Read Peter Davies’ summary of this meeting, organized by Eva-Maria Mandelkow and Ulrike Beisiegel.
Previous studyies have indicated that Aβ somehow impairs long-term potentiation, but what are the signal transduction pathways involved in this phenomenon? A paper from Michael Shelanski's lab suggests as a candidate pathway involved in memory formation.
How similar are neural stem cells to their hematopoietic brethren? Two parallel gene expression studies compare the two.
A specific apoptosis pathway is being advanced to account for the selective death of motorneurons in ALS. Also mysterious is what causes the selective neuronal death of cholinergic neurons in Alzheimer's and dopaminergic substantia nigra neurons in Parkinson's. Could this study point to new possible explanations?
BACE protein concentration and activity levels appear elevated in affected areas of human AD brain, lending support to the hypothesis that increased Ab production is at fault in AD and that BACE inhibitors should urgently be developed.
Interested in finding aggregation inhibitors? Read about this new, inexpensive screen for small molecules that disrupt huntingtin deposition.
A new model suggests that amyloid fibrils can grow because two types of specific substructures of the monomer can bind to each other, i.e. head-to-head, tail-to-tail, head-to-head, etc.
A mouse model that claims to reproduce AD pathology more completely than APP transgenics appears to respond to treatment with NGF and a cholinergic drug.
Two current reviews lay out the current understanding of the role of protein-folding assistants and protein grinders in neurodegenerative diseases.
Small interfereing RNAs are a hot new tool to manipulate gene expression. Read here about how to apply this method to primary neuronal cultures.
This week's issue of Nature features two articles that point to ways in which the targeting of molecules associated with maintenance of cognitive function might one day help boost these functions in both normal and demented older adults.
Using chronic, low-level exposure to a pesticide, Timothy Greenamyre's group has produced a new in-vitro model that recapitulates significant aspects of the cellular damage thought to underly Parkinson's disease.
Read about this update of Martin Schwab's efforts to rekindle spinal cord regeneration with antibodies against the growth inhibitor nogo.
Open reading frame point mutations are associated with a variety of diseases, including Alzheimer’s, and many of these mutations destroy the function of the protein in question. But what of the expression level of the mutated gene? This question was addressed by Kenneth Kinzler...
The tumor suppressor p53 appears to play a role in the pathogenesis of rheumatoid arthritis. What about Alzheimer's disease?