Researchers consider the data encouraging, though questions linger about the cognition results. Did regulators mess up the randomization of this trial?
By loosening their chromatin straitjackets, and reining in their RNA watchdogs, tau unleashes transposable elements into the genome.
Investors pledge new money for research into biomarkers that yield marketable tests.
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.
In knockouts that model the most severe form of Gaucher’s disease, replacing one gene calms neuroinflammation, reduces neurodegeneration, and extends lifespan.
Researchers found large deletions, inversions, or insertions in about one-fifth of edited cells, suggesting caution for therapeutic uses of the technology.
Blood from an old mouse ages the brain of a young one, but how? Researchers report that VCAM1 on brain endothelial cells facilitates the process.
At Keystone, researchers placed pathological tau on both sides of the synaptic cleft, along with complement proteins. Activated microglia gobbled up tau-laden neurons, and even may have facilitated tau’s spread in the brain.
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.
At Keystone, the work of several groups painted TREM2 as a dedicated supporter of microglial function across neurodegenerative disease models, including those for ALS.
Working with human microglia is fraught with technical challenges, but that didn’t stop researchers at Keystone from sharing a flurry of data on how these cells act in neurodegenerative disease.
Keystone Joint Symposia—Advances in Neurodegenerative Disease Research and Therapy / New Frontiers in Neuroinflammation: What Happens When CNS and Periphery Meet?
A Delicate Frontier: Human Microglia Focus of Attention at Keystone TREM2: Diehard Microglial Supporter, Consequences Be DAMed ApoE Has Hand in Alzheimer’s Beyond Aβ, Beyond the Brain Synaptic Tau Clangs the Dinner Bell for Hungry Microglia VCAM1: Gateway ...
Tiny yet mighty, small carbon structures glom onto and dissolve α-synuclein fibrils, neutralizing their toxicity in mouse models of Parkinson’s disease.
Better tissue extraction and Aβ assays could help identify the most toxic Aβ species and most promising immunotherapies.
An 856-patient, proof-of-concept trial of the anti-protofibril Aβ antibody suggests the highest dose slowed cognitive decline and cleared plaques.