Human neurons expressing presenilin and APP mutations shuttled less cholesterol to axons; inhibiting β-secretase restored normal transport, hinting that APP C-terminal fragments may be involved.
At the 2nd Kloster Seeon meeting on BACE proteases, researchers linked BACE substrates to regulation of synaptic activity.
When the brain is starved of BIN1, endocytosis goes into overdrive. Vesicles gulp more tau aggregates into neurons, feeding their spread.
Two labs report that dipeptide repeats derived from C9ORF72 latch onto TDP43, FUS, and other proteins that form liquid organelles. The liquid then gels, retarding cellular functions.
Researchers at the Kloster Seeon meeting pressed in on the question of what are the physiological functions of this protease after development is complete.
Add Private note Add An editorial note At 2nd Kloster Seeon Meeting, Renewed Optimism for Targeting BACE1 What Exactly Does BACE Do in Adults? BACE Inhibition and the Synapse—Insights from Seeon Does BACE Drive Neurites into Dystrophy, Shorting Circuits? ...
When mixed with arachidonic acid, α-synuclein formed soluble multimers rather than toxic fibrils. Researchers speculate that these multimers represent the physiological norm in synaptic compartments.
Despite concerns over potential side effects, researchers seem more enthusiastic than ever about the prospect of treating Alzheimer’s with β-secretase inhibitors.
The mysterious protein made by the ALS/FTD-associated gene may regulate the actin filaments that physically support axons.
A worldwide perspective on causes of death and disability suggests age-standardized mortality due to Alzheimer’s disease fell 2.7 percent over 10 years, even as total deaths rose almost 40 percent.
Preserved brain networks may explain the exceptional memory prowess of some older adults.
The fragment crowds into synapses and may drag full-length tau along for the ride. Researchers proposed caspase-2 as a therapeutic target.
In aging rats, the presence of bacterial amyloid in the gut accelerated the formation of α-synuclein aggregates in brain.
Can sucking in a little extra drug tide patients over until their next dose?
The largest brain-imaging project in history has sliced and diced data from the first 5 percent of its cohort. Neurodegeneration scientists deplore the lack of AD biomarkers.