From Treadmills to Transcriptomes: Consortium Charts Molecular Responses to Exercise
First papers from MoTrPAC initiative report myriad responses to endurance training in multiple organs in rats, including the brain and heart.
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First papers from MoTrPAC initiative report myriad responses to endurance training in multiple organs in rats, including the brain and heart.
In the DIAN familial AD prevention trial, plaque-busting antibody gantenerumab, but not monomer-targeting solanezumab, nudged fluid markers toward normal.
Tauopathy cranks up lipid synthesis in neurons, which slip the fats to microglia. Blocking AMP kinase greases this process.
Amyloid precursor protein CTFs accumulate in lysosomes adjacent to endoplasmic reticulum. This disrupts calcium flow between the organelles.
Scientists find the senescent subtype has a distinct protein signature, but little change in gene expression, causing it to be overlooked in transcriptomic studies.
Lysosomes deliver a plethora of mRNA transcripts, including those encoding ribosomal subunits and mitochondrial proteins, to axonal terminals for translation.
In a small Phase 2 trial, the GLP-1 analogue lixisenatide stabilized motor abilities over one year in people with early PD.
In preliminary studies in five cohorts, the two markers have similar diagnostic accuracy, and stain tangles in postmortem brain equally well.
Two studies describe how small peptides that latch onto tau have an outsize impact on fibrillization of the protein. Both point to therapeutic strategies.
Preclinical studies and early phase trials target microglial receptors CD33 and TREM2, and amyloid-stoking ASC specks.
Reactive astrocytes spell trouble for synapses, while microglial transform from protective to destructive as disease progresses.
The addition of SUMO2 to tau prevents its phosphorylation and aggregation, preserving synapses and memory in tauopathy mouse models.
An antibody against the inhibitory receptor LILRB4 prevented its binding to ApoE. The upshot? Microglia engulfed more Aβ fibrils and plaque load fell.
Two antibodies—one against the phosphoprotein, the other to tau’s N-terminus—restored proteostasis in the brain.
At AD/PD, scientists presented small molecules that break up fibrils and antibodies that target pathogenic forms of α-synuclein or hinder spread in iPSCs and mice.
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