Gerard Drewes on Clever Joining of Databases: New Way to Finger Disease Genes

COMMENT Lander and colleagues combine data from genomics, transcriptomics, and proteomics, to find the gene causing LDFC, a rare monogenetic disease. In this disease, mitochondrial function is compromised. The emerging candidate gene is (i) one of about 50 genes

Vamsi Mootha on Clever Joining of Databases: New Way to Finger Disease Genes

COMMENT Extended Author Comment by Vamsi Mootha In our manuscript we have provided a framework for

Gerard Drewes on Measuring Tyrosine Phosphorylation En Masse—Mass Spec Does the Trick

COMMENT This study demonstrates the power of current state-of-the-art technology in "phosphoproteomics." The authors study the tyrosine phosphorylation events that occur downsteam of T cell activation. They also apply their method to the inhibition of t

Alexei Koudinov on Rotterdam Study Questions Links between Fat and Dementia Risk

COMMENT This report is one of nearly 40 others on Alzheimer's disease by the same research group using the Rotterdam study data. The article sets out to test the hypothesis that "cholesterol increases and n-3 PUFA reduce dementia risk." The results

Edward Koo on HMG-CoA reductase inhibitors (statins) in the treatment of Alzheimer's disease and why it would be ill-advise to use one that crosses the blood-brain barrier.

COMMENT Interesting speculation but the proof will be in the pudding. Ultimately, we don't yet know what happens when statins are given to normal cholesterolemic individuals. 0 edkoo

Edward Koo on FK960, a potential anti-dementia drug, increases synaptic density in the hippocampal CA3 region of aged rats.

COMMENT Interesting observations. It will be even more interesting to see what happens in APP transgenic mice with amyloid pathology. 0 edkoo

Alexei Koudinov on A safer vaccine for Alzheimer's disease?

COMMENT Will Alzheimer's vaccine succeed? Why it should? See the arguments to support the alternative viewpoint at the British Medical Journal. 0 postmaster

Alexei Koudinov on The pathogenic mechanisms of prion diseases.

COMMENT To add to the mechanisms' horizons please see recent Neurobiology of Lipids article. 0 postmaster

Alexei Koudinov on Long-term accumulation of amyloid-beta in axons following brain trauma without persistent upregulation of amyloid precursor protein genes.

COMMENT discussed in greater details in my earlier comment on an ARF news item. 0 postmaster

Andre Delacourte on Frontotemporal lobar degeneration--tau as a pied piper?

COMMENT Binary phenomenon does not exist in biology. If most DLDH are really tau-less tauopathies, FTLD with a tauopathy are likely to represent most, but not all, frontotemporal dementias. Discussing this issue is interesting, and also to know if Alzheimer'

John Hardy on A patient with dementia with Lewy bodies and codon 232 mutation of PRNP.

COMMENT An interesting and provocative paper. If the M232R mutation is pathogenic, then this suggests that DLB may be a alternative expression of prion disease. It is worth noting that Ghetti has published (in abstract form only) that other prion mutations have b

Robert Tycko on Amyloid Formation—One Amino Acid Can Make a Difference

COMMENT Novel experiments by David Teplow, George Benedek, and their colleagues provide important new information about the nature of oligomeric aggregates that form rapidly in aqueous solutions of the β-amyloid peptides, prior to the formation of protofibrils an

Richard Mayeux on Rotterdam Study Questions Links between Fat and Dementia Risk

COMMENT This is a report of a large cohort study finding no association between dietary fat consumption and risk of dementia. The large size and long follow-up of the cohort, and the use of validated measures of dietary intake and diagnosis of dementia support th

Benjamin Wolozin on Rotterdam Study Questions Links between Fat and Dementia Risk

COMMENT See comment by Benjamin Wolozin See reply by Monique Breteler Comment by Benjamin Wolozin:

Russell Swerdlow on New Drug Treats Early Parkinson's Symptoms, Similar to Older One

COMMENT This study from the Parkinson’s Study Group indicates rasagiline should benefit persons with very early Parkinson’s disease. These benefits seem modest, and are similar to those observed with another MAO-B inhibitor, selegiline. The impact that rasagiline