Could Greasing the Wheels of Lipid Processing Treat Alzheimer’s?
Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.
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Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.
Long-term treatment with the anti-sense oligonucleotide led to motor benefits in an extension trial of children 2 to 15 years old.
Diagnostics Accelerator to fund projects that develop dementia biomarkers from patient data.
People who take leisurely walks, garden, and tackle household chores had bigger brains than those who were more sedentary. Vigorous exercise brought neither additional benefit nor harm.
By slipping human microglia inside the mouse brain, researchers hope to better monitor their response to pathologies, such as Aβ.
By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
At AD/PD 2019, scientists implicated both peripheral and central innate immunity in promoting propagation.
The global agency’s report recommends physical activity, a healthy diet, stopping alcohol abuse and smoking, and managing one’s weight, blood pressure, and diabetes.
Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
In a new, inducible mouse model, poly(GR) damages mitochondria, but its effect is reversible. In flies, turning off transcription of hexanucleotide expansion protects cells.
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? Drug Reported to Help Alzheimer’s Patients Sleep Better American Academy of Neurology 2019 Annual Meeting
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
Phase 1b data show that Biogen’s BIIB092 lowers N-terminal tau fragments in cerebrospinal fluid by more than 90 percent.