Making deeper inroads into Alzheimer’s systems biology, groups of genes co-expressed in the cortex associated with clinical and pathological traits of the disease, notably the slope of cognitive decline.
New data suggest that the proteasome takes the first stab at dissolving these protein conglomerates, with autophagy coming in later to mop up.
Contradicting current opinion, a randomized trial made people stronger but, if anything, left their mental function weaker. What gives?
Antisense oligonucleotides are raising hopes for tackling a wide range of brain disorders—is the enthusiasm warranted?
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 ...
At AAN, the latest data from Phase 3 trials and open-label extensions of RNA-targeting therapies reveal a bit of benefit, but no cure.
Genetic adaptations that gave humans their smarts may promote diseases of aging, including cancer, Alzheimer’s, and Parkinson’s. One adaptation counteracted REST, a proposed protector against AD.
High vascular risk scores and Aβ burden independently associate with cognitive decline, but combined, they speed things up.
Prior evidence for protective effect evaporates after adjustment for demographic differences in high- and low-lithium communities.