Next-Gen Antisense and Small Protein-Protein Disruptors Benefit SOD1 Models
Oligonucleotides that suppress SOD1, and small molecules that limit its binding to the protein Derlin-1, delay disease onset and extend lifespan in rodent models of ALS.
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Oligonucleotides that suppress SOD1, and small molecules that limit its binding to the protein Derlin-1, delay disease onset and extend lifespan in rodent models of ALS.
Investors pledge new money for research into biomarkers that yield marketable tests.
BAN2401 Removes Brain Amyloid, Possibly Slows Cognitive Decline On Target: Crenezumab Reduces Aβ Oligomers in CSF PET Ligand Lights Up AAIC, May Detect Synapse Loss in AD Could Better Blood Pressure Management Preserve Cognition? Focused Ultrasound Breach
In SPRINT MIND trial, strict control of systolic pressure slashed MCI incidence by almost 20 percent.
In mice, aggregates of oxidized SOD1 accumulated with age, and endoplasmic reticulum stress made it worse. Does this explain SOD1 aggregates found in spinal cords of patients with sporadic ALS?
Data from the first human study hints the procedure could help deliver drugs to the brain, or even work as a therapy in its own right. A flurry of animal studies presented at AAIC support the idea.
The acetylcholinesterase inhibitor failed to slow cognitive decline in people with both depression and mild cognitive impairment.
The drug, patisiran, targets messenger RNAs that cause transthyretin amyloidosis, a rare inherited neurodegenerative disease. Approval paves the way for other RNAi-based therapies.
A zinc-finger protein and a long noncoding RNA are now implicated in late-onset Alzheimer’s disease.
Sensitive cognitive tests detect deficits in preclinical Alzheimer’s even before an amyloid scan reads positive. And CSF Aβ42 drops a decade before that—pushing research ever farther into the preclinical phase.
At AAIC, competitors vied for advantage, and discussion moved swiftly to the issue of assay standardization.
At AAIC, technology improves on pen-and-paper tests of early cognitive decline. Think learning Chinese, think smartphone burst, think digital clock.
At AAIC, scientists said that alterations in how the aging female brain uses energy and metabolizes fat may leave APOE4 carriers particularly susceptible to tau pathology.
Greater lifetime estrogen exposure protects cognition, while hormone replacement therapy taken at menopause has no cognitive effects at all.
Data from two independent cohorts suggest that the risk to the brain from high blood pressure and cardiovascular disease begins in a person’s 40s or before.
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