A protein instigates axon degeneration by promoting destruction of the essential enzyme cofactor, NAD+.
In a Solomonic move, a prestigious prize for research in neurodegenerative disease goes to a veteran tauist and a self-professed inhabitant of “amyloid land.”
A new study suggests that tau oligomers as small as trimers enter neurons and corrupt native tau proteins inside.
At AD/PD, researchers further tied TREM2 to phagocytosis and enumerated markers that may distinguish beneficial microglia from harmful ones.
The growth factor turns off microglia, major support cells for neurons.
Genetic and animal studies hint that B and T cells control amyloid accumulation, though the mechanisms remain unclear.
A mouse model that was previously thought to express a transgene predominantly in the entorhinal cortex may be much leakier than previously thought. This complicates interpretation of some previous studies reporting propagation of toxic tau aggregates.
Deep brain stimulation helps many people with Parkinson’s, but how it does so remains a mystery. A new study suggests it normalizes brain rhythms.
The notion that misfolded forms of tau, Aβ, and other proteins spread throughout the brain via connected synaptic circuits has become widely accepted. One model used to support this idea allowed researchers to restrict expression of a protein to the entorhinal cortex and watch it spread to other regions of the mouse brain. Now, a study reports that expression in this model, called Nop-tTA, "leaks" much more than previously thought. The finding does not negate the concept of protein transmission, but it questions the relative contribution of locally made versus propagated protein in some regions of the brain.
Alzforum’s coverage of AD/PD 2015 wrapped up last week with a look at the latest in inflammation research. Scientists in Nice outlined a surprising contribution of the adaptive immune system in dampening Alzheimer’s pathology, supported by genetic findings and in vivo studies. Others debated what makes the brain’s microglia a force for good or ill. Controversy continued over the role of TREM2 and whether it is expressed by central or peripheral phagocytes. Meanwhile, speakers added to the evidence that TREM2’s effects on phagocytosis are crucial for ameliorating disease. For the full rundown, read Madolyn Rogers' final two stories from Nice.
Register by May 3 for the upcoming symposium on Mechanisms of Neurodegeneration hosted by the European Molecular Biology Laboratory (EMBL) to be held June 14-17 in Heidelberg, Germany. Find further details and instructions for registration at the meeting website.
- Isidro Ferrer on Accumulation of Basic Amino Acids at Mitochondria Dictates the Cytotoxicity of Aberrant Ubiquitin.
- Elizabeth Molnar on New Treatments for Alzheimer’s Behavioral Symptoms on Horizon
- Julie Harris, Lennart Mucke and Sumihiro Maeda on Propagation Blues? Reporter Expression Clouds Reports of Traveling Tau, Aβ
- Bradley Hyman on Propagation Blues? Reporter Expression Clouds Reports of Traveling Tau, Aβ
- Rockland Wiseman on Phosphatase Inhibitor Promotes Protein Folding, Helps ALS Mice
- Michael Sasner on Transgene expression in the Nop-tTA driver line is not inherently restricted to the entorhinal cortex.
- Lary Walker on Transgene expression in the Nop-tTA driver line is not inherently restricted to the entorhinal cortex.