Monthly Archives: September 2013

The amyloid cascade hypothesis is widely accepted as central to Alzheimer disease pathogenesis. It proposes that abnormal production of beta amyloid protein is the cause of Alzeimer disease and that the neurotoxicity is due to beta amyloid itself or its … Continue reading →

Channelrhodopsins are a group of molecules used to optogenetically depolarize neurons. Here, Tsien and colleagues report their development of a red-activatable channelrhodopsin (ReaChR), that is optimally excited with orange to red light (λ ∼590-630 nm) and offers improved membrane trafficking, … Continue reading →

Cognitive enhancers are used to treat dementia, but their effectiveness for mild cognitive impairment (MCI) is unclear. The authors of this study performed a meta-analysis of the efficacy and safety of donepezil, rivastigmine, galantamine or memantine for MCI. They found … Continue reading →

The efficacy of IFN-β for treatment of multiple sclerosis can be reduced if patients develop neutralizing antibodies to the drug. Hedström and colleagues studied 695 patients with multiple sclerosis and found that the chance of developing neutralizing antibodies to IFNβ-1a … Continue reading →

 Alpha-secretase-mediated processing of cellular prion protein and amyloid precursor protein is decreased in prion and Alzheimer’s diseases. In this paper, Pietri and colleagues show that activity of the kinase PDK1 is increased in the brain following prion infection and with … Continue reading →

Age-dependent loss of dopaminergic neurons is the defining feature of Parkinson’s disease. Mutations and inactivation of parkin, an ubiquitin E3 ligase, induce Parkinson’s disease through accumulation of pathogenic substrates. The authors of this study report that overexpression of  parkin substrate, … Continue reading →