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Convergent biochemical and genetic evidence indicate that the main component of Alzheimer's plaques, the amyloid β peptide (Aβ), plays an initiating role in a complex cascade that culminates in dementia and ultimately death (1,2).
During his lifetime, Alois Alzheimer described five cases of the “characteristic sickness of the cerebral cortex” that his boss, the eminent psychiatrist Emil Kraepelin, later would name in honor of his late colleague. Now, neurologists in Alzheimer’s home state of Bavaria are investigating how these early patients’ family members fared. One patient, Johann F., turns out to have belonged to a large clan afflicted with an early-onset, heritable form of the disease. Many descendants still live in Bavaria, some in the U.S.
Viral vectors are an effective means to deliver small interfereing RNAs into target cells and organs in vivo, according to University of Iowa researchers. The authors demonstrated the therapeutic potential of this technique by inhibiting the expression, in neural cell lines, of eGFP chimeras that contained a polyglutamine (polyQ) tract.
The Notch signaling pathway is of considerable interest to those studying Alzheimer's disease because the Notch receptor and the amyloid-β precursor protein (AβPP) are proteolytically processed much the same manner. Now the Notch pathway may contribute to the progression of another neurodegenerative disease, multiple sclerosis (MS)....
Conference Report "Cell and Molecular Biology of Alzheimer's Disease" Cell and Molecular Biology of Alzheimer's Disease
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.
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