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.
In mice, rolofylline perks up neurons laid low by aggregates of tau.
Transgenic animals develop muscle weakness and paralysis similar to people with the disease.
The kinase prevents tau degradation, raising levels and kicking off hyperphosphorylation.
A mouse that expresses ApoE only in the blood loses synapses in the brain, but appears to learn and remember normally.
Discoverer of ApoE4 risk allele died of a heart attack.
Schenk loses two-year battle with pancreatic cancer.