Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.
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.
At a Keystone meeting, researchers agreed that ApoE stokes damaging neuroinflammation in response to tau pathology. The E4 allele ramped up cholesterol biosynthesis in microglia and astrocytes, and even promoted neuronal damage when expressed outside of the brain.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
Apolipoprotein E4 clearly plays a role in AD and could be a therapeutic target, but scientists are not sure whether they should raise or lower it in the brain...
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.
Institute to chart new translational research territory.
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.
As RNA Therapies Come of Age, Efficacy Remains Weak At AAN, Sights Set on Antisense Therapies for Diseases of the Brain New Alzheimer’s and Parkinson’s Immunotherapy Data at AAN Will RNA molecules that bump up or tamp down gene expression live up to their ...
A fleet of patient-derived neurons show that while an APP mutation shifts where γ-secretase takes its first bite, PS1 mutations blunt the enzyme’s second cut. Eventually, all mutations drive up the Aβ42:40 ratio.
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
Phase 1b data show that Biogen’s BIIB092 lowers N-terminal tau fragments in cerebrospinal fluid by more than 90 percent.