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.
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 More than 700 participants hailing from 35 countries gathered in ...
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.
Variants in the gene cluster MS4A associate with levels of soluble TREM2 in human cerebrospinal fluid. MS4A encodes transmembrane receptors implicated in lipid sensing.
Microfluidic tri-culture of neurons, astrocytes, and microglia models how glia impose deadly neuroinflammation on top of amyloid and tau pathology.
The proinflammatory molecule binds to Aβ oligomers and fibrils and slows nucleation in vitro, hinting it could have beneficial effects in the early stages of AD.
Herpes viruses that are commonly found in human brain promote rapid Aβ fibrillization and deposition in AD model systems.
Get up close and personal with the GABAA receptor, a key mediator of inhibitory signaling in the brain and a drug target in a wide range of disorders, including Alzheimer’s.
Chronic inhibition of protein synthesis, and slowing the dispersal of stress granules, contribute to neurodegeneration in C9ORF72 ALS/FTD.
In healthy neurons, small vesicles at the presynapse and larger ones in neurites harbor Aβ42, according to super-resolution microscopy.
Males are inflammatory, females are neuroprotective: Profiling of microglia from adult mice suggests sex-specific phenotypes, likely set at birth.
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