of a human H ferritin gene construct driven by the rat tyrosine hydroxylase promoter were shown to be less

Craig Atwood on Ironing out the Role of Metals in Neurodegenerative Diseases

COMMENT Chelation, Metals and Parkinson’s Disease This paper by Julie Andersen and colleagues highlights the importance of iron in the pathogenesis of Parkinson’s disease (PD). Reduction of reactive iron in the brains of mice either by genetic (overexpression of

Edward Koo on A scaffold protein JIP-1b enhances amyloid precursor protein phosphorylation by JNK and its association with kinesin light chain 1.

COMMENT In a detailed and carefully performed study, Inomata and colleagues provide some intriguing new observations about what JIP-1b may be doing when it interacts with AβPP. Last year, several labs reported that AβPP interacts with JIP-1b, the JNK interacting

Edward Koo on Aβ's Shadowy Sibling—What Becomes of the Intracellular Domain?

COMMENT In a detailed and carefully performed study, Inomata and colleagues provide some intriguing new observations about what JIP-1b may be doing when it interacts with AβPP. Last year, several labs reported that AβPP interacts with JIP-1b, the JNK interacting

Christopher Larsen on Spongiform degeneration in mahoganoid mutant mice.

COMMENT This interesting report introduces a new enzyme, Mahogunin, which is a ubiquitin ligase implicated in neuronal metabolism. Through caffeine mutagenesis, a Jackson Lab strain produced a mouse with coat color like that of the spongioform mouse Attractin. Th

Michal Schwartz on Therapeutic vaccine for acute and chronic motor neuron diseases: implications for amyotrophic lateral sclerosis.

COMMENT Reply by Michal Schwartz. Studies over the last five years have provided evidence that the body’s ability to withstand injurious conditions in the CNS, regardless of their primary cause, is dependent on the peripheral immune system. Our group showed, for

Benjamin Wolozin on Inactivation of TSE agents: safety of blood and blood-derived products.

COMMENT Yang and colleagues have published an elegant study investigating the function of parkin (Yang et al., 2003). Loss of parkin is known to cause ARJP, but the reason for the toxicity is unknown. Parkin is known to bind and ubiquitinate the receptor protein

Mark Cookson on Inactivation of TSE agents: safety of blood and blood-derived products.

COMMENT Following on from earlier work from the Takahashi lab showing that parkin ubiquitinates pael-r (see ARF related news story), Lu et al. now show in-vivo evidence that this substrate damages dopaminergic neurons when forcibly accumulated. One of the nice th

Tennore Ramesh on Therapeutic vaccine for acute and chronic motor neuron diseases: implications for amyotrophic lateral sclerosis.

COMMENT The role of the immune system in ALS remains very controversial. Recent advances in understanding the role of inflammation in several neurodegenerative conditions have focused many researchers towards inflammation, now dubbed "neuroinflammation."