IFITM3 Forges Link Between Neuroinflammation and Aβ Production
The antiviral protein enhances γ-secretase processing of APP. More of it is present in Alzheimer’s disease.
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The antiviral protein enhances γ-secretase processing of APP. More of it is present in Alzheimer’s disease.
Carriers of a rare hypomorphic gene variant develop a frontotemporal dementia that features Alzheimer’s-like neurofibrillary tangles.
The first steps of endocytosis faltered in astrocytes expressing ApoE4, but pumping in PICALM reversed the problem. A new study places two Alzheimer’s risk factors into the same cellular mechanism.
The panel considered the evidence for efficacy to be weak, and was troubled by too-close collaboration between the sponsor and the FDA.
In a mouse model of cortical multiple sclerosis, microglia and monocytes swooped in to gobble up synapses when dendritic calcium rose. Spines grew back once inflammation subsided.
Two papers advance the drive to develop an Alzheimer's vaccine, one looking at the antibody response in some of the Elan trial participants, the other using sophisticated methods to analyze the epitope recognized by antibodies generated in response to Aβ42 immunization.
Learning tests may prove more informative in clinical trials of early AD. A new one claims it can spot a difference in six days.
In therapy-like paradigm, suppressing ApoE4 in astrocytes toned down tauopathy. This assuaged microglia, neurodegeneration, and revived nest-building.
Epidemiology study reveals 1.5-times higher risk of dementia after herpes virus infection. Short-term antiviral treatment appears to lower risk.
The first whole-genome manipulation of protein expression in neurons by CRISPR reveals a deadly chain of events. Bad processing by lysosomes leads to build-up of lipids and iron. Oxidative stress revs up. Neurons die by ferroptosis.
In this month’s Brain, researchers at the Universities of Milan and Genoa, Italy, report that immunizing C57/Bl6 mice with Aβ42 generated an inflammatory response similar to an autoimmune disease in the brains of these mice...
In tomorrow's Nature Medicine, Bruce Yankner at Children's Hospital in Boston offers up a partial explanation for one of the abiding questions in Parkinson's research: Why do neurons die in such a selective pattern?...
Despite its long and distinguished history in Alzheimer’s research, the microtubule-stabilizing protein tau still poses many a riddle to scientists. They do know that excessive phosphorylation of tau somehow figures in neurodegeneration...
randomized trial to test the feasibility of using the COX-2 inhibitor nimesulide as a chronic treatment in Alzheimer's patients...
The job description of presenilins (PS) in the business of neuron health and disease may be getting more complicated...