Liquid Phase Transition: A Deluge of Data Points to Multiple Regulators
Transportins, methylation, and RNA all regulate LLPS and the behavior of pathogenic RNA-binding proteins.
Transportins, methylation, and RNA all regulate LLPS and the behavior of pathogenic RNA-binding proteins.
At AAT-AD/PD, scientists said an α-synuclein PET tracer is headed into trials. And marmosets model PD behaviors better than rodents. (Spoiler alert: They kick their partners while they sleep.)
Systemic inflammation can alter the epigenome of microglia, dictating whether the cells clean up Aβ pathology, or exacerbate it.
Massive meta-analysis finds no link with AD or PD.
Volunteers kept awake all night retained more florbetaben in their hippocampi and thalami in morning-after PET scan.
In animal models, a PD risk gene revs up the immune system to fight infections, while probiotic bacteria slow α-synuclein aggregation.
Researchers at AAT-AD/PD discussed investigational PD treatments that aim to modify disease by hitting genetic risk factors.
For the first time, NIA-AA proposal bases diagnosis in living people solely on biomarkers for plaques and tangles.
A raft of papers on liquid-liquid phase transition implicate nuclear import receptors, posttranslational modifications, and high RNA concentrations as physiological regulators of the process, which is intimately tied to neurodegeneration.
As you peruse Alzforum news from the AAT-AD/PD conference held last month in Turin, Italy, you may want to catch our three most recent stories on therapeutic approaches, microbial influences, and emerging research tools for Parkinson’s disease. Read the whole series, or download a PDF, for the latest on therapeutic tau antibodies, PET imaging, and blood biomarkers for Alzheimer’s disease, as well as a DIAN-ADNI data comparison and a story on the provocative idea that the incidence of AD is rising, not falling, as has been reported.
Bouts of systemic inflammation have long-lasting effects on microglia in the brain, according to a new study. Researchers reported that depending on how many times mice were injected with bacterial lipopolysaccharides, microglia either slowed the growth of Aβ plaques, or accelerated it. Exposure to systemic inflammation, and/or to Aβ pathology within the brain, influenced the epigenomes of microglia, in turn altering their gene-expression profiles and function.
Toppling the long-standing syndromic definition of AD, scientists now embrace a biologically based concept to diagnose Alzheimer’s disease in living people. Using biochemical tests and scans to detect pathologic protein accumulation, they separate the diagnosis from symptoms. The proposal marks a seismic shift away from distinct, clinically defined entities and toward a continuous disease process defined by its underlying pathophysiology. It is for research use only.
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