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?
Can a little grease smooth the assembly of α-synuclein multimers? According to a new study, arachidonic acid—the most common fatty acid in the brain—cajoles α-synuclein to form α-helical-rich, soluble oligomers that are harmless to neurons. Without the fatty acid, α-synuclein forms toxic fibrils instead. The findings support growing evidence that α-synuclein can exist as a native tetramer, and make sense in light of recent studies that identified multimers of α-synuclein mingling with synaptic vesicle membranes, which house fatty acids.
Just when you thought the menagerie of tau species involved in neurodegenerative disease couldn’t get any larger, a new fragment—dubbed Δtau314—has arrived on the scene. Researchers report that caspase-2 generates the small, soluble fragment, which resists fibrillation yet winds up in dendritic spines. The fragment coaxes human full-length mutant tau to congregate at synapses as well, claim the authors, which leads to synaptic dysfunction and memory problems in mice. The fragment popped up in the brains of people with dementia, too. Researchers propose caspase-2 as a therapeutic target.
Researchers report a fresh line of evidence to bolster the hypothesis that microbes could initiate neurodegenerative disease. When aging rats swallowed E. coli that produce a type of bacterial amyloid, deposition of α-synuclein in the rat brains accelerated. Likewise, bacterial amyloid boosted α-synuclein deposits in transgenic worms. If the findings hold up in people, they would hint at new angles for the prevention and treatment of neurodegenerative disease.
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